ci: cubitus interruptus Wings showing from no interruption (extreme left) to complete absence (extreme right) of the cubital vein. From Stern and Kodani, 1955, Genetics 40: 343-73. # ci: cubitus interruptus location: 4-0 [most proximal mutant in 4 (Sturtevant, 1951, Proc. Nat. Acad. Sci. USA 37: 405-7)]. phenotype: Vein L4 shows one or more gaps both distal and prox- imal to posterior crossvein, generally nonterminal. Anterior crossvein shortened or absent. Other gaps and scattered branch veins in region of crossveins. At 19, nearly all flies have a mutant phenotype; at 25, there is slight overlap with wild type; at 30, virtually all flies are wild type. Dosage effect such that ci/0 haplo-4's are more extreme than ci/ci diplo-4's, which are more extreme than ci/ci/ci triplo-4's. Suppressed by su(Hw)2 (Kotarski). For interactions of ci with en, H, ve, and cg, see House (1953, Genetics 38: 199-214, 309-27; 1955, Anat. Record 122: 471; 1959, Genetics, 44: 516; 1961, Genetics, 46: 871). Expression of ci sensi- tive to genetic background; selection possible for more and less extreme phenotypes (House and Yeatts, 1962, Genetics 47: 960); contribution of chromosome 2 more important than that of 3 (House and Pernaveau, 1971, Genetics 68: s29). Phenotypic effect visible in prepupa by absence of the longer longitudinal vein. RK1 at 19 and higher rank with higher tem- peratures. alleles: Two types of alleles: mutant alleles tabulated below and described in more detail following the table; wild-type isoalleles described separately. allele origin discoverer synonym ref ( comments | _____________________________________________________________________________ ci1 spont Terentieva, 30b 1, 5, 6 gypsy insert ci36 spont Curry, 36l 2 4.0 kb insert ci57 X ray Hochman, 57g 3 800 bp deletion ciD X ray Ruch, 32a18 1 molecular rearrangement ciD-G Gloor 4 ciW spont Wallace, 36d20 It: Interrupted 2 4.0 kb insert/ ( 1 = Bridges, 1935, Biol. Zh. (Moscow), 4: 401-20; 2 = CP627; 3 = Hochman, 1971, Genetics 67: 235-52; 4 = Scharloo, 1963, DIS 38: 32; 5 = Terentieva, 1931, Eksperim. Biol. 7: 187-90 (fig.); 6 = Tiniakov and Teren- tieva, 1933, Genetics 18: 117-20 (fig.). | Molecular results from Kotarski. / Different from the insert in ci36. cytology: Placed in salivary chromosome region 101F2-102A5, on the basis of its inclusion in Df(4)M63a = Df(4)101F2- 102A1;102A2-5. molecular biology: Region cloned and restriction mapped by Locke and Kotarski; all molecular lesions indicated in the table occur in the same 5.8 kb Bgl fragment. This fragment hybridizes to a 2.0 kb RNA that shows peak concentrations in late pupae. other information: The expression of ci+ can be altered in direction of ci by certain chromosome rearrangments that have one break in vicinity of ci locus. Rearranged fourth chromo- somes carrying a mutant allele of ci, R(ci), may also show altered expression of gene [Stern and Kodani, 1955, Genetics 40: 343-73 (fig.)]. R(ci) and R(ci+) terminology not retained here; interaction with ci included in descriptions of aberrations involving chromosome 4. #*ci+2: cubitus interruptus-wild-type isoallele origin: On fourth chromosome carrying ey2. references: Stern and Schaeffer, 1943, Proc. Nat. Acad. Sci. USA 29: 361-67. phenotype: Homozygote wild type at 14 and 26. ci+2/Df(4)M wild type at 26; shows some thinning and interruption of L4 at 14. ci+2/ci wild type at 26; at 14, fewer flies show thinning or interruption of L4 than ci+C/ci. ci+2/ciW shows significantly greater amount of thinning and interruption of L4 than ci+C/ciW. RK3. alleles: ci isoalleles superscripted *+2, +3, and *+C described by Stern and Schaeffer (1943), +5 by Hochman (1961, Evolution 15: 239-46). Relative strengths are +C > +5 > +3 > +2. # ciD: cubitus interruptus-Dominant phenotype: Wings show interruptions of L4 in two places: proximal to and distal to anterior crossvein. L5 also shows distal interruption. L3 and L5 thick. Consider- able plexus effect and knotting of veins. Wings broader, warped or concave upward, regularly extended, and bent back- ward. Alula fused with and in same plane as blade of wing. Black dried haemolymph from axillary spiracle. Slight scal- loping of inner wing margin, with hairs and tufts. Direction and extent of temperature effects depends on genetic back- ground (Scharloo). In general, no overlapping of wild type. Inviable in combination with Ax/Ax or Ax/Y (House and Lutes, 1975, Genetics 80: 542-43). H/+ inhibits scalloping of ciD but greatly enhances L4 interruption (House, 1959, Genetics 44: 516). Fully dominant in triplo-4's (Sturtevant, 1936, Genetics 21: 448). Two doses of ciD reduce survival of triplo-4 flies (Parker, 1969, Mutat. Res. 7: 393-407). Homoz- ygotes lethal in embryo (Hochman, 1971, Genetics 67: 235-52). Embryonic segment polarity disrupted; anterior portions of segments with their denticle belts duplicated in mirror-image fashion; posterior portions missing; each segment almost entirely covered with denticles (Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801). Fine hairs eliminated from dorsal abdominal segments; replaced with clear cuticle and socketed denticles (Orenic, Chidsey, and Holmgren, 1987, Dev. Biol. 124: 50-56). Embryonic CNS relatively normal (Patel, Schafer, Goodman, and Holmgren, 1989, Genes Dev. 3: 890-904). Genotype of oocyte with respect to ciD without effect on phenotype of progeny (Orenic et al.). ciD/l(4)102ABc dies as embryo, ciD/l(4)102ABb as embryo or larva; in ciD/Ce2 death usually delayed until pupal stage (Hochman, 1971). Survival of ci/ciD/Df(4)M101-63a argues for nonallelism or pseudoallelism of ci and ciD (Hochman, 1971). RK1. alleles: ciD-G, a less severe derivative of ciD, recovered as a recombinant between ciD and spapol (CP627). ciD-l is a revertant of the ci phenotype in combination with either _ or ci, which has retained the lethal phenotype (Puro). Ten simi- lar revertants induced by / rays isolated by Orenic et al.; three were cytologically normal and seven were translocations with breakpoints in or near the chromocenter. ciDrv [ciD-l of Haavisto (see Puro, 1982, DIS 58: 205)] reverted for ci phenotype but not for recessive lethality; complements ci. cytology: Salivary study by Bridges revealed no chromosomal aberration. other information: Not allelic with ci, at least with respect to its lethality, since ciD/Df(4)M101-63a survives, whereas ci/Df(4)M101-63a is mutant (Hochman, 1965, DIS 40: 60). Based on location, phenotype, and complementation, ciD and Ce postulated to be part of a single complex (Orenic et al.). # ciW: cubitus interruptus of Wallace phenotype: Homozygote is extreme ci type. Wings sometimes almost twice normal width, arclike, and virtually lack veins. Often present is a well-organized pattern of venation in which the posterior crossvein flows smoothly into L5. Legs lumpy, sex combs larger than normal, antennae enlarged, eyes smaller, and extra bristles present. Heterozygote shows gap in L4 in 80% of flies. ciW enhanced by H, en, and Cy (House, 1953, Genetics 38: 669-70; 1959, Genetics 44: 516) and by Tp(4;Y) (Benner, 1972, Genetics 71: s4). Temperature effect described by House (1955, Genetics 40: 576). RK2. # cin: cinnamon location: 1-0 (1.7 x 10-3 unit to the left of y; Padilla and Nash, 1977, Mol. Gen. Genet. 