# fs 2.: see fs(2)E # fs(1)-: female sterile on chromosome 1 There have been three concerted searches for female sterile mutations on the X chromosome. The first to be reported is that of Gans, Audit, and Masson (1975, Genetics 81: 683-704), the second is by Mohler (1977, Genetics 85: 259-72), the third is by Komitopoulou, Gans, Margaritis, Kafatos, and Mas- son (1983, Genetics 105: 897-920). These series of mutants are designated fs(1)A, fs(1)M, and fs(1)K respectively. In designating loci the order of priority is A>M1-M63>K; e.g., all alleles of mutants first recovered (Gans et al.) are designated fs(1)A-, and the nominate allele is the one with the lowest acquisition number; alleles found by Audit are num- bered, consecutively, alleles of Mohler are designated by the superscript M, and those by Komitopoulou by K. Allelism among these mutants has been incompletely tested; the number of loci is certainly lower than the tables indicate. In addition to these extensive searches there are other female sterile mutants whose designations are more ad hoc. # fs(1)5: see yl # fs(1)5e location: 1-37.5. origin: Induced by ethyl methanesulfonate. references: Perez-Chiesa, Cintron, and Morales, 1985, DIS 61: 215. phenotype: Homozygous females sterile; males fertile. 95% of heterozygous females are fertile when reared at 25, but only 5% are fertile when reared at 29, or when reared at 25 but shifted for three days to 29. Eggs produced are permeable to neutral red and burst when dechorionated in a 3% sodium hypo- chlorite solution. # Fs(1)10A location: 1-33.52. synonym: hfs: haplo female sterile. references: Lefevre, 1969, Genetics 63: 589-600. Zhimulev, Pokholkova, Bgatov, Semeshin, and Belyaeva, 1981, Chromosoma 82: 25-40. phenotype: Locus inferred from the infertility of females heterozygous for vermilion deficiencies. cytology: Placed in 10A8 by deficiency analysis; included in Df(1)v65b = Df(1)9F12-23;11A8-9 and Df(1)RA37 = Df(1)10A5-6;- 10B17-C1 but not Df(1)vL3 = Df(1)9F10;10A7-8 or Df(1)KA7 = Df(1)10A8-9;10F10. # fs(1)11 to fs(1)14: see otu # fs(1)29: see yl # fs(1)42 location: 1-13.3. origin: Induced by ethyl methanesulfonate. discoverer: Denell, 1971. references: Rizzo and King, 1977, J. Morphol. 152: 329-40 (fig.). phenotype: Viability and longevity normal. Oogenesis in homoz- ygous females proceeds through stage 8; chambers then degen- erate. Dying follicle cells seen in chambers at all positions in ovarioles; profolicle cells also die in germaria and clus- ters of cystocytes delayed in achieving full complement of covering follicle cells. Egg chambers in vitellarium contain about 60% the normal number of follicle cells; these have greater lateral dimensions, and their nuclei and nucleoli are larger than normal. Follicular envelope of mutant chambers often contains gaps through which projections from cystocytes protrude. # fs(1)117: see yl # fs(1)205: see yl # fs(1)209: see otu # fs(1)288 origin: Induced by ethyl methanesulfonate. references: Waring, DiOrio, and Hennen, 1983, Dev. Biol. 100: 452-63. cytology: Placed in 12A6-D3 based on its inclusion in Df(1)HA92 = Df(1)12A6-7;12D3. # fs(1)445: see yl # fs(1)1001: see otu # fs(1)1163: see Yp1ts1 # fs(1)1304b: see otu # fs(1)1396: see otu # fs(1)1401: see otu # fs(1)1867 location: 1-62.9 (0.4 cM to the right of car). origin: Induced with ethyl methanesulfonate. references: Wieschaus, 1979, Cell Lineage, Stem Cells, and Cell Determination (Le Douarine, ed.). Elsevier/North Holland Biomedical Press, pp. 291-302. Szabad and Szydonya, 1980, Development and Neurobiology of Drosophila (Siddiqui, Babu, Hall, and Hall, eds.). Plenum Press, New York, pp. 95-108. phenotype: Homozygotes and hemizygotes exhibit delayed develop- ment and Minute-like or missing bristles; eclosion delayed about four days compared to heterozygous sibs; gynandromorphs delayed in development in proportion to quantity and indepen- dent of the quality of fs(1)1867 tissue. Homozygous females sterile, never lay eggs; ovarioles develop normally until stage 10 after which degeneration and resorption occurs. Oocytes in fs(1)1867 ovaries transplanted into wild-type hosts unable to develp, but fs(1)1867 oocytes in wild-type ovaries do develop. fs(1)1867 follicle cells fail to become columnar; defect concluded to be follicular. # fs(1)4077: see otu # fs(1)A: female sterile of Audit A series of ethyl-methanesulfonate-induced sex-linked reces- sive female sterile mutations first reported by Gans, Audit, and Masson (1975, Genetics 81: 683-704). The mutants were apportioned to the following phenotypic classes: Class I - females produce few if any eggs; Class II - females produce morphologically abnormal eggs; and Class II - females lay numerous normal appearing eggs. Class III is subdivided into IIIA for cases where fertilization by a sperm carrying the normal allele of the mutant for which the mother is homozygous rescues the eggs and produces an offspring and IIIB in which a sperm bearing a normal allele is unable to effect rescue. All classes have been described briefly by Gans et al.; Class II mutants have been described in more detail by Komitopoulou, Gans, Margaritis, Kafatos, and Masson [1983, Genetics 105: 897-920 (fig.)], and Class IIIB by Zalokar, Audit, and Erk [1975, Dev. Biol. 47: 419-32 (fig.)]. Information on mapping, allelism, and phenotypic class of these mutant presented in following table followed by phenotypic descrip- tions from above references. genetic mutant location phenotype allelism ( cytology ____________________________________________________________ fs(1)A59 II 2A, 1K 8F-9A fs(1)A73 IIIB fs(1)Ya fs(1)A97 1-31 IIIB fs(1)A99 IIIA fs(1)A107 IIIA fs(1)A116 I otu fs(1)A117 II fs(1)A120 1-46.9 II 6A fs(1)A125 II t.s. fs(1)A147 1-0 II 2A, 3M 1B10-1E3 fs(1)A148 1-48 II yl 12E1-13A5 fs(1)A180 1-36 II t.s. fs(1)A214 1-38 IIIB 2A fs(1)A231 I otu fs(1)A248 I *fs(1)A265 I otu *fs(1)A267 II dec-1 fs(1)A273 1-65 Ii 1A, 1K, 1M 18E1-20A fs(1)A305 II yl fs(1)A321 II fs(1)A330 IIIB fs(1)A331 IIIB fs(1)332 II yl *fs(1)A336 II fs(1)A343 II fs(1)A1202 fs(1)A371 1-0.3 II fs(1)N 1E4-2B12 fs(1)A379 II fs(1)N fs(1)A383 1-62 IIIB 2A fs(1)A384 II dec-1 fs(1)A387 IIIA fs(1)A426 IIIB fs(1)A427 I fs(1)A436 IIIA fs(1)A456 ec-cv II 4F1-5A1 fs(1)A457 1-49 IIIA 1M 3A fs(1)A462 I t.s. fs(1)A473 ct-v II t.s. 7E-8A fs(1)A475 IIIA fs(1)A476 IIIA fs(1)A489 II fs(1)A1203 fs(1)A508 1-18 II 7C3-D1 or 5D6-6E1 fs(1)A543 I t.s. fs(1)A571 II fs(1)A1204 fs(1)A572 IIIB fs(1)A573 IIIB gd fs(1)A1001 I t.s. fs(1)A1010 II fs(1)A1024 IIIA fs(1)A1031 IIIB fs(1)A2142 fs(1)A1038 II fs(1)N fs(1)A1042 IIIB fs(1)A1057 I sn fs(1)A1059 II 1A, 1K 4F1-5A2 fs(1)A1061 II yl fs(1)A1071 IIIA r fs(1)A1074 IIIA fs(1)A1081 II yl fs(1)A1103 IIIB par fs(1)A1122 IIIB par fs(1)A1130 II yl fs(1)A1140 1-62 IIIB fs(1)A1145 I t.s. fs(1)A2482 fs(1)A1162 IIIB fs(1)A3832 fs(1)A1168 IIIB fs(1)A4572 fs(1)A1182 IIIB mh fs(1)A1186 II yl fs(1)A1187 IIIB fs(1)A1190 II fs(1)A1205 fs(1)A1198 II fs(1)A1206 fs(1)A1203 IIIB fs(1)A4573 fs(1)A1242 1-26 IIIB 7E-8A fs(1)A1245 I fs(1)A1246 I fs(1)A12452 fs(1)A1248 I fs(1)A12453 fs(1)A1268 II fs(1)A1304 1-19 I fs(1)A1336 II dec-1 fs(1)A1361 IIIA r fs(1)A1369 II fs(1)A1472 fs(1)A1371 1-9 IIIB 3K, 1M fs(1)A1456 IIIA t.s. fs(1)h fs(1)A1459 v-f IIIB 2M fs(1)A1497 1-13.7 IIIB swa fs(1)A1501 1-20.7 II dec-1 fs(1)A1502 IIIB swa fs(1)A1509 IIIB fs(1)A1526 IIIB fs(1)A1528 IIIB fs(1)A1559 IIIA fs(1)A1561 ct-v II 9B-C fs(1)A1569 I t.s. lz fs(1)A1578 1-55 IIIB fs(1)A1621 1-11.7 I liz; snf 4F1-5A1 fs(1)A1630 IIIA rA3 ( Mutants allelic to previously recognized or more recently renamed loci are listed as alleles of those loci. For newly recognized loci the numbers of subsequently identified alleles in the A, K, and M series are indicated. # fs(1)A59 phenotype: Eggs show limited flaccidity; chorion with slightly shortened dorsal appendages. Mosaic analysis with fs(1)A59K1 shows normal allele to function in somatic tissue (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)A97 phenotype: Homozygous females sterile at 29 but not 16. Pro- duce haploid embryos at 29 which form abnormal blastoderms. # fs(1)A99 phenotype: Cold sensitive; death occurs during larval stage; normal development at 29. # fs(1)A107 phenotype: Development ceases late in embryogenesis. # fs(1)A117 phenotype: Embryogenesis arrested at various stages; low fecun- dity. # fs(1)A120 phenotype: Embryogenesis arrested at various stages; dependent on culture medium. Somatic-cell-specific function (Wieschaus, Audit, and Masson, 1981, Dev. Biol. 88: 92-103). # fs(1)A125 phenotype: Low fecundity; dorsal appendages fused; partially fertile at 16 and 23. # fs(1)A147 phenotype: No initiation of development; fine structure of chorion normal. # fs(1)A180 phenotype: Fertile at 16 and 23. Mosaic analysis suggests that normal allele functions in somatic tissue (Wieschaus, Audit, and Masson, 1981, Dev. Biol. 88: 92-103). Chorion ultras- tructure normal (Komitopoulou, Gans, Margaritis, Kafatos and Masson, 1983, Genetics 105: 897-920). # fs(1)A214 phenotype: No evidence of cleavage; Feulgen-positive material accumulates during first two hr. No evidence that fertiliza- tion takes place regularly. (Figured by Zalokar, Audit, and Erk, 1975, Dev. Biol. 47: 419-32). fs(1)A2142 fertile at 16 but not 29. # fs(1)A248 phenotype: Adult phenotype normal but females retain eggs. fs(1)A2482- females fertile at 16. # fs(1)A273 phenotype: Chorion appendages of fs(a)A273K1 females show abnormal size and shape. About 5% of eggs produce adults. Mosaic results ambiguous (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)A321 phenotype: Homozygous females have short bristles; lay flaccid eggs. # fs(1)A330 phenotype: Time of developmental failure varies - at fertiliza- tion, blastoderm formation, gastrulation, or in embryo. Such development as does occur is abnormal. # fs(1)A331 phenotype: Various times of developmental arrest. # fs(1)A383 phenotype: Embryos apparently normal but few larvae hatch. Many eggs of fs(1)A3832 females cease mitosis during first hour, forming a few polyploid nuclei; others reach blastoderm which displays a peculiar mosaicism of an area with large swollen nuclei sharply separated by a line of pycnotic nuclei from an area with nuclei having more condensed chromatin. Occasionally two such areas in succession divided by lines girdling egg. Preblastoderm mitoses diploid and synchronous. # fs(1)A387 phenotype: Embryos fail late in development; some rescue by fertilization with sperm carrying normal allele. # fs(1)A426 phenotype: Embryonic development arrested at various times dur- ing development at 29; some adult survival at 16. # fs(1)A427 phenotype: Phenotype of adults normal, but females retain eggs. # fs(1)A436 phenotype: Development fails at advanced stage of embryo- genesis. Rescue effected by fertilization with sperm carrying normal allele. # fs(1)A456 phenotype: Mosaic analysis shows normal allele to function in somatic tissue. Chorion ultrastructure normal (Komitopoulou, Gans, Margaritis, Kafatos, and Masson, 1983, Genetics 100: 897-920). # fs(1)A457 phenotype: Haploid development to abnormal blastoderm or gas- trula stages. Nuclei smaller than normal and their numbers in blastoderm may exceed 10,000. In at least one case a Y chro- mosome was seen suggesting proliferation of paternal pronu- cleus. Few develop to late embryonic stages. # fs(1)A462 phenotype: Adults normal but females retain eggs; partially fertile at 16. Clones of homozygous germinal cells in hetero- zygous female produce oviposited eggs (Wieschaus, Audit, and Masson, 1981, Dev. Biol. 88: 92-103). # fs(1)A473 phenotype: Eggs partially devoid of chorion; females fertile at 16 and 23. Mosaic studies show gene function to be specific to soma (Wieschaus, Audit, and Masson, 1981, Dev. Biol. 88: 92-103; Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)A475 phenotype: Mutant females lay eggs at 23 but not at 29. Fer- tilization with sperm carrying normal allele produces some progeny at 23. # fs(1)A476 phenotype: Development arrested in late embryo; rescue occurs with sperm carrying normal allele. # fs(1)A508 phenotype: Adults display twisted bristles and delayed develop- ment. Eggs produced by homozygous females vary in size, often smaller than normal. # fs(1)A543 phenotype: Adults have short wings; homozygous females retain eggs at 29 but are fertile at 16. # fs(1)A572 phenotype: Early blastoderm apparently normal; later at nuclear elongation nuclei appear constricted and some forced out of peripheral layer and into deeper regions of the egg. Exces- sive numbers of blastoderm nuclei (>10,000), but not due to haploidy. Gastrulation appears normal; development arrested at time of first muscular contractions. Difficulties of nuclear separation in early cleavage stages observed. # fs(1)A1001 phenotype: Adults normal in appearance. Females retain eggs but are partially fertile at 16. Mosaic results at 29 indi- cate mutant interferes with somatic function of normal allele. # fs(1)A1010 phenotype: Development arrested in second and third cleavage; in metaphase, excessive numbers of punctiform and filamentous chromosomes; spindles appear normal. A few escapers appear at 16-18; many are agametic. # fs(1)A1024 phenotype: Offspring of homozygous mothers usually die in late pupal stages; about 30% escapers have unexpanded wings and die within a few days of eclosion. # fs(1)A1042 phenotype: Development arrested in second and third cleavage; in metaphase, excessive numbers of punctiform and filamentous chromosomes; spindles appear normal. A few escapers appear at 16-18; many are agametic. # fs(1)A1059 phenotype: Egg development and chorion morphology of fs(1)A1059K1 females at 19 normal. At 29 chorion resembles that of previously identified chorion-protein-gene- amplification-defective mutants [fs(1)K451 and fs(1)K1214]. At 29 follicle cells show at least a three-to-five-fold suppression of amplification of the chorion-protein genes on both the X and third chromosomes compared to 24 (Komitopoulou, Kouyanou, and Kafatos, 1986, Dev. Genet. 7: 75-80). alleles: Although not explicitly stated, it seems that lack of complementation has been demonstrated in the following combi- nations: fs(1)A10591/fs(1)A1059K1 (Komitopoulou), fs(1)A10592/fs(1)A1059M1, and fs(1)A1059K1/fs(1)A1059M1 (Mohler). allele origin synonym ref ( __________________________________________ fs(1)A10591 EMS 1 fs(1)A10592 EMS fs(1)A1371 1 fs(1)A1059K1 EMS fs(1)K575 2 fs(1)A1059M1 EMS fs(1)M60 3 ( 1 = Gans, Audit and Masson, 1975, Genetics 81: 683-704; 2 = Komitopoulou, Gans, Margaritis, Kafatos, and Masson, 1983, Genetics 105: 897-920; 3 = Mohler and Carroll, 1984, DIS 60: 236-41; # fs(1)A1074 phenotype: At 29 eggs fail to develop; at 23 development ceases during embryogenesis or larval or even pupal stages. Some rescue at 23 by fertilization with sperm carrying the normal allele. # fs(1)A1140 phenotype: Preblastoderm formed more or less normally, but nuclei irregularly placed within periplasm; many polyploid mitoses. Gastrulation abnormal; death precedes onset of mus- cular movement. # fs(1)A1187 phenotype: Homozygous females fertile at 16 but not at 29. Blastoderm abnormal containing haploid nuclei. # fs(1)A1242 phenotype: Eggs arrest after a few nuclear divisions; have polyploid groups of chromosomes or deeply stained masses of chromatin. Mosaic studies indicate germ-line function of nor- mal allele (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)A1245 phenotype: Viability reduced when raised at 29 and development delayed 1-3 days depending on allele. Oogenesis normal until stage 11-12 of King [stage 9 for fs(1)A12453]. Appendages of chorion absent. Mosaic analysis using fs(1)A12452 suggest germ line function of gene (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)A1304 phenotype: Most egg chambers of homozygous females degenerate after King stage 6; a few cysts escape to produce stage 14 oocytes which are retained in the ovariole. Vitellogeneis severely inhibited and uptake of protein from the hemolymph apparently impaired. (Khipple Mulligan and Rasch, 1980, J. Exp. Zool. 212: 343-54). Nucleoli of nurse cells morphologi- cally aberrant (Khipple Mulligan and King, 1976, Int. J. Insect. Morphol. Embryol. 5: 127-35). Oocytes grow at reduced rate and become covered by multiple layers of follicle cells, which secrete abnormal egg coverings (Khipple Mulligan and King). Phenotype insensitive to ecdysone administration and pole-cell-transplantation in studies by Lamnissou and Galti-Douka (1986, Dev. Genet. 6: 239-46), (Khipple Mulligan and Rasch). Mosaic studies by Wieschaus, Audit, and Masson (1981, Dev. Biol. 88: 92-103) indicate that the gene func- tions in the germ line, presumably in the nurse cells. # fs(1)A1371 phenotype: Homozygous females produce few offspring at 29; at 16 nuclei begin to degenerate in preblastoderm stage leading to irregular blastoderm and irregular gastrula. Claimed to be an allele of fs(1)1059K1 and fs(1)1059M1 by Mohler and Carroll (1984, DIS 60: 236-41) but phenotype is not concordant with such a claim. # fs(1)A1459 phenotype: Homozygous females produce progeny at 16 but not at 29. Blastoderm develops normally at 29, but at nuclear elon- gation stage, nuclei move irregularly from surface into peri- plasm; nuclei degenerate, cell wall formation irregular. # fs(1)A1509 phenotype: Blastoderm and early gastrulation normal; orifice of midgut remains widely separated from cephalic furrow, inter- vening space filled with yolky ooplasm covered with a layer of flat epithelium; area may subsequently evert exposing internal organs. Cyst-like diverticles formed within embryo. Develop- mental arrest at time of first muscular contractions. Primary defect is failure of germ band elongation. # fs(1)A1526 phenotype: Few nuclear divisions resulting in polyploid groups of chromosomes or in deeply stained masses of chromatin. # fs(1)A1528 phenotype: Most eggs remain unfertilized. # fs(1)A1559 phenotype: Developmental arrest in late embryo; a few larvae hatch. # fs(1)A1561 phenotype: Mosaic studies indicate somatic function of normal allele (Perrimon and Gans, 1981, Dev. Biol. 100: 365-73). # fs(1)A1578 phenotype: Most eggs remain unfertilized. # fs(1)A1621 location: 1-11.7. origin: Induced with ethyl methanesulfonate. synonym: liz; snf. references: Gans, Audit, and Masson, 1975, Genetics 81: 683- 704. Gollin and King, 1981, Dev. Genet 2: 203-18. Wieschaus, Audit, and Masson, 1981, Dev. Biol. 88: 92-103. Perrimon and Gans, 1983, Dev. Biol. 100: 365-73. Steinmann-Zwicky and Nothiger, 1985, Cell 42: 877-87. Cline, 1988, Genetics 119: 829-62 Oliver, Perrimon, and Mahowald, 1988, Genetics 120: 159-71. Steinmann-Zwicky, 1988, EMBO J. 7: 3889-98. phenotype: Homozygous females viable but semisterile; males normal. Young females produce ova which can be fertilized and develop normally into adults. Older females cease production of oocytes, producing at first only pseudo nurse cells and subsequently tumorous germaria containing hundreds or thousands of cells of apparently germinal origin. Tumoro- genesis takes place earlier at higher temperatures. fs(1)A1621/Df(1)C159 hemizygous for mutant; more temperature sensitive; the germ-line phenotype more severe than in homozy- gote but viability seems unaffected (Gollin and King). Mosaic studies suggest that gene function is germ line autonomous (Wieschaus et al.; Perrimon and Gans); however, the leakiness of the mutant phenotype introduced an element of ambiguity, raising the possibility of a somatic contribution to oogenesis as well. Interactions with Sxl alleles studied by Cline (1989), Steinmann-Zwicky (1988), and Oliver et al. (1988). Fertility of fs(1)A1621 homozygotes is rescued by the presence of SxlM1. Trans heterozygotes of fs(1)A1621 or Df(1)HC244 with Sxlf1 show very low viability when fs(1)A1621 is inher- ited from the female; survivors are sterile and show patchy transformations to maleness, such as sex-comb bristles and pigmentation of tergites 5 and 6. Viability of heterozygotes produced by the reciprocal cross also reduced but less so; surviving heterozygotes display reduced fertility. Viability effects appear to arise mostly from a maternal effect of the gene, whereas masculinizing and sterility effects result from decreased zygotic expression. The maternal effect of fs(1)A1621 also reduces survival of Sxlf1/+ daughters; sur- vival is cold sensitive. The presense of SxlM1 rescues fs(1)A1621/Sxlf1 females; Df(1)HC244, SxlM1/Sxlf1 are viable and fertile without male transformations. SxlM1 is also able to rescue Sxlf1/+ from the maternal effect of fs(1)A1621/+, and fs(1)A1621 is able to rescue male viability and fertility of SxlM1 in fs(1)A1621 SxlM1 double mutants. In contrast to the sis genes, which also interact with Sxl, the zygotic dose of fs(1)A1621 has little or no influence on the sexual pheno- type of 2X;3A animals; moreover, fs(1)A1621 interacts little if at all with sis-a. Thus although fs(1)A1621+ clearly has a positive involvement in Sxl+ functions, its precise placement in the sex determination hierarchy is currently unclear. It has been suggested that it is involved in the positive autore- gulatory aspect of Sxl function that maintains female develop- ment. Females heterozygous for fs(1)A1621 and either ovoD1, ovoD2, or ovoD3 have ovarian tumors (Oliver, Pauli, and Mahowald, 1990, Genetics 125: 535-50). cytology: Placed in 4F7-12 based on its inferred inclusion in Df(1)HC244 = Df(1)3E8;4F11-12 but not Df(1)A113 = Df(1)3D6;4F7-8 (Steinmann-Zwicky, and Nothiger, 1985; Cline, 1988). # fs(1)BP location: 1-32.67. discoverer: Bgatov. phenotype: Adults normal; fertility lesion not characterized. alleles: Six; fs(1)BP1 to fs(1)BP6 isolated as F58, F129, F403, F417, F456, and F469, respectively. cytology: Placed in 9F3-5 based on inclusion in Df(1)HC133 = Df(1)9B9-10;9F2-5 but not Df(1)ras-P14 = Df(1)9E1-2;9F3-4 (Zhimulev, Pokholkova, Bgatov, Umbetova, Solovjeva, Khudyakov, and Belyaeva, 1987, Biol. Zentralbl. 106: 699-720; 1987, DIS 66: 194-97). # fs(1)cor-36: see Cp-36n1 # fs(1)C A small series of ethyl-methanesulfonate induced mutants produced and partially characterized by D. Mohler and A. Car- roll (1984, DIS 60: 236-41). mutant location synonym phenotype cytology ____________________________________________________________________ fs(1)C1 dec-1 7C1 fs(1)C2 dec-2 7E10-8A5 fs(1)C3 cv-v no eggs laid; chorion thin 8B-C with short appendages fs(1)C4 cv-v no eggs laid; thin chorion disorganized ovaries fs(1)C5 cv-v no eggs laid; thin chorion disorganized ovaries fs(1)C6 cv-v no eggs laid; thin chorion disorganized ovaries # fs(1)de: female sterile (1) defective eggs A subset of hybrid-dysgenesis-induced, X-linked female- sterile mutations that are characterized by the production of morphologically abnormal eggs that fail to hatch [Orr, Galano- poulos, Romano, and Kafatos, 1989, Genetics 122: 847-58 (fig.); see also Galanopoulos, Orr, Szabad and Kafatos, 1989, Dev. Genet. 10: 87-97 (fig.)]. The loci are numbered from 1 through 17 with alleles of fs(1)de1 designated by lower case letters in the superscript. The X chromosomes in these lines harbor multiple P elements, thus complicating cytological localization. No case of allelism with previously identified sex-linked female sterile mutations and one case of allelism to a known lethal mutation in the BRC detected. Various defects in respiratory appendages and chorionic architecture described in above references. number locus location of alleles comments _________________________________________________________ fs(1)de1 near cv 7 germ line dependent fs(1)de2 f-car 1 fs(1)de3 near car fs(1)de4 double mutant? fs(1)de5 f-car 1 fs(1)de6 m-f fs(1)de7 near car fs(1)de8 f-car 1 fs(1)de9 near car 1 fs(1)de10 m-f 1 germ line dependent fs(1)de11 ct-m 1 fs(1)de12 sc-ec 1 nprfs; soma dependent fs(1)de13 m-f fs(1)de14 m-f fs(1)de15 near car fs(1)de16 m-f fs(1)de17 f-car 1 germ line dependent # fs(1)h: female sterile (1) homeotic location: 1-21.65 (0.05 cM to the left of mys). synonym: l(1)7Da; fsh. references: Gans, Audit, and Masson, 1975, Genetics 81: 683- 704. Zalokar, Audit, and Erk, 1975, Dev. Biol. 47: 419-32 (fig.). Gans, Forquignon, and Masson, 1980, Genetics 96: 887-902. Forquignon, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 132- 38. Digan, Haynes, Mozer, Dawid, Forquignon, and Gans, 1986, Dev. Biol. 114: 161-69. phenotype: Many mutant alleles at this locus are nonconditional lethals, but there are three temperature-sensitive hypomorphic alleles. fs(1)h1 is the weakest of these and many of the phenotypic studies have been carried out on it and on Df(1)C128, which is deficient for the locus. Temperature- sensitive genotypes display two periods of sensitivity to elevated temperature; one is during oogenesis and affects embryonic development and the other is during the pupal stage and affects adult survival. Adult survival of fs(1)h1 homozy- gotes and fs(1)h1/Df(1)C128 heterozygotes is normal at 20 and 25, but 10% and 0 respectively at 28.5. As mentioned above, the TSP for lethality is the pupal stage. fs(1)h15 shown to be lethal in germ-line clones (Perrimon, Engstrom, and Mahowald, 1984a, Dev. Biol. 105: 404-14). Fertility of fs(1)h homozygotes and fs(1)h/Df(1)C128 temperature sensitive with the former becoming completely sterile at 29 and the latter at 25; temperature-sensitive periods for fs(1)h/Df(1)C128 females during pregastrulation embryogenesis and perhaps late oogenesis. Eggs laid at restrictive tempera- tures exhibited normal preblastoderm development, although about half the nuclei are haploid; nuclear behavior during blastoderm formation disrupted and development arrested in blastoderm or early gastrulation. Larvae and adults surviving semi-permissive temperatures display homeotic anomalies; dead embryos, and newly hatched larvae frequently have missing thoracic and anterior abdominal segments; surviving adults exhibit a sex ratio skewed in favor of males and frequently show missing halteres and less frequently third legs; effects are more severe in progeny of fs(1)h/Df(1)C128 than homozygous fs(1)h females, in daughters than sons, and at 25 than 23; small areas of homeotic transformations of anterior metathora- cic to anterior mesothoracic structures also seen. The mater- nal effect of fs(1)h interacts synergistically with Ubx130, Df(3R)red, and