155: 171-77). references: Baker, 1973, Dev. Biol. 33: 429-40. phenotype: cin/Y and cin/cin embryos of cin/cin mothers almost completely lethal; rare surviving adults have reddish-brown eyes; both survival and normal eye pigmentation affected by the presence of cin+ in either the mother or the zygote; how- ever, cin progeny of cin+ mothers exhibit mutant phenotype when raised on 0.02% allopurinol (Padilla and Nash, 1977, Mol. Gen. Genet. 155: 171-77). Survival of the double mutant cin3 v is also sensitive to allopurinol (Bentley and Williamson, 1982, DIS 58: 23). Mosaic and transplantation analysis (Nis- sani and Fellinger, 1978, Dev. Biol. 65: 117-27) indicate that the maternal effect of cin+ on eye color requires the presence of cin+ in the oocyte, whereas cin+ in ovarian meso- derm contributes to the maternal effect on viability. Affected progeny lack activity for four different molybdenum hydroxylases-all known to require a molybdenum-containing cofactor for catalytic function. These are aldehyde oxidase (Bentley and Williamson, 1982, Can. J. Genet. Cytol. 24: 1- 9), pyridoxal oxidase, xanthine dehydrogenase (Browder and Williamson, 1976, Dev. Biol. 53: 241-49), and sulfite oxidase (Bogaart and Bernini, 1981, Biochem. Genet. 19: 929-46). Inactivity of xanthine dehydrogenase accounts for the eye color phenotype. Level of low-molecular-weight molybdenum cofactor severely reduced. cin progeny of cin mothers CRM negative for pyridoxal oxidase (Warner, Watts, and Finnerty, 1980, Mol. Gen. Genet. 180: 449-53). Aldehyde oxidase CRM found in hemolymph of cin1 (100%) and cin9 (60%) larvae and in extracts of cin9 (32%) adults. Both alleles show about 70% normal quantities of xanthine dehydrogenase CRM (Browder, Wilkes, and Tucker, 1982, Biochem. Genet. 20: 111-24). Eye color expression nonautonomous in gynandromorphs (Padilla and Nash, 1977). alleles: All alleles induced by ethyl methanesulfonate except the spontaneous cin2 and perhaps cinB. allele ref ( phenotype __________________________________________ cin1 1 cin2 3 temperature sensitive cin3 6 cin3N 7 female sterile cin4 2 cin4N 7 | cin5 2 cin6 2 cin7 2 cin8 2 cin9 2 | cin10 2 / cin11 2 / cin12 2 cin13 2 cin14 2 cin15 2 | cinB 4 cinlk ` 5 ( 1 = Baker, 1973, Dev. Biol. 33: 429-40; 2 = Bentley and Williamson, 1979, Can. J. Genet. Cytol. 21: 457-71; 3 = Courtright, 1976, Genetics 83: s17; 4 = Courtright, unpublished; 5 = Hickey and Singh, 1982, DIS 58: 74-76; 6 = Mohler, 1977, Genetics 85: 259-72; 7 = Padilla and Nash, 1977, Mol. Gen. Genet. 155: 171-77. | Males carrying this allele produce cin+ sons in crosses to C(1)RM, cin y females. / Males carrying this allele produce cin sons in crosses to C(1)RM, cin y females. Males carrying other alleles produce no sons from such crosses. ` cinlk considered to be a hypomorphic or leaky allele of cin; it produces low levels of aldehyde oxidase and xanthine dehydrogenase activity and is genetically very close to yel- low; however, cin1/cinlk are wildtype both with respect to eye color and enzyme activity and may not therefore be an allele. cytology: Duplication analysis by Padilla and Nash place cin distal to arth and proximal to l(1)J1. other information: Four complementation groups described by Baker; a fifth observed by Warner. # cinnabar: see cn # cinnamon: see cin # ck: crinkled (M. Ashburner) location: 2-51.0 (estimated). discoverer: Bridges, 30c30. synonym: l(2)br27, l(2)35Ca, D group of O'Donnell et al. (1977). references: O'Donnell, Mandel, Kraus, and Sofer, 1977, Genetics 86: 553-66. Ashburner, Tsubota, and Woodruff, 1982, Genetics 102: 401-20. Gubb, Shelton, Roote, McGill, and Ashburner, 1984, Chromosoma 91: 54-64 (fig.). phenotype: Recessive lethal or semilethal. ck embryos exhibit denticles thickset and forked; hairs basally fused; sensory hairs blunt [Nusslein-Volhard, Wieschaus, and Kluding, (fig.)]. Hemizygous survivors, or survivors among heteroal- lelic combinations that partially complement for viability, have stubbly chaetae, multiple trichomes, and feathery aristae (Gubb et al.). Variable expression of a wavy, crinkled wing phenotype. Cell viable in clones of adult epidermis; bristle and hair phenotypes autonomous; useful as a cell marker in 2L for clonal analysis (Struhl). alleles: 13 named alleles, all but ck1 induced by ethyl methanesulfonate. Four additional EMS-induced alleles, including one weak allele, isolated by Nusslein-Volhard, Wieschaus, and Kluding (1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82). allele isolation # ref ( phenotypic class | _________________________________________________ ck1 ck2 BMW13 1, 2 2 ck3 BMW14 1, 2 3 ck4 BMW26 1, 2 1 ck5 HG22 1, 2 1 ck6 HG29 1, 2 1 ck7 HG32 1, 2 2 ck8 64-106 2 1 ck9 64-1564 2 1 ck10 GM12 2, 3 3 ck11 CH11 3, 4 ? ck12 CH39 3, 4 3 ck13 CH52 3, 4 2 ( 1 = Ashburner, Tsubota, and Woodruff, 1982, Genetics 102: 401-20; 2 = Gubb, Shelton, Roote, McGill, and Ash- burner, 1984, Chromosoma 91: 54-64; 3 = Maroni (unpub- lished); 4 = O'Donnell, Mandel, Kraus, and Sofer, 1977, Genetics 86: 553-66. | Class 1 survival at 1% or less, class 2 at 5%, and class 3 greater than 10% expected value. cytology: Placed in 35B10-C1 based on its inclusion in Df(2L)64j = Df(2L)34D1-2;35B9-C1 and Df(2L)fn30 = Df(2L)34C6- 7;35B9-C1, but not in Df(2L)AR-R1 = Df(2L)35A3-4;35B9-C1. other information: Allelism of l(2)35Ca and ck inferred from similarities in phenotype and map position. Insertion TE35B between 35B9 and 35C1 results in a class 2 ck allele (Gubb et al.). # CkII (: Casein kinase II, ( subunit location: 3-{47}. references: Saxena, Padmanabha, and Glover, 1987, Mol. Cell. Biol. 7: 3409-17. phenotype: The structural gene for the catalytic subunit of casein kinase II (CKII). CKII is a cyclic-nucleotide- independent, Ca2+ and calmodulin-insensitive protein kinase. It phosphorylates serine and threonine residues of a broad range of nuclear and non-nuclear proteins with functions in development, cell division, and oncogenesis. It exists as a 130,000 molecular weight (2|2 tetramer. Purification of the Drosophila enzyme described by Glover, Shelton, and Brutlag (1983, J. Biol. Chem. 258: 3258-65). molecular biology: cDNA sequence isolated by antibody screening of a \gt11 expression library. Nucleotide sequence shows an open reading frame encoding a 336-amino-acid polypeptide with strong homology to calf thymus CKII( and homology to the yeast homologue; also shows weak homology to the yeast Cdc28 gene. Drosophila CkII ( and | can rescue casein kinase II deficient yeast (Glover). cytology: Placed in 80A by in situ hybridization (Glover). # CkII |: Casein kinase II, | subunit location: 1-{36}. references: Saxena, Padmanabha, and Glover, 1987, Mol. Cell. Biol. 7: 3409-17. phenotype: The structural gene for the autophosphorylated, regulatory | subunit of casein kinase II (CKII). molecular biology: cDNA sequence isolated by antibody screening of a \gt11 expression library. Nucleotide sequence shows an open reading frame encoding a 215-amino-acid polypeptide with strong homology to calf thymus CKII| and homology to the yeast homologue. Genomic sequence reveals five introns in the protein-coding region and at least one more upstream from the initiating ATG (Saxena, Carney, Bruley, and Glover, 1989, Genetics 122: s25). Drosophila CkII ( and | can rescue casein kinase II deficient yeast (Glover). cytology: Placed in 10E by in situ hybridization (Glover). # cl: clot location: 2-18.83 (Kotarski, Pickert, and MacIntyre, 1983, Genetics 105: 371-86). origin: Spontaneous. discoverer: Bridges, 27a3. phenotype: Eye color dark maroon to sepialike with age, is less extreme than sepia. Severely deficient in one of three enzyme activities required for the conversion of dihydroneopterin triphosphate to pyrimidodiazepine, a precursor of the dro- sopterins (Wiederrecht, Paton, and Brown, 1984, J. Biol. Chem. 259: 2195-2200). Claimed to accumulate 2-amino-4- hydroxypteridine, biopterin, sepiapterin, and xanthopterin (Nikla, 1972, Can. J. Genet. Cytol. 14: 105-11). Eye color autonomous when larval optic disk is transplanted into wild- type host (Beadle and Ephrussi, 1936, Genetics 21: 230). Larval Malpighian tubes pale yellow, distinguishable from wild type (Brehme and Demerec, 1942, Growth 6: 351-56). RK1. alleles: cl2 (CP627). cl3 and cl4 induced by ethyl methanesul- fonate in CyO (Kotarski, Pickert, and MacIntyre, 1981, DIS 56: 191); clCA1 associated with T(1;2)clCA1 (Ashburner, Faithfull, Littlewood, Richards, Smith, and Velissariou, 1980, DIS 56: 186). cytology: Placed in salivary chromosome bands 25E1-2 (Ashburner and Velissariou, 1980, DIS 55: 196). # claret: see ca #*cld: cloudy location: 2-96 to -101. origin: / ray induced. discoverer: Wallbrunn, 61j6. references: 1964, DIS 39: 59. phenotype: Wings opaque from fluid between upper and lower mem- branes; occasionally, fluid forms small blisters. Males sterile; females highly infertile. RK2. # cleft: see cf # clf: see wtwclf # cli: clift (C. Nusslein-Volhard) location: 2-17. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.). phenotype: Embryonic lethal. Defect in head involution. No segmental movements. Shows abdominal transformations in com- bination with Pc-like mutants. alleles: Two. #*Cli: Clipped wings location: 1- (to the left of f). discoverer: Agol. references: 1936, DIS 5: 7. phenotype: Dominant wing mutant (no description given). Viable in male and homozygous female. RK3. # Clift: see Cli # clip wing: see dpo2 # clipped: see cp # Clipped wings: see Cli # Clipt: see Cpt # Clk: Clock (J.C. Hall) location: 1-1.4 (0.015 map units to the right of per01). origin: Induced by ethyl methanesulfonate. discoverer: Konopka and Orr. references: Dushay, Konopka, Orr, Greenacre, Kyriacou, Rosbash and Hall, 1990, Genetics 125: 557-78. synonym: Clk-6. phenotype: The normal 24 hour period of the circadian rhythms of adult locomotor activity and of eclosion are shortened by approximately 1.5 hours. Clk/+ heterozygotes have a period phenotype intermediate between wild-type and mutant homozy- gotes. The period of the phase-resetting response of the activity rhythm is shortened by 1-2 hours per cycle; adults entrain well to 12 hour light: twelve hour dark cycles, but evening peak of locomotor activity is advanced relative to wild-type; courtship song rhythms of mutant males have essen- tially normal one-minute periods. Temperature compensation of circadian period is normal (Q10 approximately equal to 1.0), in tests of locomotor activity rhythms. cytology: Series of deletions and duplications running from X distal tip to white; all failed to uncover and ameliorate effects of Clk. other information: Clk is close enough to per01 mutation so that it could be allele of the period gene; however, Clk/per01 indistinguishable from Clk/+. #*clm: clumpy marginals location: 1-32.6. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3205). discoverer: Fahmy, 1953. references: 1958, DIS 32: 68. phenotype: Irregularly bent marginal hairs, especially on pos- terior border of wings. Bristles stiff and frequently bent or split. Viability and fertility of males good. Homozygous females reduced in viability and fertility. RK2. other information: One allele each induced by 2-chloroethyl methanesulfonate and DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine. # clo: close down (T. Schupbach) location: 2-77. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female-sterile; homozygous females contain egg chamber which degenerate before yolk uptake. Occasionally normal egg chambers are found which take up yolk and form eggs. Such eggs often have fused dorsal appendages and remain unfertilized. alleles: clo1 to clo3 isolated as WG, WK, and WU. # Clock: see Clk # close down: see clo # clot: see cl # cloudy: see cld # cloven thorax: see clv # club: see cb # clubfoot: see cbf # club wing: see clw # clumpy marginals: see clm # clt: cricklet location: 2-96. origin: Induced by ethyl methanesulfonate. references: Shirras and Bownes, 1989, Proc. Nat. Acad. Sci. USA 86: 4559-63. phenotype: Yolk protein synthesis reduced approximately twenty fold in homozygous females; such females are also defective in the synthesis of larval-serum protein 2 (LSP2) although LSP2 synthesis in larvae is unaffected. Adult fat body normal in morphology and in other secretory functions. Larval fat body persists into adult stage; oocyte development arrested in pre- vitellogenic stage. Methoprene, a juvenile hormone analogue, which stimulates fat-body synthesis of yolk and vitellogenesis in starved wild-type females, has no effect in clt females; however, ovarian transplant experiments indicate that clt females have sufficient JH concentrations to promote oogenesis. Ecdysone, on the other hand, stimulates LSP2 and yolk-protein synthesis in clt females, but has no effect on larval-fat-body regression or oogenesis. #*clv-1: cloven thorax no. 1 location: 1-0.0. origin: X ray induced. discoverer: Muller, 19h. references: 1935, DIS 3: 29. phenotype: Thorax often has long cleft; partially dominant. Semilethal at low temperature; viable at high temperature. RK3. #*clv-2 location: 1-42.0. origin: X ray induced. discoverer: Muller, 26l11. references: 1935, DIS 3: 29. phenotype: Thorax has longitudinal cleft, sometimes half thorax. One wing often reduced or like vg. Partially dom- inant. Semilethal. RK3. alleles: *clv-252b completely recessive (CP627). *clv-2D [formerly Clv3 (Maroni, 1968, DIS 43: 60)] is a fully dom- inant allele associated with T(1;2)clv-2D. cytology: Placed in 11A7-8 based on association of clv-2D with T(1;2)11A7-8;27E2-3 (Kirschbaum). # Clv3: see clv-2D # clw: club wing location: 1-21 (same as sn; inferred from instability corre- lated with that of sn49s). origin: Presumably induced by P-factor in chromosome isolated from natural population; arose simultaneously with sn49s. references: Golubovsky and Zakharov, 1979, Genetika (Moscow) 15: 1599-1609. 