trx, but not bx3 or pbx. alleles: Most alleles are nonconditional lethals; fine struc- ture mapping places two nonconditional alleles tested distal to the three tested conditional alleles. Relative strengths of the mutant alleles estimated as follows: Df(1)C128 = fs(1)h5 = fs(1)h4 > fs(1)h18 > fs(1)h3 > fs(1)h8 > fs(1)h17 > fs(1)h2 > fs(1)h6 > fs(1)h1, the last three being conditional. allele origin discoverer synonym ref ( comments | _________________________________________________________________________ fs(1)h1 EMS fs(1)A1456 3 temperature sensitive fs(1)h2 EMS 1 temperature sensitive fs(1)h3 EMS 1 fs(1)h4 EMS 1 8 kb insert in 38.4 to 38.9 kb fs(1)h5 HD l(1)R10.4 1 Inversion and deletion fs(1)h6 EMS fs(1)M16, fshM 6, 7 temperature sensitive fs(1)h7 X ray Lefevre l(1)HF339 4 T(1;3)7D;75C-D1 fs(1)h8 X ray Lefevre l(1)N72 4 T(1;3)7D3-4;61F; breakpoint in 43.1 to 46.8 kb fs(1)h9 X ray Lefevre l(1)RA50 4 In(1)7D3;18E5-F1 fs(1)h10 X ray Lefevre l(1)RF29 4 T(1;2;3)3D3-4; 7D3-6;41;93F fs(1)h11 EMS Lefevre l(1)DA548 5 fs(1)h12 EMS Lefevre l(1)DF911 5 fs(1)h13 EMS Lefevre l(1)EF422 5 fs(1)h14 EMS Lefevre l(1)EF491 5 In(1)7C9-D1;20 fs(1)h15 EMS Lefevre l(1)VA75 5 fs(1)h16 EMS Lefevre l(1)VE728 5 fs(1)h17 spont Schalet l(1)16-18, fshS 8 copia-like insert in 45.4 to 47.8 kb fs(1)h18 HD l(1)26/62A, fshE 2 two copies of 37 to 47 kb in tandem sepa- rated by 0.8 kb ( 1 = Digan, Haynes, Mozer, Dawid, Forquignoni, and Gans, 1986, Dev. Biol. 114: 161-69; 2 = Eeken, Sobels, Hyland, and Schalet, 1985, Mutat. Res. 150: 261-75; 3 = Gans, Audit, and Masson, 1975, Genetics 81: 683-704; 4 = Lefevre, 1981, Genetics 99: 461-80; 5 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 6 = Mohler, 1975, Genetics 85: 259- 72; 7 = Mohler and Carroll, 1984, DIS 60: 236-41; 8 = Schalet, 1986, Mutat. Res. 163: 115-44. | Origin of molecular coordinates a SacI site just proximal to the proximal breakpoint of Df(1)C128 = Df(1)7D1;7D5-6, positive values to the left. cytology: Localized to 7D1-5 based on its inclusion in Df(1)C128 = Df(1)7D1;7D5-6. molecular biology: Region cloned in an 120 bp chromosome walk from a genomic clone shown to be deleted by Df(1)C128. South- ern blots identify lesions associated with four alleles, which map to positions 39 to 51 kb distal to the proximal breakpoint of Df(1)C128. Poly(A)+RNAs migrating as a doublet at 7.6 kb and a band at 5.9 kb are transcribed from this region in ovaries; these transcripts are present in 0 to 4 h embryos but are not detectable at later stages. During pupal stages a 2.4 kb transcript is detected. The largest RNAs are derived from a 20-kb chromosomal region encompassing the sites of all mapped fs(1)h alleles. The fs(1)h transcription unit is less that 500 base pairs distal to that of mys. # fs(1)K10 location: 1-0.5 (based on 191 recombinants between y and w). origin: Induced by ethyl methanesulfonate. references: Wieschaus, Marsh, and Gehring, 1978, Wilhelm Roux's Arch. Dev. Biol. 184: 75-82 (fig.). Wieschaus, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York and London, pp. 89-94 (fig.). phenotype: Homozygous females lay eggs with hyperplasia of the anterior chorionic appendages to form a collar around the micropile. Pole-cell-transplantation studies demonstrate chorionic phenotype to depend on germ-line genotype; pattern of overlying follicle cells apparently depends on cues from oocyte. In situ hybridization and antibody staining indicate that expression is confined to the primary oocyte and that the protein product is sequestered in the oocyte nucleus (Prost, Deryckere, Roos, Haenlin, Pantesco, and Mohier, 1988, Genes Dev. 2: 891-900). Eggs of mutant females seldom fertilized; those that are exhibit abnormalities of gastrulation with the anterior ends showing dorsal patterns of development both ven- trally and literally. Some larvae produced with dorsal cuticu- lar pattern covering entire circumference; last few segments have normal ventral hypoderm pattern. Ventralizing mutants grk and top both epistatic to the dorsalizing effects of fs(1)K10 (Schupbach, 1987, Cell 49: 699-707). Germ-line mosa- ics produced by mitotic exchange indicate fs(1)K10 activity required during oogenesis (Marsh, Wieschaus, and Gehring, 1976, Experientia 32: 803). Ovarian clones of homozygous cells useful in investigating kinetics of oogenesis (Wieschaus and Szabad, 1979, Dev. Biol. 68: 29-46). alleles: Four ethyl-methanesulfonate-induced alleles; fs(1)K101 isolated by Wieschaus et al. (1978); fs(1)K102, fs(1)K103, and fs(1)K104 isolated as fs(1)M9 by Mohler (Mohler, and Car- roll, 1984, DIS 60: 236-41). cytology: Placed 2E2-F1 based on its being deleted by Df(1)278 = Df(1)2E2-F3;3A5-B4 but not Df(1)2F1;3A4. (Perrimon, Engstrom, and Mahowald, 1984, Genetics 108: 559-72). molecular biology: Region cloned in a 200-kb chromosomal walk initiated from cloned sequences from microdissected polytene region 2E2-F1 (Haenlin, Steller, Pirrotta and Mohier, 1985, Cell 40: 827-37). fs(1)K10 mutants rescuable by transforma- tion with a 5-kb sequence. This sequence detects mRNA molecules of four different sizes on Northern blots; all have apparently the same initiation sites; species of 3.1 and 2.8 kb have different polyadenylation sites and both have had an 854-bp intron removed; a 4.0-kb species retains the intron and has the same polyadenylation site as the 3.1 kb molecule; a low-abundance mRNA of 6.0 kb retains the intron and extends beyond the known polyadenylation sites. The 3.1 and 2.8 mes- sages are expressed in the ovaries and early embryos; the two larger transcripts are more generally expressed. Transcrip- tion from left to right (Haenlin, Roos, Cassab, and Mohier, 1987, EMBO J. 6: 801-07). Sequencing of cDNA clones yields a conceptual polypeptide of 463 amino acid residues of 51.5 kd and an isoelectric point of pH 11.2; the molecule has three domains: the amino terminal domain up to residue 225 contains seven eight-residue repeats with consensus sequence GlnGlnGlnHisProSerPro and variants thereof; the middle domain of ca. 112 amino acids is apolar, containing 37% proline; the carboxyterminus contains a helix-turn-helix motif in residues 390-418 (Prost et al.). # fs(1)K79-fs(1)K1563: Female sterile of Komitopoulou A series of ethyl-methanesulfonate-induced, sex-linked- recessive female-sterile mutants reported by Komitopoulou, Gans, Margaritis, Kafatos, and Masson (1983, Genetics 105: 897-920). The same classification scheme as used in the fs(1)A series was employed for fs(1)K mutants. Only class II mutants have been characterized. Information on mapping, allelism, and phenotypic class are presented in the accompany- ing table; additional phenotypic description follows the table. genetic mutant location phenotype allelism ( cytology ____________________________________________________________ fs(1)K79 II 8E-9B1 fs(1)K93 near sc II 3C4-11 fs(1)K155 ovo fs(1)K163 near ct II fs(1)K184 II yl fs(1)K254 1-17 II t.s. 5D5-E1 fs(1)K294 II yl fs(1)K313 II fs(1)A59K1 fs(1)K418 II sn fs(1)K451 near g II 12A6-D3 fs(1)K467 II dec-1 fs(1)K473 II sn fs(1)K499 II fs(1)A1459K1 fs(1)K524 I fs(1)K575 II t.s. fs(1)A1059K1 4F-5A2 fs(1)K621 II yl fs(1)K646 1-15 II fs(1)M3K1 5C5-D6 fs(1)K718 II dec-1 fs(1)K741 cv-ct I t.s. 5D-6E fs(1)K743 II sn *fs(1)K811 II fs(1)K1075 II fs(1)A273K1 fs(1)K1090 II dec-1 fs(1)K1124 II dec-1 fs(1)K1103 ovo fs(1)K1134 I fs(1)K1193 rt. of g II fs(1)K1214 1-18.17 II 5D5-E1 fs(1)K1221 I fs(1)K1232 II dec-1 fs(1)K1237 ovo fs(1)K1274 I t.s. fs(1)K1281 II fs(1)N fs(1)K1347 II fs(1)N fs(1)K1421 II sn fs(1)K1511 II dec-1 fs(1)K1540 II fs(1)N fs(1)K1563 1-44.7 II t.s. 12D3-E1 ( Mutants allelic to previously recognized or more recently renamed loci are listed as alleles of those loci. # fs(1)K79 phenotype: Actually fs(1)K79 females, either homozygous or hem- izygous, are fertile, but their eggs display short and fragile dorsal appendages. # fs(1)K93 phenotype: Homozygous females produce flaccid eggs, which readily take up neutral red. # fs(1)K163 phenotype: Survival severely reduced and development delayed; wings short and thin. Eggs of homozygous females flaccid; embryogenesis blocked at various stages; rescue effected by sperm carrying normal allele. # fs(1)K254 phenotype: Pupal lethal at 29; female survival reduced at 23 and 25. Female fertility reduced at 23 and abolished at 25 and 29. Eggs of homozygous females have short thin dorsal appendages; ultrastructure of chorion abnormal; chorion defects not temperature sensitive. Mosaic analysis shows gene to function in somatic tissue (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)K451 phenotype: Reduced viability, especially of females; abnormali- ties of posterior legs, also especially in females. fs(1)K451/Df(1)g-l does not survive. Homozygous females pro- duce eggs with short thin dorsal appendages and ultrastructur- ally defective chorions. All major chorion proteins underpro- duced owing to failure of chorion protein gene amplification. Cp genes on the third chromosome more severely affected than those on the X (Orr, Komitopoulou, and Kafatos, 1984, Proc. Nat. Acad. Sci. USA 81: 3773-77). In mosaic experiments fs(1)K451 behaves as a locus required in both somatic and ger- minal tissues (Perrimon and Gans, 1983, Dev. Biol. 100: 365- 73). # fs(1)K524 phenotype: At 29 eyes rugose and bristles short and fine; abdominal etching as well at 20. Ovaries extremely atrophied, resembling ovaries without germ cells; however, occasional stage 14 cysts encountered. # fs(1)K741 phenotype: Viability good; ovaries atrophied at 29. Female fertile at 23. #*fs(1)K811 phenotype: Low fecundity; dorsal appendages of chorion may be fused; chorion ultrastructurally normal. # fs(1)K1134 phenotype: Follicular development arrested at stage 8; transformation of larval to adult fat body appears to be blocked. May be a juvenile hormone deficiency. # fs(1)K1193 phenotype: Viability normal; homozygous females produce some- what flaccid eggs. Development rarely proceeds to pupal stage. Mosaic studies indicate that gene functions in germ line (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)K1214 phenotype: Viability and fecundity of homozygous females reduced; sterility virtually complete, but a few progeny escape. Dorsal appendages of chorion short and thin. All major chorion proteins underproduced owing to a defect in amplification of Cp genes on both the X and chromosome 3 (Orr, Komitopoulou, and Kafatos, 1984, Proc. Nat. Acad. Sci. USA 81: 3773-77). Mosaic analysis indicates somatic function of gene (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)K1221 phenotype: Oogenesis normal but mature eggs retained by homozy- gous female. # fs(1)K1274 phenotype: Viability good at 29 but ovaries of homozygous females severely atrophied, probably with tumorous follicles. At 25 cysts contain 16 nurse cells and no oocyte; females fer- tile when raised at 23. Mosaic studies indicate germ-line function of gene (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)K1563 phenotype: Viability normal; eggs produced by homozygous females have thin, short dorsal chorionic appendages at 29 but not 23; sterile at both temperatures; partially dominant at 29. Chorion ultrastructurally abnormal. Mosaic studies indi- cate somatic function for gene (Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). # fs(1)L186-fs(1)L211: see yl # fs(1)M: female sterile of Mohler A series of ethyl-methanesulfonate-induced sex-linked- recessive female-sterile mutants reported by Mohler (1977, Genetics 85: 259-72; Mohler and Carroll, 1984, DIS 60: 236-41). The mutants were mapped and tested for comple- mentation. The accompanying table lists the complementation groups. _______________________________________________________________________________________________________________________ locus genetic #M allelism cytology phenotype location __________________________________________________________ alleles ( | oviposits eggs rescue stage of arrest | | | | | develop / _______________________________________________________________________________________________________________________ fs(1)M1 1-10.2 1 + fs(1)M2 1-1 5 + + preblastoderm fs(1)M3 1-15 5 5C5-D6 fs(1)M4 1-0 6 + + preblastoderm fs(1)M5 3 fs(1)A147M1 fs(1)M6 5 fs(1)N fs(1)M7 1 mk fs(1)M8 y-cv 1 + + leaky; rescuable fs(1)M9 3 fs(1)K10 fs(1)M10 8 pcx fs(1)M11 y-cv 1 + - leaky fs(1)M12 3 fs(1)Ya fs(1)M13 1-14 5 5C7-D6 + + leaky, fragile chorions; some eggs collapse fs(1)M14 near cv 2 5A8-C1 + - fs(1)M15 near cv 2 + + + fs(1)M16 fs(1)h fs(1)M17 1-15 1 + + preblastoderm fs(1)M18 6 gd fs(1)M19 1-37 11 11A3-B2 + fs(1)M20 v-f 2 12E1-13A5 + + + preblastoderm fs(1)M21 v-f 1 + + + preblastoderm fs(1)M22 1 fs(1)A457M1 fs(1)M23 2 fs(1)A1459M1 fs(1)M24 v-f 3 + + + fs(1)M25 14 yl fs(1)M26 v-f 2 10A4-B3 + + leaky fs(1)M27 v-f 1 + + + fs(1)M28 v-f 1 + + + fs(1)M29 1-53 6 + + + postgastrula fs(1)M30 v-f 1 + - leaky; collapsed eggs fragile chorions fs(1)M31 near f 1 + ? leaky fs(1)M32 near f 2 + + + fs(1)M33 near f 1 + - eggs collapse with fragile chorions fs(1)M34 15 r fs(1)M35 1 Yp2 9A-B + ? fs(1)M36 1-58 6 + + pregastrula; some eggs collapse fs(1)M37 5 mei-41 fs(1)M38 1-10.2 1 + - eggs collapse; fragile chorion fs(1)M39 cv-v 1 + ? fs(1)M40 y-cv 1 + + + pregastrula fs(1)M41 y-cv 1 + + + fs(1)M42 2 dnc fs(1)M43 cv-v 1 10B1-17 ` + - fs(1)M44 3 swa fs(1)M45 4 sn fs(1)M46 near v 2 10A4-B3 + - fs(1)M47 1 pt fs(1)M48 cv-v 1 + - eggs collapse; fragile chorions fs(1)M49 cv-v 3 9A + - some eggs collapse fs(1)M50 cin fs(1)M51 v-f 1 + - small eggs; some collapse; fragile chorions fs(1)M52 cv-v 1 8E-F + - leaky fs(1)M53 near v 1 + + pregastrula fs(1)M54 v-f 1 + + fs(1)M55 near f 1 + - leaky, some eggs collapse fs(1)M56 v-f 1 + + + fs(1)M57 f-sfa 4 + + postgastrula, some eggs collapse; fragile chorion fs(1)M58 f-sfa 1 + + + fs(1)M59 f-sfa 1 + fs(1)M60 1 fs(1)1059M1 fs(1)M61 fs(1)M62 cv-v 1 10A4-B3 + fs(1)M63 v-f 2 + - leaky; small eggs fs(1)M64 y-cv 1 + fs(1)M65 y-cv 1 + fs(1)M66 1 fs(1)A456M1 fs(1)M68 cv-v 2 + fs(1)M69 2 lz fs(1)M70 cv-v 1 + fs(1)M71 1 ptg fs(1)M72 1-23.6 1 7E10-8A5 + - no sperm stored in hemizygous female; homozygotes fertile fs(1)M73 cv-v 1 7C-D + fs(1)M74 cv-v 1 + fs(1)M76 cv-v 1 + fs(1)M77 cv-v 1 + fs(1)M78 v-f 1 9E3-11B2 + fs(1)M79 v-f 1 12D + fs(1)M81 v-f 1 + fs(1)M82 v-f 1 + fs(1)M83 near f 1 + fs(1)M84 near f 1 + fs(1)M85 v-f 1 + fs(1)M86 f-sfa 1 + fs(1)M87 f-sfa 1 + fs(1)M88 f-sfa 1 + fs(1)M89 f-sfa 1 + fs(1)M91 w-v 1 + fs(1)M93 w-v 1 + leaky fs(1)M94 w-v 1 7E10-8A5 + leaky fs(1)M95 w-v 1 7E10-8A5 + fs(1)M101 14 otu fs(1)M103 1-5 2 + + fs(1)M104 1-1.8 3 - ovaries with misshapen yolky eggs fs(1)M105 1-1.9 3 - ovaries have misshapen yolky eggs fs(1)M106 2 Sxl fs(1)M108 1-52 1 + fs(1)M111 1-21 5 7D1-6 - females retain normal appearing eggs fs(1)M112 1-25.1 2 7E10-8A5 - stage 8 & 9 eggs accumulate; adults with disturbed ocellar bristle pattern fs(1)M114 1 fs(1)A273M1 fs(1)M116 1-30 2 9E3-10A1 - stage 8 oocytes accumulate fs(1)M120 1-0.5 1 + fs(1)M121 near f + fs(1)M122 21.64 1 7C-D + ( The number of alleles for each complementation group recovered by Mohler. | Allelism to previously named or recently renamed loci; e.g., fs(1)M5 alleles fail to complement fs(1)A147; Mohler's three alleles are accordingly designated fs(1)A147M1, fs(1)A147M2, and fs(1)A147M3. / fs(1)-bearing ova from homozygous females rescued by fer- tilization with fs(1)+-bearing sperm. ` 1 = Zhimulev, Belyaeva, Pokholkova, Kotcheneva, Fomina, Bgatov, Khudyakov, Patzevitch, Semeshin, Baritcheva, Aizenzon, Kramers, and Eeken, 1981, DIS 56: 192-96; 2 = Zhimulev, Pokholkova, Bgatov, Umbetova, Solovjeva, Khu- dyakov, and Belyaeva, 1987, Biol. Zentralbl. 106: 699- 720. # fs(1)N: female sterile (1) of Nasrat location: 1-0.0 (closely linked to sc). origin: Induced by an unspecified chemical mutagen. discoverer: Nasrat, 1952. references: Counce and Ede, 1957, J. Embryol. Exp. Morphol. 5: 404-21 (fig.). Degelmann, Hardy, Perrimon, and Mahowald, 1986, Dev. Biol. 115: 479-89 (fig.). synonym: fs(1)nas. phenotype: Maternal lethal. Developmental study of fs(1)N1 by Counce and Ede. Eggs of fs(1)N/fs(1)N females will not support development of normal embryos. About half the eggs contain little or no yolk; development may or may not begin in such eggs but never progresses beyond a highly abnormal cleavage. In eggs containing more yolk, major effect is on synchrony of cleavage and blastoderm mitoses. Twenty percent of these embryos cease development before blastoderm formation. The remainder have abnormal blastoderms and aberrant gastrulation. Final pattern of damage determined by degree of abnormality of earlier stages, but some embryos show larval differentiation. A few of the least abnormal embryos may emerge but never move about or feed. Formation of polar granules abnormal. RK3. alleles: Homozygous fs(1)N12 females produce embryos with defects in anterior and posterior development (Degelmann et al.). Head involution fails; anterior endodermal derivatives are deficient and the absence of pharyngeal musculature causes collapse of the cephalopharyngeal apparatus. Embryos lack all posterior endodermal derivatives as well as structures charac- teristic of abdominal segments 8 to 10 usually, but have six abdominal denticle belts, and occasionally partial seventh or seventh and eighth. In addition, posterior midgut, hindgut, Malpighian tubules, filzkorper, spiracles, anus, anal pad, and anal tuft absent; lateral tracheal trunks end blindly, usually in the sixth segment; posterior disorganization of CNS seen. Pole cells form abnormally and seldom migrate to form the gonad; posterior blastoderm nuclei fail to cellularize and the centrosome position vis a vis the blastoderm nuclei erratic; remarkably free of microtubules. Six rather than seven stripes of ftz transcription seen in blastoderm, with the sixth stripe wider than normal and separated from the fifth by a wider-than-normal space. At gastrulation neither posterior midgut invagination nor proctodeal invagination occur nor- mally. allele origin discoverer synonym ref ( comments ___________________________________________________________________ fs(1)N1 Nasrat,1952 fs(1)N2 EMS fs(1)A371 1 fs(1)N3 EMS fs(1)A379 1 fs(1)N4 EMS fs(1)A1038 1 fs(1)N5 EMS fs(1)K1281 2 fs(1)N6 EMS fs(1)K1347 2 fs(1)N7 EMS fs(1)K1540 2 fs(1)N8 EMS Mohler fs(1)M612-1166 3 fs(1)N9 EMS Mohler fs(1)M612-1420 3 fs(1)N10 EMS Mohler fs(1)M614-574 3 fs(1)N11 EMS Romans fs(1)M612N2X2D 3 fs(1)N12 EMS Engstrom fs(1)N211 3 fs(1)N13 EMS Morales fs(1)Ndvm 4 ( 1 = Gans, Audit and Masson, 1975, Genetics 81: 683-704; 2 = Komitopoulou, Gans, Margaritis, Kafatos and Masson, 1983, Genetics 105: 897-920; 3 = Mohler and Carroll, 1984, DIS 60: 236-41; 4 = Perez-Chiesa, Ramos, Morales, Caceres, Car- dona and Vazquez, 1983, DIS 59: 160. cytology: No detectable chromosomal rearrangements (Slizynska). Placed in 1E1-2A by Per'z-Chiesa. # fs(1)ne: female sterile (1) no eggs A subset of hybrid-dysgenesis-induced, X-linked female- sterile mutations that are characterized by the oviposition of few if any eggs [Orr, Galanopoulos, Romano, and Kafatos, 1989, Genetics 122: 847-58 (fig.); see also Galanopoulos, Orr, Sza- bad, and Kafatos, 1989, Dev. Genet. 10:87-97 (fig.)]. The loci are numbered between 1 and 13 with alleles designated by lower case letters in the superscript. The X chromosomes in these lines harbor multiple P elements thus complicating cyto- logical localizations. No case of allelism with previously identified sex-linked female sterile mutations detected. Various defects in respiratory appendages and chorionic archi- tecture of hand dissected eggs described in above references. number locus location of alleles comments _________________________________________________________ fs(1)ne1 sc-ec 8 soma dependent fs(1)ne2 sc-ec 2 fs(1)ne3 2 double mutant? germ-line dependent fs(1)ne4 f-car 2 germ-line dependent fs(1)ne5 near car fs(1)ne6 double mutant? fs(1)ne7 f-car fs(1)ne8 ct-m 1 germ-line dependent fs(1)ne9 near car 1 germ-line dependent fs(1)ne10 ct-m fs(1)ne12 double mutant? fs(1)ne13 double mutant? # fs(1)pcx: see pcx # fs(1)Ya: female sterile of Young location: 1-[between l(1)zw7 and l(1)zw5; to the right of fs(1)Yb]. origin: Induced by ethyl methanesulfonate. discoverer: Young. references: Young and Judd, 1978, Genetics 88: 723-42. Lin and Wolfner, 1989, Mol. Gen. Genet. 215: 257-65. phenotype: Homozygous females completely sterile; lay normal numbers of eggs. Eggs remain vacuolated after deposition. No evidence of syngamy (Zalokar, Audit, and Erk, 1975, Dev. Biol. 47: 419-32). alleles: Expression female germ-line autonomous (Perrimon, Engstrom, and Mahowald, 1986, Genetics 113: 695-712); no expression detectable in daughters of tud females (Lin and Wolfner). Transcript detectable in nurse cells and oocyte as early as stage 7; evenly distributed throughout cytoplasm of 0-2 h embryos, but not detectable later (Lin and Wolfner). allele discoverer synonym ref ( _______________________________________________ fs(1)Ya1 Young fs(1)Y2 3 fs(1)Ya2 Young fs(1)Y5 3 fs(1)Ya3 Young fs(1)Y6 3 fs(1)Ya4 fs(1)A73 1 fs(1)Ya5 Mohler fs(1)M1213-1970 2 fs(1)Ya6 Mohler fs(1)M1213B-76 2 fs(1)Ya7 Mohler fs(1)M1213F-50 2 ( 1 = Gans, Audit and Masson, 1975, Genetics 105: 897-920; 2 = Mohler and Carroll, 1984, DIS 60: 236-41; 3 = Young and Judd, 1978, Genetics 88: 723-42. cytology: Placed in 3B4-6 by deficiency mapping. molecular biology: Identified on the basis of homology with a 2.4-kb female-specific transcript within a 32-kb walk through region 3B4-6. Germ-line transformants with an 8.5-kb fragment of wild-type DNA with homology to only the above transcript rescue fertility of both fs(1)Ya and fs(1)Yb females. Tran- scription unit shown to be 2.7 kb long and to be transcribed from left to right (Lin and Wolfner). # fs(1)Yb location: 1-[between l(1)zw7 and l(1)zw5; to the left of fs(1)Ya]. origin: Induced by ethyl methanesulfonte. discoverer: Young. references: Young and Judd, 1978, Genetics 88: 723-42. phenotype: Homozygous females semisterile; lay reduced numbers of eggs, most of which remain vacuolated after deposition; a few develop into normal-appearing adults. Mutation without effect on males. alleles: fs(1)Yb1, fs(1)Yb2, and fs(1)Yb3 recovered as fs(1)Y1, fs(1)Y3, and fs(1)Y7, respectively. cytology: Placed in 3B4-6 by deficiency mapping. # fs(1)yolkless: see yl # Fs(2)1: see Fs(2)M # fs(2)3A-fs(2)308A: see fs(2)HO3-fs(2)HO308 # fs(2)A A series of mutants that have been subjected to complementa- tion and physiological analysis but not mapped genetically. origin: Induced by ethyl methanesulfonate. references: Bakken, 1973, Dev. Biol. 33: 100-22 (fig.). # fs(2)A1 phenotype: Homozygous females anatomically normal; lay eggs that do not hatch. alleles: Two alleles recovered among 79 second-chromosome female-sterile mutants analyzed. # fs(2)A2 phenotype: Homozygous females anatomically normal; lay eggs that do not hatch. First cleavage division normal; subsequent divisions often contain extra chromosomes; both clumped and scattered chromosomes observed. Some eggs have large spheri- cal masses of fragmented chromosomes. No peripheral migration of nuclei. alleles: Seven alleles recovered among 79 mutants analyzed. # fs(2)A3 phenotype: Homozygous females anatomically normal; lay eggs that do not hatch. # fs(2)A4 phenotype: Homozygous females anatomically normal; seem to be ovulation deficient since they accumulate normal-appearing stage-14 oocytes in their ovarioles. alleles: 39 alleles recovered among 79 mutants analyzed. # fs(2)A5 phenotype: Homozygous females anatomically normal; lay eggs that do not hatch. # fs(2)A6 phenotype: Homozygous females anatomically normal but do not oviposit; ovaries may be abnormal. # fs(2)A7 phenotype: Homozygous females anatomically normal; lay eggs that do not hatch. Abnormal cleavage figures seen after the fourth division. Peripheral migration of nuclei restricted to only a part of the egg surface. Many blastoma nuclei large and reticulate; others small and condensed. Yolk nuclei clumped and unevenly disposed. # fs(2)A8 phenotype: Homozygous females anatomically normal; lay eggs that do not hatch. # fs(2)A9 phenotype: Homozygous females anatomically normal; lay eggs with fragile chorions, which do not hatch. Some eggs reach syncytial blastema but not cellular blastoderm formation; blastema nuclei unequal in size, irregularly shaped, and some- times pycnotic. Distribution over egg surface nonuniform. alleles: Two alleles among 79 mutants analyzed. # fs(2)A10 phenotype: Homozygous females anatomically normal; seem to be ovulation deficient since they accumulate stage-14 oocytes in their ovarioles. # fs(2)A11 phenotype: Homozygous females anatomically normal. Distribu- tion of nuclei in syncytial blastema irregular. Oldest embryos show abnormal gastrulation. # fs(2)A12 phenotype: Homozygous females anatomically normal; lay foreshortened eggs with truncated anterior tip and short fat chorionic filaments. Eggs similar to stage-11 oocytes, some with adhering follicle and nurse cells. A few eggs lack stainable chromatin; most have one to three large spherical masses of fragmented chromosomes or tripolar spindles and abnormally elongated mitotic figures. alleles: Six alleles among 79 analyzed mutants. # fs(2)A13 phenotype: Homozygous females anatomically normal, lay eggs that do not hatch. Eggs have abnormal cleavage figures, mul- tipolar spindles, nonuniformity of chromosome contraction dur- ing anaphase, mitotic asynchrony, and uneven distribution of mitotic figures through ooplasm. In some, no mitotic figures are recognizable; only large masses of fragmented chromosomes or amorphic clumps are seen. # fs(2)A14 phenotype: Homozygous females anatomically normal; lay eggs that do not hatch. Most eggs display meiotic metaphase II chromosomes, without visible spindle fibers, and a sperm head lying close by. Oocyte chromosomes may be scattered or regu- larly grouped. # fs(2)A15 phenotype: Homozygous females have small abnormally organized ovaries; ovaries approximately 200 um long; no ovariole forma- tion; no organized follicles; no recognizable oocytes. Nuclei of different sizes and shapes but not in groups expected from cystocyte divisions; some are pycnotic. # fs(2)A16 phenotype: Homozygous females have small (400-600 um long) abnormally organized ovaries. Ultrastructural studies by King and Buckles (1980, DIS 55: 74-75) reveal that oogonial cysts appear to be normal; surrounded by wedge-shaped follicle cells but not separated by interfollicular stalks so that the con- ventional moniliform vitellarium is not observed. Posterior end of ovariole filled with fusing follicles. # fs(2)A17 phenotype: Homozygous females have smaller-than-normal ovaries with nurse cell nuclei arrested in stage 4. Follicle cells continue normal differentiation for some time before degen- erating. Vitellogenesis defective; oocyte arrests in stage 7. Transplantation experiments (Postlethwait and Handler, 1978, Dev. Biol. 67: 202-13) show that fs(2)A17 ovaries develop autonomously in wild-type hosts and that fs(2)A17 hosts sup- port vitellogenesis in implanted normal and ap ovaries. alleles: Six alleles among 79 analyzed mutants. # fs(2)A18 phenotype: Most egg chambers of homozygous females arrested in stage 7; no evidence of vitellogenesis. Height of follicular columnar epithelium increased. Posterior half of ovarioles filled with degenerating stage-8-sized egg chambers. Tran- splantation experiments (Postlethwait and Handler, 1978, Dev. Biol. 67: 202-13) show that fs(2)A18 is ovary autonomous when transplanted into a wild-type host but nonautonomous when transplanted into a fs(2)A17 host. fs(2)A18 hosts support some vitellogenesis of + and ap implants. # fs(2)adp: see adpfs # fs(2)B: female sterile (2) of Bridges location: 2-5. origin: Spontaneous. discoverer: Bridges, 29c25. synonym: fes. references: King, Sang, and Leth, 1961, Exp. Cell. Res. 23: 108-17 (fig.). King, Koch, and Cassens, 1961, Growth 25: 45-65 (fig.). Koch and King, 1964, Growth 28: 325-69 (fig.). King, 1969, Nat. Cancer Inst. Monogr. 