1980, DIS 55: 49-55. Zakharov and Golubovsky, 1980, Genetika (Moscow) 16: 1603-12. Zakharov and Yurchenko, 1984, Genetika (Moscow) 20: 266-73. Yurchenko, Zakharov, and Golubovsky, 1984, Mol. Gen. Genet. 194: 279-85. phenotype: Wings fail to expand; retain pupal conformation. Penetrance low, 11% in males and 0.6% in homozygous females; inversely related to temperature; penetrance in XO males less than in XY males. Unstable, clw sn49s can mutate to wild type, either unstable (i.e., can regenerate clw sn49s) or stable, or to a stable clw+ with an unstable sn phenotype of intermediate strength. Interpreted as owing to an insertional sequence between clw and sn. cytology: Placed in 7D based on its presumed contiguity with sn. Since it may have been carried in by a transposon, there may not be a normal allele at this position in wild-type chro- mosomes. other information: May be allelic to cb. # cm: carmine location: 1-18.9. origin: Spontaneous. discoverer: Mohr, 27d27. references: 1927, Z. Indukt. Abstamm. Vererbungsl. 45: 403-5. phenotype: Eye color translucent dark ruby. With st, eye color deep orange; with brown, slightly lighter than bw alone. Lar- val Malpighian tubes very pale yellow. RK1. alleles: allele origin discoverer synonym ref ( comments _______________________________________________________________________ cm1 spont Mohr, 27d27 4 cm2 mustard Sobels, 57l cm28-4 5 cm3 X ray Valentin, 67j cm67j 6 cm4 Gerasimova cmMR1 1, 2 unstable allele | cm5 EMS Lefevre cmVEM119 3 ( 1 = Gerasimova, 1983, DIS 59: 38; 2 = Gerasimova, and Ilyin, 1984, DIS 60: 111-12; 3 = Lefevre, and Watkins, 1986, Genetics 113: 869-95; 4 = Mohr, 1927, Z. Indukt. Abstamm. Vererbungsl. 45: 403-05; 5 = Sobels, 1958, DIS 32: 84; 6 = Valentin, 1971, DIS 46: 40. | Arose in a stock carrying a transposable element in ct and reverts spontaneously; inserted element neither P nor gypsy (their mdg4). cytology: Located in 6E5-6 (CP627; Lefevre, 1981, Genetics 99: 461-80). # cm: see cmp Cm: Crimp Edith M. Wallace, unpublished. #*Cm: Crimp location: 3-43.5. origin: Spontaneous. discoverer: Bridges, 28a28. phenotype: Heterozygote has crimped wings ruffled on rear edge. Classification good in first 4 days' hatch, then Cm overlaps wild type progressively. Better at 25 than at 19. Homozygous lethal. RK2 as lethal; RK3 as dominant. # Cma: Comma location: 3-57.5 (between jvl and sbd). origin: X ray induced. discoverer: Lewis, 1971. references: Craymer, 1980, DIS 55: 197. phenotype: Cma/+ has a pair of comma-like depressions at the anterior edge of the dorsal mesothorax similar to those of some dp alleles, inturned dorsocentral bristles, a sr-like phenotype, and a soft-appearing cuticle. Cma/+ imparts domi- nance to the vortex effects of dp, dpv, dpov, and dpolv alleles. Cma/+ flies flightless, have abnormal myofibrils of indirect flight muscles (Mogami). Homozygous lethal. RK1. cytology: Location in 88C-F inferred from its map position and its survival in combination with Df(3R)sbd105 = Df(3R)88F9- 89A1;89B4-5 and the failure of a synthetic deficiency to the left that includes 88C to include jvl (Craymer). # cmd: carminoid location: 3-68.2. origin: Spontaneous. references: Mostashfi and Koliantz, 1970, DIS 45: 34. phenotype: Eye color resembles that of cm. # cMdh: see Mdh1 # cMhc-1: see Mhc-c # cml: caramel location: 2-71.2 (said to complement sf and ake). origin: Spontaneous. references: Ribo, 1968, DIS 43: 59. phenotype: Eye color brownish orange at eclosion, darkens with age but not as dark as se. Produces orange eye in combination with cn. RK1. # cmp: crumpled location: 3-93. origin: Spontaneous. discoverer: Bridges, 22d2. synonym: cm. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 247. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 223. phenotype: Wings about two-thirds normal size and greatly crum- pled or blistered. Marginal hairs irregularly clumped. Legs irregularly shortened and gnarled. Bristles somewhat short and thick. Posterior scutellars slightly divergent. Branches of aristae bent anteriorly near middle, with apices parallel to main axes of aristae. Viability and fertility may be low. RK3. cmp: crumpled Edith M. Wallace, unpublished. #*cmt: comet location: 3-57.2 (based on 35 cu-sr recombinants). origin: Induced by ethyl methanesulfonate. references: Garcia-Bellido and Dapena, 1973, DIS 50: 179. 1974, Mol. Gen. Genet. 128: 117-30 (fig.). phenotype: Homozygous lethal; however, clones of homozygous cells survive in cuticle. Wing cells like mwh but with fewer trichomes per cell and smaller angles between trichomes. Less distinct in tergites but accompanied by loss of pigment. # cn: cinnabar location: 2-57.5. origin: Spontaneous. discoverer: Clausen, 20i8. references: 1924, J. Exp. Zool. 38: 423-36. phenotype: Eye color bright red, like v or st. Ocelli color- less. Eye color darkens with age, but ocelli remain color- less. Larval Malpighian tubes pale yellow (Beadle, 1937, Genetics 22: 587-611). cn defective in ommochrome synthesis; blocks conversion of kynurenine to 3-hydroxykynurenine, which has been identified as the cn+ hormone (Butenandt, Weidel, and Schlossberger, 1949, Z. Naturforsch. 4b: 242-44). cn homozy- gotes devoid of kynurenine 3-hydroxylase activity (Ghosh and Forrest, 1967, Genetics 55: 423-31). Enzyme activity propor- tional to the number of doses of cn+; cn+ therefore concluded to be the structural gene for kynurenine 3-hydroxylase (EC 1.14.13.9) (Sullivan, Kitos, and Sullivan, 1973, Genetics 75: 651-61). Also cn defective in the uptake of kynurenine by eye discs and Malpighian tubules, where it is normally con- verted to 3-hydroxykynurenine (Sullivan, Grillo, Kitos, 1974, J. Exp. Zool. 188: 225-34). Nonautonomous in development of pigment of transplanted eye disks (Beadle and Ephrussi, 1936, Genetics 21: 230); however, ethyl methanesulfonate-induced mutants recovered as mosaics in homozygous red background (Paton and Sullivan, 1978, Biochem. Genet. 16: 855-65); furthermore, even though st has no detectable 3- hydroxykynurenine, it is able to rescue cn in transplants (Phillips, Simmons, and Bowman, 1970, Biochem. Genet. 4: 481-87). Enzyme activity developmentally regulated with a peak of activity in early third instar and a five-fold higher peak in the second half of pupal development (Sullivan et al.). Heterozygotes in all pairwise combinations of 13 ethyl methanesulfonate-induced alleles exhibit mutant phenotype (Paton and Sullivan, 1978). RK1. alleles: allele origin ref ( comments ______________________________________________________________________ cn1 3, 4 cn2 3, 4 hypomorph in In(2R)Cy cn2P 5 amorphic derivative of cn2 in In(2LR)CyO cn3 3 amorphic allele cn4 amorphic allele in In(2LR)bwV1 cn4P-30P EMS 7 cn12P and three other alleles hypomorphic cn31P EMS 7 amorphic derivative of cn2 in In(2LR)SM1 cn35k 3 hypomorphic allele *cn36c 3 cn38j 6 hypomorphic allele cn78 spont 2 amorphic allele in In(2LR)Gla cn80c / ray amorphic allele cnlvI X ray 1 amorphic allele cnrbr 8 detail follows *cns 3, 4 ( 1 = Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186; 2 = Ashburner, Faithfull, Littlewood, Richards, Smith, Velissariou, and Woodruff, 1980, DIS 55: 193; 3 = CP552; 4 = CP627; 5 = Craymer, 1980, DIS 55: 197; 6 = Ives, 1968, DIS 43: 64; 7 = Paton and Sullivan, 1978, Biochem Genet. 