31: 323-45. phenotype: External morphology and sexual behavior normal (Bur- net, Connolly, Kearney, and Cook, 1973, J. Insect Physiol. 19: 2421-31). Males fertile; females sterile. After rearing on glucose diet mutant females are less receptive to copula- tion attempts and more vigorously courted than wild-type vir- gins (Cook and Connolly, 1976, J. Insect Physiol. 22: 1727- 35). Germaria of ovaries of homozygous females larger than normal; cysts contain 3 times the normal number of cells; metaphase figures found throughout germarium. Just over half the oogonia undergo complete cleavage with the loss of ring canal connections to other cells; remaining cells in small clusters with tenuous connections (Johnson and King, 1972, Biol. Bull. 143: 525-47). Vitellaria subdivided into a series of sausage-shaped cell aggregates, each surrounded with an ill-defined follicular epithelium and filled with hundreds to thousands of mitotically active oogonia-like cells [King, Burnett, and Staley, 1957, Growth 21: 239-61 (fig.)]. These cells occasionally differentiate into cells resembling nurse cells, which may have polytene chromosomes, and rarely into oocytes. fs(2)B ovaries transplanted into wild-type hosts in late larval stages and reciprocal transplants develop auto- nomously (Clancy and Beadle, 1937, Biol. Bull. 72: 47-56; Klug, Bodenstein, and King, 1968, J. Exp. Zool. 167: 151-56). The cells of the corpus-allatum corpus-cardiacum complex of homozygous fs(2)B females appear to be prevented from releas- ing their hormone products and undergo degenerative changes; these effects reversable by vitellogenic activity of wild-type ovary implanted into the abdomen of the fs(2)B female (King, Aggarwal, and Bodenstein, 1966, J. Exp. Zool. 161: 151-76; Aggarwal and King, 1971, J. Morphol. 134: 437-46). Abdominal fat cells of fs(2)B females 1.5 times size of those in wild type. They resemble male fat cells in having more fat and less glycogen than those of normal females; return to normal size and composition following implantation of wild-type ovary (Butterworth and Bodenstein, 1968, J. Exp. Zool. 167: 207- 18). fs(2)B ovaries show reduced levels of thymidylate syn- thetase (Carpenter, 1973, Genetics 75: 113-22). RK3. # Fs(2)D: see Fs(2)G # Fs(2)D10 location: 2 (unmapped). origin: Induced by ethyl methanesulfonate. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Dominant female sterile. Development ceases before cellularization of blastoderm; syncytial nuclear division appears normal. # Fs(2)D-M: see Fs(2)M # fs(2)E: female sterile (2) Edmondson origin: A series of nine ultraviolet-induced mutations at dif- ferent loci. references: Edmondson, 1952, DIS 26: 61-62. 1960, DIS 34: 49. CP627. genetic mutation location synonym phenotype ______________________________________________________________ fs(2)E1 ( 2-57.6 fs2.1 no eggs; rudimentary gonads *fs(2)E2 2-22.0 fs2.2 eggs don't hatch *fs(2)E3 2-47.5 fs2.3 no eggs; narrow curved wings *fs(2)E4 2-48.5 fs2.4 narrow curved wings; few eggs, don't hatch *fs(2)E5 2-50.4 fs2.5 embryos degenerate; few larvae hatch *fs(2)E6 2-54.4 fs2.6 eggs don't hatch *fs(2)E7 2-55.2 fs2.7 vitelline membrane defective *fs(2)E8 2-62.6 fs2.8 no eggs *fs(2)E9 2-35.6 fs2.9 eggs don't hatch ( Dorsal appendages of chorion convoluted or fused (King and Koch, 1963, Quant. J. Microscop. Sci. 104: 297-320). # fs(2)eo: female sterile (2) early oogenesis (T. Schupbach) A group of female-sterile mutations on the second chromosome which affect early stages of oogenesis (before yolk uptake). They were all induced by ethyl methanesulfonate, and recovered in screens by Schupbach and Wieschaus (1989, Genetics 121: 110-17). genetic locus location synonym phenotype ______________________________________________________________________ fs(2)eo1 2-30 fs(2)eoPV30 few if any egg chambers; early oogenic arrest fs(2)eo2 2-54 fs(2)eoPL3 few if any egg chambers; early oogenic arrest fs(2)eo3 ( 2-{54} fs(2)eoRV64 many degenerating egg chambers fs(2)eo4 2-64 fs(2)eoPB6 egg chambers with variable number of nurse cells and degenerating material in ovaries fs(2)eo5 2-85 fs(2)eoWP19 ovarian tumors with many small, undifferentiated cells in ovaries fs(2)eo6 2-105 fs(2)eoQS2 ovarian tumors with many small, undifferentiated cells in ovaries fs(2)eo7 2-105 fs(2)eoPP22 few if any egg chambers; early oogenic arrest ( Placed in 36E4-38A7 on the basis of its inclusion in Df(2L)TW50 = Df(2L)36E4-F1;38A6-7. # Fs(2)G: Female sterile (2) of Grell location: 2- (not located). origin: Induced by ethyl methanesulfonate. discoverer: E. H. Grell, 65e. synonym: Fs(2)D. references: Yarger and King, 1971, Dev. Biol. 24: 166-77 (fig.). phenotype: Heterozygous females raised at 25 or 30 completely sterile; minimal development noted of zygotes resulting from eggs of females raised at 20; heterozygous males fertile. Ten percent as many egg chambers as normal, and 10% of chambers have fewer than 16 cells, generally lacking an oocyte. Ovaries of heterozygous females developing at 30 frequently fail to attach to oviducts. At 25 and 30, heterozygous females take one day longer to develop than controls; viabil- ity of Fs(2)G/+ females 70-75% at 20 and 25, 5% at 30. Wings of heterozygotes normal at 20, frequently incised at 30, greatly reduced and crumpled at 30. Bristles short; thorax broad and flattened with air bubbles under cuticle. RK3. # fs(2)HO: female sterile (2) of Hardy and Orevi A series of female-sterile mutations isolated from a sample of lethal-free ethyl-methanesulfonate treated second chromo- somes produced by Hardy and Orevi. mutation synonym ref ( ______________________________ fs(2)HO3 fs(2)3A fs(2)HO8 fs(2)8B 1 fs(2)HO20 fs(2)20B 1 fs(2)HO100 fs(2)100A 1 fs(2)HO103 fs(2)103B fs(2)HO144 fs(2)144A fs(2)HO164 fs(2)164A fs(2)HO192 fs(2)192A 1 fs(2)HO260 fs(2)260A fs(2)HO294 fs(2)294A fs(2)HO297 fs(2)297A fs(2)HO308 fs(2)308A ( 1 = Postlethwait and Handler, 1976, Dev. Biol. 67: 202-13. phenotype: Females homozygous for all four mutants dealt with by Postlethwait and Handler have oogensis aborted at early previtellogenic stages, are ovary autonomous in transplants into wild-type females, and support vitellogenesis in implanted wild-type ovaries. # fs(2)K: female sterile (2) of Kikkawa location: 2-100. origin: Spontaneous. discoverer: Kikkawa, 1960. synonym: fes(2)K. references: 1960, DIS 34: 51. phenotype: Female sterile; male fully fertile. RK3. # fs(2)lto: female sterile (2) late oogenesis (T. Schupbach) A group of female-sterile mutations on the second chromosome which lead to defects in later stages of oogenesis (during yolk uptake, chorion synthesis, or egg laying). They were all ethyl methanesulfonate induced and isolated in screens by Schupbach and Wieschaus (1989, Genetics 121: 101-17). genetic locus location synonym phenotype __________________________________________________________________________ fs(2)lto1 2-51 fs(2)ltoPN48 Homozygous females lay eggs with fragile chorions, which remain unfertilized. fs(2)lto2 2-{54} ( fs(2)ltoHD43 Homozygous females lay collapsed eggs. fs(2)lto3 2-{54} ( fs(2)ltoRE57 Homozygous females lay eggs which often lack dorsal appendages, and appear more pointed at the posterior end. fs(2)lto4 2-62 fs(2)ltoQB3 Homozygous females lay tiny eggs, which remain unfertilized. fs(2)lto5 2-{86} | fs(2)ltoDF6 Homozygous females lay short eggs. ( In Df(2L)TW50 = Df(2)36E4-F1;38A6-7. | In Df(2R)PC4 = Df(2)55A;55F. # Fs(2)M: Female sterile (2) of Meyer location: 2- [between al (2-0.4) and dp (2-13.0), (Szabad, Erdelye, Hoffman, Szidonya, and Wright, 1989, Genetics 122: 823-35)]. origin: X ray induced. synonym: Fs(2)1, Fs(2)D-M. references: Meyer, 1966, DIS 41: 167. phenotype: Sterile Fs(2)M/+ females deposit very few, mostly flaccid eggs that never bear dorsal chorionic appendages (Sza- bad, Erdelye, Hoffman, Szidonya, and Wright, 1989, Genetics 122: 823-35). Flies slightly reduced in size with discernably reduced eyes. Fs(2)M/Cy females show less curled wings than +/Cy (Craymer). # fs(2)OW: female sterile (2) of Oshima and Watanabe A series of up to 34 different complementation units iso- lated from a natural population 3 times during the year; as many as 7 more isolated from cage populations. The loci inferred are numbered from 101 to 107, 202 to 217, and 801 to 812 from the natural population and c1 to c7 from the population cage. Complementation testing was the only pro- cedure to which these recessive female-sterile mutants were submitted. The designator OW did not appear in the original publication. origin: Spontaneous. references: Oshima and Watanabe, 1973, Genetics 74: 351-61. # fs(2)Q342: see Vm26A2 # Fs(2)Sz: Female sterile (2) of Szabad A series of ethyl-methanesulfonate-induced dominant-female- sterile mutations on the second chromosome described by Sza- bad, Erdelye, Hoffmann, Szidonya, and Wright (1989, Genetics 122: 823-35). Meiotic mapping possible in germ-line- independent and incompletely penetrant mutants; remainder mapped mitotically. X-ray- or EMS-induced revertants usually recessive lethals; complementation analysis of revertants identify 13-15 loci. The mutants named for Hungarian families that vanished by the beginning of the 14th century, as indi- cated in the following table. locus name location comments ( ____________________________________________________________________ Fs(2)Sz1 Barsa 2-(nub-stw) little or no embryogenesis Fs(2)Sz2 Billa 2-(nub-lt) little or no embryogenesis (Reuter) Fs(2)Sz3 Dorog 2L dorsal appendages reduced Fs(2)Sz4 Etre 2-71.4 thin chorion; not germ line dependent (Wright) Fs(2)Sz5 Himca 2L pre-pronuclear-fusion arrest Fs(2)Sz6 Hont 2-(al-dp) meiotic defects (Wright) Fs(2)Sz7 Ketel 2-(lt-sca) meiotic defects Fs(2)Sz8 Kompolt 2-(al-dp) abnormal nuclear divisions Fs(2)Sz9 Tarhos abnormal nuclear divisions Fs(2)Sz10 Tekele 2-(al-nub) abnormal nuclear divisions Fs(2)Sz11 Told 2-(nub-sca) 15% of embryos->head defects Fs(2)Sz12 Ugra 2-18 agametic; germ line independent Fs(2)Sz13 Vaja 2-15.1 Incompletely penetrant; variable head defects; may be BicD allele ( Phenotype of eggs laid by Fs(2)Sz/+ females; parentheses indicate origin of alleles not found in Szeged. # fs(2)TLM: female sterile (2) of Trippa, Louverre, and Micheli location: 2-89.7 (between L and Pin). origin: Spontaneous. references: Trippa, 1977, DIS 52: 3 (fig.). Trippa, Loverre, and Michele, 1977, DIS 52: 75. Trippa, Loverre, and Cicchetti, 1980, Genetics 95: 399-412 (fig.). Trippa, Loverre, and Cicchetti, 1980, J. Exp. Zool. 214: 277-85. phenotype: Homozygous females sterile, produce no eggs, have underdeveloped ovaries; fewer ovarioles than normal; vitello- genesis apparently absent. One third of homozygous males sterile; remainder show normal fecundity, become sterile dur- ing first week of life. Testes abnormally shaped and reduced in size. # fs(2)TW1: female sterile (2) Ted Wright 1 location: 2-54 (estimated from cytological location). origin: Induced by ethyl methanesulfonate. discoverer: T.R.F. Wright in saturation studies of the Df(2L)130 region. phenotype: Eggs produced by homozygous females show no visible signs of development (Schupbach, and Wieschaus, 1989, Genetics 121: 101-17). alleles: Eight independent occurrences recovered by Wright, four more by Schupbach. cytology: Placed between 37C2 and 37D1 on the basis of its inclusion in the region of overlap of Df(2L)E71 = Df(2L)36F2- 6;37C6-D1 and Df(2L)VA12 = Df(2L)37C2-D1;38B2-C1. # Fs(2)X10 location: 2 (unmapped). origin: Induced by ethyl methanesulfonate. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Dominant female sterile, gives cup-like eggs. # Fs(2)Y12 location: 2 (unmapped). origin: Induced by ethyl methanesulfonate. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Semidominant female sterile, gives cup-like eggs. # fs(3)6m45 location: 3- (not mapped). discoverer: Rice. references: Bownes and Hames, 1978, J. Embryol. Exp. Morphol. 47: 111-20. phenotype: Oocytes of homozygous females show no signs of vitellogenesis. Yolk proteins accumulate in hemolymph. fs(3)6m45 ovaries transplanted fail to take up yolk proteins and are nonvitellogenic. Wild-type ovaries take up yolk pro- tein and develop normally in fs(3)6m45 host. # fs(3)108-350 locus location origin discoverer ref ( ___________________________________________________________ fs(2)108-17 3-(ss-k) EMS Nusslein-Volhard 2 fs(2)110-8 EMS Nusslein-Volhard 1 fs(2)272-9 3-(st-cu) EMS Nusslein-Volhard 1, 2 fs(2)293-19 3-(st-ss) EMS Nusslein-Volhard 1, 2 fs(2)350-7 3R EMS Nusslein-Volhard 2 ( 1 = Snyder, Galanopoulous, and Kafatos, 1985, Genetics 110: 53; 2 = 1986, Proc. Nat. Acad. Sci. USA 83: 3341-45. # fs(3)108-17 phenotype: Eggs of homozygous females have short thin chorionic respiratory appendages. Endochorionic structures disrupted; chorionic protein levels normal. # fs(3)110-8 phenotype: Eggs of homozygous females deficient in the first- deposited inner endochorionic layers; early chorion proteins deficient, although transcript levels appear normal. # fs(3)272-9 phenotype: Egg shells produced by homozygous females extremely disrupted. Deficiency of endochorionic material. All six chorion proteins and their mRNA's present at reduced levels; deficiency in the level of chorion-gene amplification in fol- licle cells. alleles: Two; fs(3)272-91 recovered by Nusslein-Volhard; fs(3)272-92 EMS induced by Lindsley; originally designated fs(3)SD78. # fs(3)293-19 phenotype: Eggs of homozygous females defective in late- deposited outer layers of endochorion; endochorionic material deficient. Late-gene expression as measured by mRNA or pro- tein levels defective; deficiency in the level of chorion-gene amplification in follicle cells. # fs(3)350-7 phenotype: Eggs of homozygous females have short thin chorionic respiratory appendages; endochorion structure disrupted; chorionic-protein levels normal. # fs(3)A A series of mutants that have been subject to complementa- tion and phenotypic analysis but have not been mapped geneti- cally. origin: Induced by ethyl methanesulfonate. references: Baaken, 1973, Dev. Biol. 33: 100-22 (fig.). # fs(3)A1 phenotype: Oocyte development normal through stage 7, then arrested. Every ovariole has the normal number of 6 folli- cles. No vitellogenesis. Very little degeneration seen. Effects of mutant not affected by transplantation of fs(3)A1 ovaries into wild-type hosts; fs(2)A1 hosts support vitello- genesis of implanted wild-type ovaries poorly (Postlethwait and Handler, 1978, Dev. Biol. 67: 202-13). alleles: Two alleles recovered. # fs(3)A2 phenotype: Homozygous females morphologically normal; lay eggs that do not hatch. # fs(3)A3 phenotype: Same as fs(3)A2. # fs(3)A4 phenotype: Same as fs(3)A2. # fs(3)A5 phenotype: Homozygous females morphologically normal; oocytes contain mature eggs but ovoposition does not take place. # fs(3)A6 phenotype: Same as fs(3)A5. # fs(3)A7 phenotype: Same as fs(3)A5. # fs(3)A8 phenotype: Same as fs(3)A5. alleles: Two alleles recovered. # fs(3)A9 phenotype: Same as fs(3)A5. # fs(3)A10 phenotype: Ovaries ~180 um long; appear immaturely developed rather than malformed,. Ovariole formation proceeds halfway down the ovary; stage 3 or 4 the most mature follicles seen. Posterior half of ovary contains degenerating egg chambers. # fs(3)A11 phenotype: Homozygous females morphologically normal; lay eggs that lack all discernable chromatin and fail to hatch. # fs(3)A12 phenotype: Same as fs(3)A11. # fs(3)A13 phenotype: Homozygous females produce eggs that appear to develop normally for the first 10 hr following fertilization but fail to hatch. # fs(3)A14 phenotype: Mostly the same as fs(3)A11; a few eggs produced by homozygous females contain large amorphous chromatin bodies; one embryo observed to reach syncytial blastema stage. # fs(3)A15 phenotype: Fertilized eggs of homozygous females have tripolar spindles, longitudinally split metaphase plates with too many chromosomes, precocious pulling of some chromosomes to poles, and numerous anaphase bridges. Some eggs had 1-3 large spher- ical or fragmented chromosomes. # fs(3)A16 phenotype: Ovaries of homozygous females show retardation of oocyte growth; stage 7 oocytes smaller than nurse cells; many egg chambers begin degenerating at stage 7. Some continue to grow, and nurse cells and follicle cells differentiate nor- mally, but follicle is dwarfed. # fs(3)A17 phenotype: A few ovaries produce one or two yolky oocytes and the rest of the posterior half is filled with degenerating egg chambers. Most ovaries show very long slender stage-10 and stage-11 chambers. The globular appearance of the ooplasm suggests that many are degenerating. # Fs(3)Apc location: 3- 39.5 (63/81 the distance of h to th). origin: Induced by ethyl methanesulfonate. discoverer: Szabad and Erdelye. references: Szabad and Hoffman, 1989, Dev. Biol. 131: 1-10. phenotype: Majority of eggs produced by Fs(3)Apc/+ females col- lapse; 1-5% not flaccid. Respiratory appendages of chorion rudimentary as in the anterior chorion. When fertilized, resulting embryos rarely develop cuticular derivatives. Fol- licle cells in ovarioles fail to migrate between the oocyte and nurse cells. Mutant does not successfully revert. Germ- line chimaeras demonstrate that fs(3)Apc is follicle-cell autonomous. # fs(3)G2 phenotype: Females almost sterile; produce rare surviving pro- geny. Oogenesis incomplete, usually stops in early phases of vitellogenesis. Most (89%) follicles contain 32 cells instead of normal 16 as a result of an extra oogonial division. The 32 cells of an incipient cyst enclosed in two chambers in 6% of the cases. Position of oocyte in follicle abnormal in 28% of cases. Males partially sterile. Viability low. RK3. # fs(3)G3 phenotype: Oogenesis incomplete; most follicles stop develop- ment during yolk deposition (after stage 9). Males fertile. RK3. # fs(3)G5 phenotype: Oogenesis incomplete; ovarioles contain excessive numbers of follicles, which usually stop developing at or before stage 9. Males fertile. RK3. # fs(3)H: female sterile (3) of Handler location: 3- (not mapped). origin: Two complementing mutants, fs(3)H23 and fs(3)H172, induced by ethyl methanesulfonate. discoverer: Handler. references: Postlethwait and Handler, 1978, Dev. Biol. 67: 202-13. # fs(3)H23 phenotype: Follicles cease development at early previtellogenic stage; the few vitellogenic follicles that do appear are highly abnormal. Ovary autonomous in transplants, but some vitellogenesis induced by administration of juvenile hormone analogue, ZR-515. fs(3)H23 females support vitellogenesis in implanted wild-type ovaries. # fs(3)H172 phenotype: Oocytes occasionally begin vitellogenesis, but pro- cess halts prematurely and only rarely do mature oocytes develop. Mature follicles look normal. Ovary autonomous in transplants into wild-type host and supports vitellogenesis in implanted wild-type ovaries. # fs(3)HO: female sterile (3) of Hardy and Orevi A series of female-sterile mutations isolated from a sample of lethal-free, ethyl-methanesulfonate-treated third chromo- somes produced by Hardy and Orevi. genetic mutation location synonym ref ( __________________________________________ fs(3)HO5A | 3-46.3 fs(3)f15A 1 fs(3)HO5B | 3-48.4 fs(3)f25A 1 fs(3)HO29 3- fs(3)29A 2 fs(3)HO115 3- fs(3)115A 2 fs(3)HO127 3- fs(3)127A 2 fs(3)HO133 3- fs(3)133A 2 fs(3)HO191 3- fs(3)191A fs(3)HO231 3- fs(3)231A ( 1 = Nishida, 1980, Jpn. J. Genet. 55: 427-39 (fig.); 2 = Postlethwait and Handler, 1978, Dev. Biol. 67: 202-13. | Isolated from same mutagen-treated chromosome along with ms(3)HO5A and ms(3)HO5B. # fs(3)H05A phenotype: Homozygous females do not lay eggs; oocyte develop- ment arrested in a previtellogenic stage. Attachment of ovaries to ovoduct fragile. Germania filled with polytene cells; no vitellana. cytology: Polytene chromosomes normal. # fs(3)HO5B phenotype: Homozygous females lay fertilized eggs, which fail to develop. Maternal effect lethal. cytology: Polytene chromosomes normal. # fs(3)HO29 phenotype: Oocytes exhibit abortive vitellogenesis. Mutant effect is ovary autonomous in transplants into wild-type hosts and mutant females support development of implanted wild-type ovaries. # fs(3)HO115 phenotype: Oocyte development arrested in late previtello- genesis. Mutant-effect ovary autonomous in transplants into wild-type hosts and mutant females support vitellogenesis in implanted wild-type ovaries. # fs(3)HO127 phenotype: Similar to that of fs(3)HO115. # fs(3)HO133 phenotype: Similar to that of fs(3)HO115. # fs(3)K1 location: 3- (not mapped). discoverer: Mohler. references: King and Mohler, 1975, Handbook of Genetics (R.C. King, ed.). Plenum Press, New York, and London, Vol. 3, pp. 83. phenotype: Homozygous females produce eggs with abnormal dorsal chorionic appendages. # Fs(3)Sz: Female sterile (3) of Szeged A series of ethyl-methanesulfonate-induced dominant or incompletely dominant female-sterile mutations on the third chromosome described by Erdelye and Szabad (1989, Genetics 122: 111-27). X-ray- or EMS-induced revertants identify 27- 34 loci. The mutants are named for Hungarian families that vanished by the beginning of the 14th century, as indicated in the following tables. _____________________________________________________________________________ Table I: Complete Dominants locus name location comments ( _____________________________________________________________________________ Fs(3)Sz1 Apc 3-39.5 incomplete anterior egg coverings; flaccid eggs with rudimentary chorionic append- ages Fs(3)Sz2 Avar 3-36.3 agametic; retains eggs Fs(3)Sz3 Baksa 3L eggs fertilized, but sperm pronuclei do not divide and there is no development Fs(3)Sz4 | Bercel 3-(ru-h) only chitin granules in embryos Fs(3)Sz5 Bojla 3L eight sperm nuclei along A-P axis Fs(3)Sz6 Botond 3L eggs fertilized, meiosis completed, but no further development Fs(3)Sz7 | Damasa 3L eggs fertilized, meiosis com- pleted, but usually no further development Fs(3)Sz8 Farkas 3-(ru-sr) several divisons of pronuclei without fusion Fs(3)Sz9 Gerec 3-(h-th) pronuclei approach but no fusion or division Fs(3)Sz10 Hodos 3-(ru-h) several divisons of pronuclei without fusion Fs(3)Sz11 Horka 3R pronuclei approach but no fusion or division Fs(3)Sz12 / Huba 3L pronuclei may or may not divide; no fusion; cleavage may or may not occur Fs(3)Sz13 Jutas 3R meiotic figures among cleavage nuclei Fs(3)Sz14 ` Kavar 3L head lesions in embryos; some posterior structures present Fs(3)Sz15 Keled 3-(cu-sr) poorly formed cuticle fragments in 50% of the embryos Fs(3)Sz16 Keve 3-(h-th) mid abdominal segments missing Fs(3)Sz17 Kun 3-(e-ca) sperm but not egg pronuclei divide a few times Fs(3)Sz18 Laborc 3L 1-3 large nuclei (probably sperm pronuclei) Fs(3)Sz19 Palat 3-(ru-h) head lesions Fs(3)Sz20 Pilis 3-(sr-e) poorly formed cuticle fragments in 50% of embryos Fs(3)Sz21 Tevel 3-(h-th) head lesions Fs(3)Sz22 ` Tomaj 3-(h-th) sperm pronuclei may or may not divide but no fusion or further development Fs(3)Sz23 Tonuz 3R sperm but not egg pronuclei divide a few times Fs(3)Sz24 Varas 3-(ru-h) sperm but not egg pronuclei divide a few times Fs(3)Sz25 Zerind 3R sperm but not egg pronuclei divide a few times Fs(3)Sz26 Zombor 3-(h-th) several divisons of pronuclei without fusion _______________________________________________________________________________ Table II: Incomplete Dominants locus name location comments ( _______________________________________________________________________________ Fs(3)Sz27 Kartal 3-(cu-ca) areas without nuclei in syncytial blastoderm; cleavage abnormalities Fs(3)Sz28 Levente 80.7 no development after syncytial blastoderm; cleavage abnormalities Fs(3)Sz29 Purdur 3-(ru-cu) eggs fertilized, meiosis completed, but no development Fs(3)Sz30 Rosd 3-(cu-sr) head lesions Fs(3)Sz31 Vencellin 28.1 head lesions Fs(3)Sz32 Zolta 3-(cu-sr) eggs rudimentary and flaccid; follicle cell epithelium ventralized during oogenesis ( Phenotype of eggs laid by Fs(3)Sz/+ females. | Two mutant alleles. / Four mutant alleles. ` Three mutant alleles. # fs(3)T: female sterile (3) of Tabriz location: 3-108.6. origin: Spontaneous. references: Mostashfi and Koliantz, 1972, DIS 48: 104. phenotype: Homozygous females sterile and exhibit a pinkish eye color. # fs(4)34 location: 4- (not mapped). origin: Spontaneous. discoverer: Hochman, 64d. references: 1972, DIS 48: 17. phenotype: Viability of homozygotes normal; males fertile; females sterile. As originally described by Hochman, ovaries morphologically normal; females can be inseminated and can oviposit, but eggs fail to develop. In subsequent work, King and Buckles (1980, DIS 55: 74-75) report altered phenotype with oogenesis arrested in the germarium, where there are large numbers of oogenia not organized into cysts anteriorly and a solid plug of profollicle cells posteriorly. cytology: Induced in neither Df(4)M = Df(4)101E-F;102B6-17 nor Df(4)G = 102E2-10; tip (Hochman, 1974, Cold Spring Harbor Symp. Quant. Biol. 38: 581-89); probably lies between. # fsh: see fs(1)h # ft: fat location: 2-12.0. origin: Spontaneous. discoverer: Mohr, 20b15. references: 1923, Studia Mendeliana (Brunae). pp. 266-87. 1929, Z. Indukt. Abstamm. Vererbungsl. 50: 113-200 (fig.). Bryant, Huettner, Held, Ryerse, and Szidonya, 1988, Dev. Biol. 129: 541-54. phenotype: Viable alleles characterized using ft1. Abdomen short and fat. Thorax broad. Wings short and broad with crossveins much closer together than normal. Scutellum shor- tened; scutellar bristles far apart. Viability good. Second- and third-instar larvae, particularly when there is little yeast in the food, show vacuoles in cytoplasm of salivary gland cells. Two waves of vacuole formation; vacu- oles may be membrane-bound lipoprotein bodies (Chandhuri, 1969, DIS 44: 118). Tip of X disfigured, possibly as a result of several small puffs intermingled with hard, non- puffed bands. In about 1% of larvae, salivary glands distally expanded and crooked [Slizynski, 1964, Cytologia (Tokyo), 29: 330-36 (fig.)]. Lethal alleles characterized in study of ft8 (formerly fd = floppy disc) by Bryant et al.. ft8 classi- fied as an amorphic mutation based on the similarity in lethal phenotype of ft8/ft8 and ft8/Df(2L)M25A-11. Larvae character- ized by imaginal-disc hyperplasia such that mutant discs are much larger and more convoluted than wild type; the disc remains a single epithelial layer but in the highly convoluted proximal regions, of the wing disc at least, the columnar cells give way to cuboidal epithelial cells, which are defi- cient in cytoskeletal elements. Pupariation is delayed 3.2 days in mutants and the discs contain 122,000 cells at the end of nine days compared to 50,000 cells in wild type discs, which attain full growth at 5 days. Disc phenotype autonomous in transplants into adult hosts. Occasional mutant pupae reach the pharate-adult stage so that adult structures can be studied. Abdomens normal; eyes often swollen and may be split into two parts; extra head bristles; distal parts of antennae and legs may be missing; wings often fail to evaginate. Legs most severely affected; joints short and thick; missing tarsal joints and claws and tarsal fusions; increased bristle densi- ties with deviant chaetal polarities; frequent outgrowths and ingrowths of cuticle; the latter giving rise to cuticle bound vesicles within the legs. alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________________ ft1 spont Mohr, 20b15 3, 4 viable allele ft2 l(2)sz32 5 viable allele ft3 l(2)sz71 5 viable allele ft4 l(2)a13 5 pupal lethal ft5 l(2)a17 5 pupal lethal ft6 l(2)a27 5 pupal lethal ft7 l(2)blo 5 pupal lethal ft8 HD l(2)ftfd 1 pupal lethal ft9 EMS l(2)gd1 2 pupal lethal ft10 l(2)h1 5 pupal lethal ft11 l(2)h27 5 pupal lethal ft12 l(2)sz12 5 pupal lethal ft13 l(2)sz29 5 pupal lethal ft14 l(2)sz37 5 pupal lethal ft15 l(2)sz44 5 embryonic lethal ft16 l(2)sz52 5 pupal lethal ft17 l(2)sz81 5 pupal lethal ( 1 = Bryant, Huettner, Held, Ryerse and Szidonya, 1988, Dev. Biol. 129: 541-54; 2 = Gateff, 1977, DIS 52: 4-5; 3 = Mohr, 1923, Studia Mendeliana (Brunae). pp. 266-87; 4 = Mohr, 1929, Z. Indukt. Abstamm. Vererbungsl. 50: 113-200 (fig.); 5 = Szidonya and Reuter, 1988, Genet. Res. 51: 197-208. cytology: Placed in 24D5-8 based on its deletion by Df(2L)sc19-1 = Df(2L)24D5-6;25C8 but not by Df(2L)dp-h28 = Df(2L)24D8;24F6-7. other information: G = Gull, a dominant allele of ft. # ftd: see qs # fty: see fru fu: fused Edith M. Wallace, unpublished. # fu: fused location: 1-59.5. origin: Spontaneous. discoverer: Bridges, 12k4. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 55-58 (fig.). Lynch, 1919, Genetics 4: 501-33. King, 1970, Ovarian Development in Drosophila melanogaster, Academic Press, New York, London. Busson, Limbourg-Bouchon, Mariol, Preat, and Lamour-Isnard, 1988, Roux's Arch. Dev. Biol. 197: 221-30. phenotype: Veins L3 and L4 fused from base to beyond anterior crossvein with elimination of anterior crossvein and first basal cell. L3 and L4 fused at tip; this fusion may reach back to basal cell. L3 may be thickened and branched to vary- ing degrees; L4 may be partially or completely absent. Mosaic wings in which the posterior compartment is nearly entirely fu/fu may develop normally; alternatively, patches of + tissue in a fu wing may develop a fu phenotype (Fausto-Sterling, 1978, Dev. Biol. 63: 358-69). Wings usually extended; flightless owing to cuticle defect (Deak). Ocelli reduced or absent; bristles of ocellar region small or absent. Eyes small and slightly rough. Phototactic response normal (Benzer, 1967, Proc. Nat. Acad. Sci. USA 58: 1112-19). Anterior scu- tellar bristles reduced in number and scutellum shortened. Female late to eclose and has decreased longevity. Ovaries histologically normal at eclosion but with half the normal number of ovarioles (Beatty, 1949, Proc. Roy. Soc. Edinburgh, B 63: 249-70); fecundity 4% normal. Developing egg chambers may fuse or become tumorous with age (King, Burnett, and Sta- ley, 1957, Growth 21: 239-61 (fig.)]. All aspects of pheno- type respond in a coordinated fashion to experimental manipu- lation (Wust and Hanratty, 1979, Can. J. Genet. Cytol. 21: 335-46). Proportion of tumorous egg chambers increases by 6% per day. Females raised at 18 show only 10% the tumor development of those raised at 25. Tumor formation also enhanced by presence of YS (King, 1969, Nat. Cancer Inst. Monogr. 31: 323-45). Ovarian effects in females carrying fu and a deficiency for fu [i.e. In(1)ClLy4R = In(1)4A5- B1;17A6-B1L1A8-B1;18A3-4R] are more extreme than those in fu homozygote (King, 1959, DIS 33: 142-43; 1970). Alleles vary in strength; measures of ovarian tumor formation revealed that fu1 = fu14 > fu7 > fu13 > fu11 = fu12 [Smith and King, 1966, J. Nat. Cancer Inst. 36: 445-63 (fig.)]. fu/fu ovaries transplanted into fu+ hosts develop autonomously in regard to fertility (Clancy and Beadle, 1937, Biol. Bull. 72: 47-56; Sobels, 1950, Experientia 6: 139-40) and tumor formation (Smith, Bodenstein, and King, 1965, J. Exp. Zool. 159: 333- 36). The few normal-appearing eggs that are laid by fu/fu females produce adults only if they have been fertilized by fu+-bearing sperm (Lynch, 1919, Genetics 4: 501-33). Eggs fertilized by fu- or Y-bearing sperm, with rare exceptions (Counce), develop into embryos that become abnormal 5-51/2 hr after fertilization. Lethal embryos exhibit incompletely penetrant segment polarity defects in which the anterior denticle-belt-bearing half of each segment shows mirror-image duplication replacing the naked cuticle of the posterior half; more pronounced in thoracic segments; penetrance in right and left hemisegments at the same level is not necessarily corre- lated. (Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801, Gergen and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 49-62). Elimination of regions of dor- sal pattern and occasional head defects are also observed. fu eggs from fu/+ mothers develop normally. Segment polarity defects autonomous in mosaics (Gergen and Wieschaus). Hetero- zygous daughters from homozygous mothers on the other hand, often have abnormal abdominal segmentation and, as embryos, have abnormal musculature. This is a maternal effect not found in the reciprocal cross, and it is temperature sensitive (Armstrong and Sobels). RK1. alleles: No complementation observed in 120 heteroallelic com- binations (Wurst and Hanratty). allele origin discoverer synonym ref ( comments | __________________________________________________________________________________________ fu1 spont Bridges, 12k4 1, 4, 9, 11, 12, 14, 17 WIWI fu2 Sturtevant 3 fu3 Stern 3 fu4 Moore fu3M 3 *fu5 heat Grossman, 1932 fug 3, 4, 7 fu6 L.V.Morgan fu20l 18 fu7 H2CO Auerbach, 1951 fuff 2, 3, 11, 12, 14 *fu8 UV Edmondson, 51e fu51e 4, 13 fu9 azm / Purdom, 57a fu57a 4, 11, 12 *fu10 azm Purdom, 57f fu57f 4, 12 fu11 spont R.F.Grell, 1959 fu59 1, 4, 11 WIWW *fu12 / ray Fahmy, 62f1 fu61f1 4, 11 *fu13 / ray Fahmy, 62f2 fu62f2 4, 11 fu14 / ray Fahmy, 62f3 fu62f3 1, 4, 11 WSWI fu15 NNG Kaufman, 1968 fu68 10 fu16 P Gans fumimi 1 SWIS fu17 Deak fuDB203 5 fu18 EMS Wurst fu15 18 fu19 EMS Wurst fu20 18 fu20 EMS Wurst fu40 18 fu21 EMS Wurst fu41 18 fu22 EMS Wurst fu67 18 fu23 EMS Wurst fu83 18 fu24 EMS Wurst fu49 18 fu25 EMS Hanratty fu429 18 fu26 EMS Hanratty fu2341 18 fu27 EMS Hanratty fu2322 18 fu28 EMS Hanratty fuKD 18 fu29 EMS Hanratty fuMH63 18 fu30 EMS Hanratty fu0A 18 fu31 EMS fumH63 1, 18 pupal lethal ` fu32 EMS fuecn 1, 6, 15 WSWS fu33 futs1; who 8 ` fu34 futs2 fu35 futs3 fu36 spont Schalet fuS 1 SWWW fu37 EMS Perrimon fu2P 16 fu38 EMS Perrimon fu9PZ 16 fu39 EMS Perrimon fuIPP7 16 pupal lethal fu40 EMS Perrimon fu9P2.3 1, 16 pupal lethal ` fu41 X ray fuA 1 SIWS fu42 DEB fuC10 1 ISWI fu43 DEB fuDB3 1 SISS fu44 DEB fuDB4 1 ISS- fu45 DEB fuDB5 1 WWIW fu46 DEB fuDB6 1 IIWW fu47 DEB fuDB9 1 IIII fu48 DEB fuDB10 1 IIWI fu49 DEB fuDB11 1 IIII fu50 DEB fuG3 1 SWSS fu51 DEB fuJ3 1 IIIS fu52 DEB fuJB3 1 WWS- fu53 DEB fuL4 1 SWWS fu54 DEB fuM1 1 SSIS fu55 DEB fuMC2 1 SISS fu56 DEB funew 1 SSWS fu57 DEB fuW3 1 SSWI fu58 DEB fuY1 1 SSS- ( 1 = Busson, Limbourg, Bouchon-Mariol, Preat and Lamour- Isnard, 1988, Roux's Arch. Dev. Biol. 197: 221-30; 2 = Counce, 1956, Z. Indukt. Abstamm. Vererbungsl. 87: 462-81; 3 = CP552 4 = CP627 5 = Deak, 1976, J. Insect Physiol. 22: 1159-65; 6 = Gergen and Wieschaus, 1986, Roux's Arch. Dev. Biol. 195: 49-62; 7 = Grossman, 1934, DIS 1: 30; 8 = Homyk and Grigliatti, 1983, Dev. Genet. 4: 501-33; 9 = Lynch, 1919, Genetics 4: 501-33; 10 = Kaufman, 1969, DIS 44: 44; 11 = King, 1970, Ovarian Development in Drosophila Melanogaster, Academic Press, New York, London; 12 = King, Burnet and Staley, 1957, Growth 21: 239-61; 13 = Meyer and Edmondson, 1951, DIS 25: 72; 14 = Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. 237: 55-58 (fig.); 15 = Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801; 16 = Perrimon and Mahowald, 1987, Dev. Biol. 119: 587-600; 17 = Smith and King, 1966, J. Nat. Cancer Inst. 36: 445-61 (fig.); 18 = Wrust and Hanratty, 1979, Can. J. Genet. Cytol. 21: 335-46. | Phenotype as determined by Busson et al. with respect to wing phenotype, viability, fecundity and maternal effect respectively; W = weak, I = intermediate, S = strong. Wing phenotype, veins L3 and L4 fused only proximally = W, at several points = I, all along length = S. Viability as the ratio of the number of fused flies to wild type in fu/+ X fu/Y: 0.75-1.0 = W, 0.5-0.75 = I, 0.25-0.5 = S. Fecundity as the ratio of eggs laid by fu/fu versus fu/+ sisters: 0.5-1.0 = W, 0.25-0.5 = I, 0-0.1 = S. Maternal effect on segmentation as percent of embryos with all segments entirely duplicated: 0-25% = W, 25-70% = I, 70-100% = S. / azm = azo-mustard. ` Phenotype described below. cytology: Placed in 17C3-D2 based on its inclusion in Df(1)fu- H4 = Df(1)17C3-7;17D1-2 (Busson, Limbourg-Bouchon, Mariol, Preat and Lamour-Isnard, 1988, Roux's Arch. Dev. Biol. 197: 221-30). molecular biology: Included in a 250-kb walk from 17C to 17E; no alterations in restriction map were observed for 12/12 viable fu alleles nor for the three pupal-lethal alleles listed in the allele table. Df(1)fu-Z4 determined to be defi- cient for 40-kb; a cosmid covering this region when injected into embryos effects partial rescue of the maternal effect of homozygosity for fu in some 2% of embryos; similar results obtained from a 14-kb subclone. Two adjacent EcoRI subclones identify four transcripts on Northern blots of mRNA from 0-4 hr embryos of 1.3 and 1.6 kb for the more distal fragment and 2.5 and 3.5 kb for the more proximal fragment; the fu tran- script or transcripts not identified (Mariol, Preat and Limbourg-Bouchon, 1987, Mol. Cell. Biol. 7: 3244-51). # fu31 phenotype: Homozygous and hemizygous females and hemizygous males die in pupal stage; lethality suppressible by Su(fu). fu31/fu41 and fu31/Y have all segments entirely duplicated; lack mouth hooks and some have no head. fu31/+ embryos from such clones exhibit very low paternal rescue; small correction of segmental phenotype, low hatch, and preadult mortality (Busson, Limbourg-Bouchon, Mariol, Preat and Lamour-Isnard, 1988, Roux's Arch. Dev. Biol. 197: 221-30). # fu33 phenotype: A temperature-sensitive allele. fu wing-vein pheno- type occurs at all temperatures; ocelli absent when raised at 22 but not at 17. TSP for absence of anterior ocellus from second instar through pupal stage, for posterior ocelli res- tricted to late third instar and early pupal stage. Flight- less when raised at 22 or 29 but not at 17; wings held hor- izontally perpendicular to body at 29. Musculature abnormal when raised at restrictive temperatures [Homyk and Grigliatti, 1983, Dev. Genet. 4: 77-97 (fig.)]