16: 855-65; 8 = Valade del Rio, 1974, DIS 51: 22. cytology: Placed in 43E3-14 by deficiency analysis (Zacharo- poulou, Yannopoulos, and Stamatis, 1981, DIS 56: 166-67); restricted to 43E6-14 by inclusion in Df(2R)CA53 = Df(2R)46E6;44B6. # cnrbr phenotype: An unstable amorphic allele that reverts with fre- quency of 3 x 10-3 (Valade del Rio, 1974, DIS 51: 22); also induces reversions of cn1 and cn2 alleles on homologous chro- mosome in heterozygotes; some of the revertants themselves mutate back to cnrbr (Valade del Rio, 1982, Experientia 38: 790-92). # cno: canoe location: 3-49. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). phenotype: Homozygous lethal; dorsal surface of embryo open. alleles: Fourteen; four weak and one temperature sensitive. # Co-3A: see 1(2)S3a # Co-7: see 1(2)S7 # Co-122: see mle # Coa: Coarse location: 3-7.7. discoverer: E.H. Grell, 1969. references: R.F. Grell, 1978, Genetics 89: 65-77. # coal: see cal # Coarse: see Coa # coatless: see ctl #*coc: collapsed ocelli location: 1-61.5. origin: Induced by D-1:6-dimethanesulfonyl mannitol (CB. 2511). discoverer: Fahmy, 1960. references: 1964, DIS 39: 58. phenotype: Ocelli small and flat. Anterior ocellar hairs fre- quently missing. Other slight alterations in body size and wing shape. RK3. cytology: Placed in salivary region 18A4 through 18B8 on the basis of its inclusion within the deficiency carrying the left end of In(1)y4 = In(1)1A8-B1;18A3-4 and the right end of In(1)sc9 = In(1)1B2-3;18B8-9 (Norton and Valencia, 1965, DIS 40: 40). # coi: coitus interruptus (J.C. Hall) location: 1-22.1. origin: Induced by ethyl methanesulfonate. discoverer: Lindsley. references: Hall, Siegel, Tompkins, and Kyriacou, 1980, Stadler Genet. Symp. 12: 43-82. phenotype: Males court females with slightly reduced vigor and mating success but mate frequently; duration of such copula- tions average 60% of normal 20 min; high proportion of mutant males also have abnormal sperm, e.g., nonmotile; females apparently unaffected by the mutation. # Coi: see Cu # Coiled: see Cu # Coiledex: see Cu # coitus interruptus: see coi # Collagen: see Cg # collapsed ocelli: see coc # com: compressed location: 3-48.5. origin: Spontaneous. discoverer: Bridges, 18k27. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 193. phenotype: Head flattened ventrally. Eyes small, displaced. Vibrissae tufted. Aristae crumpled. Humeral patches elevated. Wings droopy. Poor viability and fertility. RK3. # com: see comt # comatose: see comt #*com-d: compressed-dilapidator location: 3-68.5. origin: Spontaneous. discoverer: Bridges, 19c8. phenotype: Flies small, pale, weak, with defective legs and wings. RK3. # comb gap: see cg # comet: see cmt # Comma: see Cma # Compensatory Response: see CR # compensatory response: see Xh-cr # compressed: see com # compressed-dilapidator: see com-d # comt: comatose (J.C. Hall) location: 1-39.2. origin: Induced by ethyl methanesulfonate. synonym: com, preoccupied. references: Siddiqi and Benzer, 1976, Proc. Nat. Acad. Sci. USA 73: 3253-57. phenotype: Larvae or adults become paralyzed when exposed to high temperatures, but this requires many seconds for induc- tion; recovery from immobility on lowering of temperature is slow and directly correlated with duration of paralysis; most of the comt alleles do not induce relatively rapid paralysis until 38 (Siddiqi and Benzer, 1976), but two (com101, com102) cause pass-out at 29 (Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65); the mutations induce graded decrease and recovery of function of synapses at neuromuscular junctions as temperature is raised and lowered (Siddiqi and Benzer, 1976); several alleles are cold sensitive for paralysis as well as heat sensitive (Siddiqi and Benzer, 1976). ERG normal (Homyk and Pye, 1989, J. Neurogenet. 5: 37-48). alleles: allele isolation number discoverer ______________________________________________ comt1 ST53 Siddiqi and Benzer comt2 101 Homyk et al. comt3 102 Homyk et al. comt4 ST17 Siddiqi and Benzer comt5 ST47 Siddiqi and Benzer comt6 TP7 Siddiqi #*con: condensed location: 1-27.1. origin: Spontaneous. discoverer: Bridges, 36d11. references: 1937, DIS 7: 6. phenotype: Thorax and abdomen shortened; abdomen dilated, exposing ventral skin to side view. Eyes slightly roughened, occasionally kidney shaped, and somewhat dark. Wings short and bluntly rounded with crossveins closer together than nor- mal. Bristles shortened and somewhat fine at 19, stubby at 25. Postscutellars semierect and crossed; posterior verticals shortened or missing. Male entirely sterile. Viability 50% wild type. RK2. cytology: Salivary chromosome studies (Demerec, Kaufmann, Fano, Sutton, and Sansome, 1942, Year Book - Carnegie Inst. Washing- ton 41: 191) show locus to lie between 7C4-5 and 8C1-2. Further restricted to 8A through 8C2 on the basis of its genetic location to the right of oc at 8A. # concave wing: see ccw # concertina: see cta # condensed: see con # Confluens: see Co # Confluent: see Cf # Confluent-3: see Dlcf-3 # congested: see cgd # contorted: see ctt # Contrabithorax: see Cbx Contrabithorax: see Cbx under BXC # contrast blind: see l(1)ogre # control of female fertility: see cff # convex wing: see cvw # cop: copper location: 1-43.3. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1953. references: 1958, DIS 32: 68. phenotype: Brownish red eye color. Best classification in newly emerged flies. Occasionally, wings show cutaway inner margins. Excellent viability and fertility in both sexes. RK2. other information: Two alleles induced by L-p-N,N-di-(2- chloroethyl)amino-phenylalanine. # Cor: Corroded eye location: 3- (not located). origin: X ray induced. discoverer: Muller. references: 1946, DIS 20: 66. phenotype: Cor/+ shows slight irregular flecking of eye. In combination with v, expression enhanced, producing patchy diminution in color, especially near posterior margin of eye, giving impression that color was washed or eaten away, espe- cially from deeper layers; regions of surface often blackened. Homozygote not described. RK2. # corkscrew: see csw # corrugated wing: see corr #*corr: corrugated wing location: 2-36. origin: Spontaneous. discoverer: Mayeda, 61g. references: 1963, DIS 38: 31. phenotype: Wings wrinkled and wavy, reduced to three-fourths normal size. Whole wing corrugated at 20, only posterior third at 25. Good classification. RK2. # Corroded eye: see Cor # corrugated wing: see corr # cort: cortex (T. Schupbach) location: 2-49. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal mutant; homozygous females lay eggs in which a narrow halo of clear cytoplasm appears in the cortex around the time when nuclei would be expected to migrate to the periphery, but no cellularization takes place. alleles: Two, cort1 and cort2, isolated as QH and RH. # cos: costa (P. Simpson) location: 2-57.4. synonym: cos2. references: Whittle, 1976, Dev. Biol. 51: 257-68 . Grau and Simpson, 1987, Dev. Biol. 122: 186-200 (fig.). Simpson and Grau, 1987, Dev. Biol. 122: 201-09 (fig.). phenotype: Homozygotes, hemizygotes, and heteroallelic hetero- zygotes for class I alleles die as embryos with a normal cuticular phenotype. When derived from homozygous ovarian clones, however, abnormal deletion-duplication patterns in each segment are observed; posterior rows of abdominal denti- cles are replaced by mirror-image duplications of the anterior rows, including the segmental boundary, which is thereby duplicated; thoracic denticle belts missing; cos1 especially severely affected in this regard, including loss of entire segments. Heterozygotes derived from homozygous ovarian clones show slightly abnormal segmental patterning. Flies heterozygous for class I alleles or cos deficiencies and at the same time heterozygous for Cos alleles display pattern duplications of wings and halteres. Class II alleles are hem- izygous lethal but homozygous viable. They display wing and haltere duplications indistinguishable from those found for cos1/Cos1 heterozygotes as described by Whittle. Flies heterozygous for class III alleles and Cos show moderately reduced viability and occasional wing duplications; flies homozygous for class III alleles show reduced viability and have wild-type phenotype, but enhance the pattern duplications associated with Cos/+; hemizygotes for class III alleles or heterozygotes with class I alleles are lethal or nearly so in the presence of Cos, the survivors invariably exhibiting pat- tern duplications of wings and halteres. alleles: Severity of class I and II alleles estimated as fol- lows: cos3 > cos2 > cos1 = cos4 = cos5 > cos6 > cos7. Simi- larly for class III alleles: cosV5 _ cosV4 = cosV1 _ cosV2 _ cosV3. allele origin discoverer comments ____________________________________________________ cos1 ( EMS Whittle class I allele cos2 X ray Grau & Simpson class I allele cos3 X ray Grau & Simpson class I allele cos4 EMS Grau & Simpson class I allele cos5 EMS Grau & Simpson class I allele cos6 EMS Grau & Simpson class I allele cos7 EMS Grau & Simpson class II allele cosV1 | Simpson class III allele cosV2 | Simpson class III allele cosV3 | Simpson class III allele cosV4 | Simpson class III allele cosV5 EMS Grau & Simpson class III allele ( Synonym: cos2W1. | Found to exist in various laboratory stocks. cytology: Placed in 43B2-C3 on the basis of its inclusion in the region of overlap of Df(2R)pk78k = Df(2r)42E3;43C3 and Df(2R)ST1 = Df(2R)43B2-C1;43E1-8. # Cos: Costal (P. Simpson) location: 2-67.2. synonym: Epa: Epaulette; Cos1. references: Whittle, 1976, Dev. Biol. 51: 257-68. Grau and Simpson, 1987, Dev. Biol. 122: 186-200 (fig.). Simpson and Grau, 1987, Dev. Biol. 122: 201-09 (fig.). phenotype: Mirror-image duplications of wings and halteres; duplications of wing begin in mid-costal region and may include entire anterior compartment; posterior compartments unaffected, even when transformed into anterior compartments in en homozygotes. Penetrance of Cos higher when maternally than when paternally inherited. Class I alleles are homozy- gous viable and display pattern duplications in both heterozy- gotes and homozygotes. Penetrance and expressivity variable and may overlap wild type. Class II alleles are lethal when homozygous or in heteroallelic combination with one another; they sometimes display pattern duplications in heterozygotes. Class III alleles are homozygous lethal and have no dominant phenotype. Flies heterozygous for alleles of any of the three classes display the phenotype when simultaneously heterozygous for lethal alleles or deletions of cos; the heterozygous expression of Cos is dependent on the number of cos+ alleles present, with the severity of wing duplication decreasing as the number of cos+ alleles increases from one to three. Flies heterozygous for Cos and homozygous or hemizygous for some viable alleles of cos die as pharate adults and display pat- tern duplications in the anterior compartment of every body segment. Homozygotes of class II and IIIK alleles die as embryos with abnormal cuticular patterns; failure to develop of variable extents of the anterior end of the embryo, i.e. head or head and thorax, as well as mirror image duplications of anterior denticle belts of abdominal segments, or more fre- quently simply disturbed denticle polarity. Embryos that are simultaneously homozygous for cosV alleles and Cos3 are more severely affected, with some exhibiting a bicaudal phenotype. cosV1 Cos2/Df(2R)CA58 flies survive poorly, but show pattern duplications in the anterior compartments of all segments. Revertants of Cos are viable and wild type in phenotype; as they are presumably null alleles, Cos mutations are presumed to be gain of function alleles. alleles: allele origin discoverer synonym ref ( comments _________________________________________________________________ Cos1 EMS Whittle, 1976 Cos1W1 2 class III allele Cos2 EMS Simpson 1 class II allele Cos3 X ray Simpson 1 class II allele Cos4 EMS Grau & Simpson 1 class III allele Cos5 X ray Grau & Simpson class II allele Cos6 X ray Grau & Simpson class III allele Cos7 X ray Grau & Simpson class III allele Cos8 EMS Mariol 1 class II allele Cos9 EMS Nusslein-Volhard 1 class II allele Cos10 / ray Harrington Epa; Cos1A1 1 class I allele ( 1 = Grau and Simpson, 1987, Dev. Biol. 122: 186-200; 2 = Whittle, 1976, Dev. Biol. 51: 257-68 cytology: Placed in 49F13-50A3 based on its inclusion in Df(2R)vg-B = Df(2R)49D3-4;50A2-3 but not Df(2R)vg104 = Df(2R)49C4;49F13 (Lasko and Pardue, 1988, Genetics 120: 495- 502). # cos2: see cos # costakink: see csk cp: clipped Edith M. Wallace, unpublished. # cp: clipped location: 3-45.3. discoverer: Mainx, 34g. references: 1936, Z. Indukt. Abstamm. Vererbungsl. 71: 303-4 (fig.). Pollitzer, 1937, DIS 8: 91. phenotype: Wing margins snipped, most often along marginal vein. At 19, character slighter but completely penetrant. Shows partial dominance in combination with Minutes (Sinclair and Suzuki, 1979, Genetics 91: s117; V. Walker). Most stocks carry closely linked modifiers; has reduced viability when phenotype is good (Craymer). RK2. alleles: cpSS305 and cpSS307 X ray induced (Ashburner, Faith- full, Littlewood, Richards, Smith, Velissariou, and Woodruff, 1980, DIS 55: 193-95). cytology: Placed between the breakpoints of T(Y;3)L131 = T(Y;3)75D4-5 (V. Walker) and T(2;3)spy = T(2;3)33D4-E3;79A4-B1 (Puro, 1983, Hereditas 62: 414-18). # Cp15: Chorion protein location: 3-{26.5} (based on in situ hybridization). Located between Cp18 and Cp19. synonym: S15: Shell. references: Spradling, Digan, Mahowald, Scott, and Craig, 1980, Cell 19: 905-14. Spradling, 1981, Cell 27: 193-201. Griffin-Shea, Thireos, and Kafatos, 1982, Dev. Biol. 91: 325-36. Levine and Spradling, 1985, Chromosoma 92: 136-42. Wong, Pustell, Spoerel, and Kafatos, 1985, Chromosoma 92: 124-35. phenotype: The second of four chorion-protein genes in a 6-kb sequence; encodes S15-1, a chorion protein estimated at 15,000 daltons by Waring and Mahowald (1979, Cell 16: 599-607) and 9700 daltons by Petri, Wyman, and Kafatos (1976, Dev. Biol. 49: 185-99). Temporal and spatial distribution of expression described by Park and Spradling (1987, Genes Dev. 1: 497- 509). alleles: Probably the locus for which Yannoni and Petri (1980, Wilhelm Roux's Arch. Entwicklungsmech. Organ. 