. # fu40 phenotype: fu40/Y sons of fu40/+ mothers die as late pupae or newly emerged adults; lethality suppressible by Su(fu). fu embryos produced by homozygous germ-line clones are mostly lethal (70%); those that hatch mostly achieve adulthood (Per- rimon and Mahowald, 1987, Dev. Biol. 119: 587-600). # Fuc: alpha-Fucosidase location: 3-35.5 [based on 45 recombinants between h(26.5) and st (44.0) (Repp)]. phenotype: Structural gene for alpha fucosidase (EC 3.2.1.51). A diffuse intermediate zone of activity in FucF/FucS heterozy- gotes suggests multimeric nature of enzyme (MacIntyre). Flies heterozygous for a null allele and a deficiency for Fuc are viable and fertile (Bond). alleles: FucF and FucS are naturally occurring alleles; also one null allele, Fucn1, induced by ethyl methanesulfonate (Bond). cytology: Placed between 67F2 and 68D6 on the basis of its inclusion in the region deleted by Df(3L)vin2 = Df(3L)67F2- 3;68D6 (Bond). # Fuh: see Fum # fum: fused mushroom bodies (J.C. Hall) location: 2- (not mapped). origin: Induced by ethyl methanesulfonate. discoverer: Heisenberg and Fischbach. phenotype: Beta lobes of mushroom bodies in dorsal brain are fused at the midline; penetrance incomplete. # Fum: Fumarase location: 1-19.9. synonym: Fuh: Fumarate hydratase. references: Madhaven and Ursprung, 1973, Mol. Gen. Genet. 120: 379-80. phenotype: The structural gene for fumarase [FUM; L-malate hydro-lyase (EC 4.2.1.2)]. Enzyme level observed depends on genetic background (Laurie-Ahlberg, Maroni, Bewley, Lucchesi, and Wier, 1980, Proc. Nat. Acad. Sci. USA 77: 1073-77). Enzyme levels higher in females than in males in midlarval, pupal, and pharate-adult stages; female levels drop and are surpassed by male levels in older adults (Whitney and Luc- chesi, 1972, Insect Biochem. 2: 367-70). Head and thorax have higher activities than abdomen (Pipkin, Chakrabarthy, and Bremner, 1977, J. Hered. 68: 245-52). Activity equally dis- tributed between mitochondrial and cytoplasmic fractions (Pip- kin et al.). alleles: Two electrophoretic alleles, FumF and FumS, found in natural populations. (Designated Fum6 and Fum4 by Research Triangle Park Group, 1978, DIS 53: 117). cytology: Placed in 5C-6C11 by method of segmental aneuploidy (Pipkin et al.). # furled: see fd # furrowed: see fw # fused: see fu # fused filament: see fft # fused mushroom bodies: see fum # fuzzy: see fy # fw: furrowed location: 1-36.85 (Lefevre, 1970, DIS 40: 45). origin: Spontaneous. discoverer: Duncan, 14k. references: 1915, Am. Naturalist 49: 575-82. Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 80. Nachtsheim, 1919, Z. Indukt. Abstamm. Vererbungsl. 20: 118- 56. phenotype: Eyes with vertical fold and furrows. Head and scu- tellum shortened. Bristles gnarled and shortened, especially the postscutellars. Best classification character is short, blunt notopleurals. RK2. Phenotype can become nearly wild type on inbreeding (Lefevre). alleles: Most information on fw alleles tabulated below. Descriptions of special phenotypic features differing from those described above for fu1 are detailed separately follow- ing the table. allele discoverer origin ref ( __________________________________________________________________________ fw1 Duncan, 14k spont 1, 2, 3, 9, 10 *fw2 | / Muller, 31a X ray in 1, 2 In(1)dl-49 *fw20c E. Wallace 1 *fw33d E. Wallace 1 *fw33e Bridges 1 fw34e / Duncan, 34e20 1, 2 fw35k Spencer, 35k4 1 *fw39k Ives 1 fw49c | / R.C. King, 49c28 32P 2,8 fw59 | / Garcia-Bellido, 59i21 X ray 2, 4 fw60 | / Garcia-Bellido, 60k8 X ray 2, 4 fw67 Hayman, 67j9 X ray 5 fw68 Kaufman nitrosoguanidine 7 *fwc Bridges, 15l27 2 *fww / Ives, 43b24 spont 6 fwwr / R.M. Valencia, 1959 X ray in 11, 12 In(1)scS1Lsc8R+dl-49 ( 1 = CP552; 2 = CP627; 3 = Duncan, 1915, Am. Nat. 49: 575- 82; 4 = Garcia-Bellido, 1963, Genet. Iber. 15: 1-102; 5 = Hayman and Maddern, 1969, DIS 44: 50; 6 = Ives, 1946, DIS 19: 46; 7 = Kaufman, 1969, DIS 44: 44; 8 = King, 1949, DIS 23: 62; 9 = Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. 237: 80; 10 = Nachsteim, 1919, Z. Indukt. Abstamm. Vererbungsl. 20: 118-56; 11 = Valencia, 1959, DIS 33: 100; 12 = Valencia, 1965, DIS 40: 36. | Only differences from the basic fu1 phenotype indicated. / Phenotype described separately below. cytology: Placed in 11A4 (Lefevre, 1981, Genetics 99: 461-80). #*fw2 phenotype: Extreme fw. Female sterile. RK2A. # fw34e phenotype: Originally showed eye surface medium folded; bris- tles much gnarled. Schultz and Curry report that stock in 1940 showed gnarled bristles and eye small but no vertical fold. RK2. # fw49c phenotype: Eyes furrowed; distal portions of aristal branches hooked; wings divergent and often stringy; scutellar groove reduced. Bristles split, bent, and often erect; acrostichal hair pattern distributed with whorls and naked areas. Late hatching, poorly viable, and mostly sterile. fw49c/fw pheno- typically intermediate but more like fw/fw than fw49c/fw49c. RK3. # fw59 phenotype: Eyes rough and creased; facets irregular, 15% fewer than normal. Eyes browner than normal; pterine concentration reduced in the eyes and, except for isoxanthopterine, increased in testis sheath. Riboflavin accumulates in Mal- pighian tubules. Large bristles of head and thorax short, thick, angled, blunt, and occasionally reduced to stumps. Arista thick with contorted and supernumerary branches. Scu- tellum small with groove between it and thorax reduced. Hatchability and larval development normal; larval anal plates swollen and surrounded by melanotic halo. Melanotic anal region persists in pupa; pupa also has melanotic spots else- where that may result in nonpigmented areas on the imaginal integument. Extrusion of anterior and posterior spiracles in prepupa incomplete. Many fw59 flies die either after 24-30 hr of pupal development or at the time of eclosion. Fecundity of female reduced owing to reduced number of ovarioles. RK2. # fw60 phenotype: Like fw59 but with lower penetrance and expres- sivity. RK2. #*fww: furrowed-weak phenotype: Affects only bristles, particularly the scutellars and postalars. Eyes normal. Normal fertility and viability. RK2. # fwwr: furrowed-wrinkled synonym: wr. phenotype: Eye surface in folds. Some bristles shortened, thickened, or curved; many doubled and may be fused. Viabil- ity low. RK2. # fwd: four wheel drive (M. Fuller) location: 3- {0}. discoverer: Wolf, 1988. synonym: ms(3)neol. origin: P-element insert marked with neomycin resistance, from the single element mobilization screen of Cooley and Sprading, 1988. references: Wolf and Fuller, unpublished. phenotype: Recessive male sterile. Failure of cytokinesis after meiosis I and meiosis II in males, usually resulting in onion stage early spermatids with four equal sized nuclei associated with a single, large mitochondrial derivative. Cells in meiosis II contain two spindles. Females fertile. cytology: Placed in 61A1-C4 based on its inclusion in Df(3L)emc-E12 = Df(3L)61A;61D3 but not in Df(3L)Ar14-8 = Df(3L)61C3-4;62A8. # fx: see fafx #*fy: fuzzy location: 2-33. origin: Spontaneous. discoverer: Ives, 39a. references: 1940, DIS 13: 49. phenotype: Hairs on abdomen and thorax irregular and directed toward midline. Hairs on wing margins erect. Hairs on legs also show abnormal polarities (Held, Duarte, and Dera- khshanian, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 145- 57). Resembles fz. Fertility and viability below normal. RK2. alleles: A possible second allele, fy2, described by Grell (1969, DIS 44: 46-47) but maps to 2-24.1. fz: frizzled From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 85. # fz: frizzled location: 3-41.7. origin: Spontaneous. discoverer: Bridges, 38b18. references: Adler, Charlton, and Vinson, 1987, Dev. Genet. 8: 99-119. phenotype: Hairs on thorax directed irregularly toward midline. Thoracic bristles also inturned and often wavy. Postverticals may turn outward. Hairs on wing edge and feet nearly erect; trichomes on wings of flies carrying weaker alleles tend to form swirls rather than lying parallel to one another and pointing distally; stronger alleles can cause random orienta- tion of trichomes. Polarity of chaetae deranged in charac- teristic ways on wings, notum, halteres, legs, tergites, and sternites; fz M+ clones in M/+ wings cause derangement of polarity in M/+ cells surrounding clone (Gubb and Garcia- Bellido, 1982, J. Embryol. Exp. Morphol. 68: 37-57). In a wild-type background clones of wing cells homozygous for fz alleles that cause eye roughening, but not of those without effect on eye texture, cause adjacent normal trichomes in regions distal, anterior, and posterior, but not proximal to the clone, to orient toward the clone rather than distally as they normally do; no effect on trichomes on opposite surface of the wing (Vinson and Adler, 1987, Nature 329: 549-51). Wing may be reduced. A low level of doubling of trichomes and splitting of chaetae observed. Sex combs may be irregular. Most alleles cause eyes to be rough. Two weak alleles, fz24 and fz34 and two neomorphic alleles, fz13 and fz20, have nor- mal eye textures. Extra leg joints tend to form as mirror- image duplications proximal to the normal joints on tarsal segments one to four. Also polarities of bristles, hairs, and bracts on legs abnormal (Held, Duarte, and Derakhshanian, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 145-57). RK2. alleles: Most alleles fit into a hypomorphic to amorphic series with many hemizygotes displaying a more severe phenotype than homozygotes. Four strong alleles are lethal in homozygotes; three are associated with chromosome rearrangements (fz3, fz26 and fz30) and one with a normal sequence (fz14); they comple- ment one another in all pairwise combinations and survive in combination with fz deficiencies; therefore lethality is not associated with the fz locus. allele origin discoverer synonym ref ( phenotype | cytology ___________________________________________________________________________ fz1 spont Bridges, 38b18 1, 3, 6 MMV fz2 spont Ives, 46f20 fz46f 5 fz3 X ray Velissariou 2 SSL / In(3L)70D6-7; 75D8 + In(3L)73D3-5; 80-81 fz4 X ray Velissariou 2 In(3L)70D6-7; 80-81 + In(3LR)79F; 87D-E fz5 X ray 4 fz6 X ray 4 fz7 X ray 4 fz8 X ray 4 fz9 EMS 4 fz10 EMS 4 fz11 EMS 4 fz12 EMS 4 fz13 EMS Adler fzF31 1, 6 MMV fz14 EMS Adler fzH41 1 SSL / + fz15 EMS Adler fzH51 1 SSV + fz16 EMS Adler fzI12 1 MMV fz17 EMS Adler fzI22 1 MMV fz18 EMS Adler fzJ21 1 MMV fz19 EMS Adler fzJ22 1 MMV fz20 EMS Adler fzN21 1, 6 MMV + fz21 EMS Adler fzP21 1 MMV fz22 EMS Adler fzR51 1 MMV fz23 EMS Adler fzR52 1 MMV fz24 EMS Adler fzR53 1 MMV + fz25 EMS Adler fzR54 1, 6 SSV + fz26 / ray Adler fzC21 1 SSL / Tp(3;2)40; 66B-D; 70D4-7 fz27 / ray Adler fzEA3 1 MMV T(2;3)40; 70D4-7 fz28 / ray Adler fzEAB 1 MMV + fz29 / ray Adler fzEF2A 1 MMV + fz30 / ray Adler fzK21 1 SSL / In(3L)70D4-7; 75A-B12 fz31 HD Adler fzCAD3 1 SSV + fz32 HD Adler fzCI9 1 MMV + fz33 HD Adler fzCT8A 1 MMV + fz34 HD Adler fzCT8C 1 WWV + fz35 HD Adler fzCT9B 1 MMV + fz36 HD Adler fzCT43 1 MMV + fz37 HD Adler fzKD4a 6 molecular deletion fz38 P derived Adler fzCT8CX2 In(3L)61C; 69A;70D4-7 ( 1 = Adler, Charlton and Vinson, 1987, Dev. Genet. 8: 99- 119; 2 = Ashburner, Angel, Detwiler, Faithfull, Gubb, Har- rington, Littlewood, Tsubota, Velissariou and Walker, 1981, DIS 56: 186-90; 3 = CP627; 4 = Gubb and Garcia-Bellido, 1982, J. Embryol. Exp. Morph. 68: 37-57; 5 = Ives, 1946, DIS 20: 65; 6 = Vincent and Adler, 1987, Nature 329: 549- 51. | Phenotypic analysis according to Adler et al.; the first letter scores thoracic-bristle phenotype and the second wing-hair disorientation (S = strong, M = moderate, W = weak); the third letter indicates viability (V) or lethality (L). / Lethal alleles complement each other as well as fz deficien- cies indicating three of the four lethal chromosomes are rearranged; they complement each other. molecular biology: Genomic sequence isolated by transposon tag- ging. A single 4-kb mRNA identified in Northern blots of pupal RNA. A full-length cDNA contains a single long open reading frame which encodes a 581-amino-acid polypeptide. The N terminus contains a putative signal sequence. Following a long N-terminal region, there are seven strongly hydrophobic regions typical of transmembrane domains three of which con- tain a proline residue. No striking homologies to other polypeptide sequences found in databases (Vinson, Conover and Adler, 1989, Nature 338: 263-64). cytology: Placed in 70D6-7 based on commonality of breakpoints in In(3L)fz3 and In(3L)fz4 (Ashburner et al.). Adler places fz in 70D4-5 based on in situ hybridization of P-element probe to polytene chromosomes of fz34. # fz13 phenotype: A neomorphic allele causing severe disruption of trichome orientation in the costal wing cell, a region little affected by most alleles; phenotype of homozygote more severe than that of hemizygote. Also unlike other alleles, homozy- gous clones of fz13 cells in the wing do not affect orienta- tion of trichomes in surrounding normal cells. A third not- able feature of fz13 is that it is without effect on eye tex- ture. # fz20 phenotype: Like fu13. # fzy: fizzy location: 2-51. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.). phenotype: Homozygous lethal; ventral outside and central ner- vous system degenerate. alleles: Eight; fzy1 and fzy2 (isolated as IB and IH) retained.