189: 17-24) detected electrophoretic variants by isoelectric focusing. cytology: Localized to 66D11-15 by in situ hybridization. Less than 1 kb from Cp18. molecular biology: Gene cloned and sequenced (Levine and Spra- dling; Wong et al.). Transcription unit estimated to be 515 nucleotides by Levine and Spradling and 590 by Wong et al.; contains a 71 nucleotide intron four codons downstream from the translation initiation site. Direction of transcription the same as for Cp16, Cp18 and Cp19. The conceptual polypeptide, which contains a signal peptide and a putative signal-peptide cleavage site, contains 115 residues and the mature chorion protein 97 residues for a calculated molecular weight of 9934 (Wong et al.) or 9467 (Levine and Spradling). Flanking sequences examined for putative regulatory sequences. Located in a chromosome region that is amplified approximately 60 fold as a series of nested bidirectional replication forks spanning approximately 100 kb in the follicle cells surround- ing maturing oocytes; amplification of the entire region under the control of ACE3, a cis-acting sequence between 615 and 187 base pairs upstream from Cp18 (Kalfayan, Levine, Orr-Weaver, Parks, Wakimoto, deCicco, and Spradling, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 527-35), and at least four amplification-enhancing regions (AERs) located one base pair downstream from each of the four second-chromosome chorion- protein genes (Delidakis and Kafatos, 1989, EMBO J. 8: 891- 901). # Cp16 location: 3-{26.5} (based on sequence proximity to Cp15 and Cp18). synonym: S16. references: Griffin-Shea, Thireos, and Kafatos, 1982, Dev. Biol. 91: 325-36. phenotype: The fourth of four chorion-protein genes in a 6-kb sequence; encodes S16-1, a 16,000-dalton chorion protein. Temporal and spatial distribution of expression described by Park and Spradling (1987, Genes Dev. 1: 497-509). cytology: Placed in 66D11-15 based on sequence proximity to Cp15 and Cp18. Approximately 1 kb from Cp19. molecular biology: Identified on genomic clone selected with cDNA probe for Cp15. S1 nuclease digest of DNA-mRNA hybrid indicates presence of small intron toward one end of gene. Located in a chromosome region that is amplified approximately 60 fold as a series of nested bidirectional replication forks spanning approximately 100 kb in the follicle cells surround- ing maturing oocytes; amplification of the entire region under the control of ACE3, a cis-acting sequence between 615 and 187 base pairs upstream from Cp18 (Kalfayan, Levine, Orr-Weaver, Parks, Wakimoto, deCicco, and Spradling, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 527-35), and at least four amplification-enhancing regions (AERs) located one base pair downstream from each of the four second-chromosome chorion- protein genes (Delidakis and Kafatos, 1989, EMBO J. 8: 891- 901). Transcriptionally most active during stages 13 and 14. # Cp18 location: 3-{26.5} (based on in situ localization). synonym: S18. references: Spradling, Digan, Mahowald, Scott, and Craig, 1980, Cell 19: 905-14. Spradling, 1981, Cell 27: 193-201. Griffin-Shea, Thireos, and Kafatos, 1982, Dev. Biol. 91: 325-36. Levine and Spradling, 1985, Chromosoma 92: 136-42. Wong, Pustell, Spoerel, and Kafatos, 1985, Chromosoma 92: 124-35. phenotype: The first of four chorion-protein genes in a 6-kb sequence; encodes S18-1 estimated at 18,000 daltons by Waring and Mahowald (1979, Cell 16: 599-607) and 15,600 by Petri, Wyman, and Kafatos (1976, Dev. Biol. 49: 185-99). Temporal and spatial distribution of expression described by Park and Spradling (1987, Genes Dev. 1: 497-509). cytology: Localized to 66D11-15 by in situ hybridization. Less than 1 kb from Cp15. molecular biology: Gene cloned and sequenced (Levine and Spra- dling; Wong et al.). Transcription unit estimated to be 650 nucleotides by Levine and Spradling and 825 by Wong et al.; contains a 176 nucleotide intron five codons downstream from the translation initiation site. Direction of transcription the same as for Cp15, Cp16 and Cp19. The conceptual polypep- tide, which contains a signal peptide and a putative signal- peptide cleavage site, contains 172 residues and the mature chorion protein 156 residues for a calculated molecular weight of 15517 (Wong et al.) or 15027 (Levine and Spradling). Flank- ing sequences examined for putative regulatory sequences. Located in a chromosome region that is amplified approximately 60 fold as a series of nested bidirectional replication forks spanning approximately 100 kb in the follicle cells surround- ing maturing oocytes; amplification of the entire region under the control of ACE3, a cis-acting sequence between 615 and 187 base pairs upstream from Cp18 (Kalfayan, Levine, Orr-Weaver, Parks, Wakimoto, deCicco, and Spradling, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 527-35), and at least four amplification-enhancing regions (AERs) located one base pair downstream from each of the four second-chromosome chorion- protein genes (Delidakis and Kafatos, 1989, EMBO J. 8: 891- 901). # Cp19 location: 3-{26.5} (based on sequence proximity to Cp15 and Cp18). synonym: S19. references: Griffin-Shea, Thireos, and Kafatos, 1982, Dev. Biol. 91: 325-36. Wong, Pustell, Spoerel, and Kafatos, 1985, Chromosoma 92: 124-35. phenotype: The third of four chorion-protein genes in a 6-kb sequence; encodes S19-1, a chorion protein estimated at 19,000 daltons by Waring and Mahowald (1979, Cell 16: 599-607) and 17,500 by Petri, Wyman, and Kafatos (1976, Dev. Biol. 49: 185-99). Temporal and spatial distribution of expression described by Park and Spradling (1987, Genes Dev. 1: 497- 509). cytology: Placed in 66D11-15 based on sequence proximity to Cp15 and Cp18. Approximately 1 kb from Cp16 on one side and less than 1 kb from Cp15 on the other. molecular biology: Gene cloned and sequenced (Wong et al.). Transcription unit estimated to be 742 nucleotides contains a 89 nucleotide intron five codons downstream from the transla- tion initiation site. Direction of transcription the same as for Cp15, Cp16 and Cp18. The conceptual polypeptide, which contains a signal peptide and a putative signal-peptide cleavage site, contains 173 and the mature chorion protein 156 residues for a calculated molecular weight of 16722 daltons. Flanking sequences examined for putative regulatory sequences. Located in a chromosome region that is amplified approximately 60 fold as a series of nested bidirectional replication forks spanning approximately 100 kb in the follicle cells surround- ing maturing oocytes; amplification of the entire region under the control of ACE3, a cis-acting sequence between 615 and 187 base pairs upstream from Cp18 (Kalfayan, Levine, Orr-Weaver, Parks, Wakimoto, deCicco, and Spradling, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 527-35), and at least four amplification-enhancing regions (AERs) located one base pair downstream from each of the four second-chromosome chorion- protein genes (Delidakis and Kafatos, 1989, EMBO J. 8: 891- 901). alleles: Electrophoretic variants identified by isoelectric focusing (Yannoni and Petri, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 301-03). # Cp36 location: 1-{23} (based on in situ localization). synonym: S36. references: Spradling and Mahowald, 1979, Cell 16: 589-98. Spradling, Waring, and Mahowald, 1979, Cell 16: 609-16. Spradling and Mahowald, 1980, Proc. Nat. Acad. Sci. USA 77: 1096-1100. Spradling, 1981, Cell 27: 193-201. phenotype: The structural gene for s36-1, a 36,000-dalton chorion protein. Synthesis primarily during stages 12 and 13 (Waring and Mahowald, 1979, Cell 16: 599-607) and during stages 11 and 12 (Petri, Wyman, and Kafatos, 1976, Dev. Biol. 49: 185-99). Approximately 1,000 daltons cleaved from pri- mary translation product to yield mature protein (Spradling et al., 1980). Temporal and spatial distribution of expression described by Park and Spradling (1987, Genes Dev. 1: 497- 509). alleles: Two-dimensional gels reveal electrophoretic variants, which we designate Cp36a and Cp36b. Null allele, Cp36n1 [formerly fs(1)cor-36] produces no 36,000-dalton chorion pro- tein (Digan, Spradling, Waring, and Mahowald, 1979, ICN-UCLA Symposium 14: 171-81). cytology: Localized to 7F1-2 by in situ hybridization. Less than 1 kb distal to Cp38. molecular biology: Resides on the same transcription unit as Cp38; separated by 1414 bp; gene 1100 bp in length and con- tains a small 5' intron (Wakimoto); nascent transcripts con- tain a ribonucleoprotein particle at each splice junction (Olsheim, Miller, and Beyer, 1985, Cell 43: 143-51). Abun- dantly transcribed producing polyadenylated mRNA in follicle cells surrounding stage-12 and -13 oocytes. Abundance markedly reduced in In(1)oc = In(1)7F1-2;8A1-2 homozygotes. Located in a chromosome region that is amplified approximately 14-16 fold as a series of nested bidirectional replication forks spanning approximately 100 kb in the follicle cells sur- rounding maturing oocytes; amplification of the entire region under the control of ACE3, a cis-acting sequence between 654 and 266 base pairs upstream from Cp38 (Wakimoto). Amplifica- tion disrupted by In(1)oc = In(1)7F1-2;8A1-2; female sterility results in homozygotes. Electron-microscope characterization of transcription unit, including length, polymerase II den- sity, and discrete termination site by Olsheim, Miller, and Beyer (1986, EMBO J. 5: 3591-96). # Cp38 location: 1-{23} (based on in situ localization). synonym: S38. references: Spradling and Mahowald, 1979, Cell 16: 589-98. Spradling, Waring, and Mahowald, 1979, Cell 16: 609-16. Spradling, Digan, Mahowald, Scott, and Craig, 1980, Cell 19: 905-14. Spradling and Mahowald, 1980, Proc. Nat. Acad. Sci. USA 77: 1096-1100. Spradling, 1981, Cell 27: 193-201. phenotype: Structural gene for s38-1, a 38,000-dalton chorion protein. Synthesis primarily during stages 12 and 13 (Waring and Mahowald, 1979, Cell 16: 599-607) and during stages 11 and 12 (Petri, Wyman, and Kafatos, 1976, Dev. Biol. 49: 185- 199). 2,000 to 3,000 daltons cleaved from primary translation product to yield mature protein (Spradling et al., 1980). Temporal and spatial distribution of expression described by Park and Spradling (1987, Genes Dev. 1: 497-509). alleles: Isoelectric focusing resolves two electrophoretic forms of s38-1 which may be designated Cp38a and Cp38b. cytology: Localized to 7F1-2 by in situ hybridization. About 1 kb proximal to Cp36. molecular biology: Resides on the same transcription unit as Cp36; separated from it by 1414 bp; gene 1516 bp in length and contains a small 5' intron (Wakimoto); nascent transcripts contain a ribonucleoprotein particle at each splice junction (Olsheim, Miller, and Beyer, 1985, Cell 43: 143-51). Abundantly transcribed producing polyadenylated mRNA in folli- cle cells surrounding stage-12 and -13 oocytes. Abundance markedly reduced in In(1)oc = In(1)7F1-2;8A1-2 homozygotes. cDNA and approximately 200 kb of genomic sequences in the region of Cp38 cloned and restriction mapped. Direction of transcription is toward the centromere. Located in a chromo- some region that is amplified approximately 14-16 fold as a series of nested bidirectional replication forks spanning approximately 100 kb in the follicle cells surrounding matur- ing oocytes; amplification of the entire region under the con- trol of ACE3, a cis-acting sequence between 654 and 266 base pairs upstream from Cp38 (Wakimoto). Amplification disrupted by In(1)oc = In(1)7F1-2;8A1-2; female sterility results in homozygotes. Electron-microscope characterization of tran- scription unit, including length, polymerase II density, and discrete termination site by Olsheim, Miller, and Beyer (1986, EMBO J. 5: 3591-96). # Cp70 location: 1-{0}. references: Yannoni and Petri, 1984, Dev. Biol. 102: 504-08. phenotype: The structural gene for a 70-dalton minor component of the chorion. alleles: Two electrophoretic alleles known. cytology: Placed in 2B3-6 based on its inclusion in Df(1)S39 = Df(1)1E1-2;2B5-6, but not in Df(1)sta = Df(1)1E1-2;2B3-4 (Peterson and Petri, 1986, DIS 63: 158). #*cpl: cupola location: 1-0.0 (no crossing over with sc in 584 males). origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1959, DIS 33: 83-84. phenotype: Small, inviable fly. Wings shorter and curved to form canopy over abdomen with tips converging toward mid- dorsal line. Head and eyes slightly deformed. Abdominal ter- gites abnormal; from irregular pigmentation to absence or gross deformation of the sixth and seventh tergites. Males sterile. RK3. #*Cpt: Clipt location: 2-43.7. origin: Spontaneous. discoverer: Sturtevant, 26b18. phenotype: Bristles short, like those of Sb. Homozygous lethal. Male sterile. RK1. #*cpw: canopy wing location: 1-2.5 [not between w and vt (Lefevre and Green, 1972, Chromosoma 36: 391-412)]. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 69. phenotype: Wings short and very broad; longitudinal veins fre- quently do not reach wing margin and often diverge. Eyes large and slightly rough. Head bristles reduced in number (ocellars most frequently affected). Thorax broad, one or more bristles occasionally absent; hairs more widely separated, with noticeable hairless areas. Males sterile. Viability 40% wild type. RK3. # cq: see rk4