# as: ascute location: 3-46. origin: Spontaneous. discoverer: Bridges, 16j21. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 170. phenotype: In as1, front of scutellum elevated, with partial obliteration of transverse furrow; deep chested. Bubble in scutellum or midline of thorax; dried black exudate, often at each side of scutellum, may appear at any of the sutures of head and thorax; black deformed lump behind cheek. Wings droop at sides. Overlaps wild type. RK3. alleles: *as1, *as2 (CP627), ashg. cytology: Placed in region 72D3-73A5 by Velissariou and Ash- burner, 1981, Chromosoma 84: 173-85. ashg: ascute-hangende origin: Spontaneous. references: Franke, 1934, DIS 2: 9. Gottschewski, 1935, DIS 4: 15. phenotype: Wings held laterally downward, ends occasionally resting on legs; eyes small and knobby. RK2. # ASC: achaete-scute complex location: 1-0.0. references: Garcia-Bellido, 1979, Genetics 91: 491-520. Carramolino, Ruiz-Gomez, Guerrero, Campuzano, and Modolell, 1982, EMBO J. 1: 1185-91. Campuzano, Carramolino, Cabrera, Ruiz-Gomez, Villares, Boronat, and Modolell, 1985, Cell 40: 327-38. Dambly-Chaudiere and Ghysen, 1987, Genes Dev. 1: 297- 306. Ghysen and Dambly-Chaudiere, 1988, Genes Dev. 2: 495-501. phenotype: The achaete-scute complex (ASC) produces a number of transcripts whose translation gene products function in the specification of diverse sensilla and their centrally project- ing neurons. Insertions of transposable elements and rear- rangement breakpoints in ASC result in the loss of certain subsets of bristles (both macrochaetae and microchaetae) and other sensilla, including their associated accessory cells, such as those forming sockets and peripheral neurons; these lesions, with few exceptions, occur outside of transcribed regions. The complex was subdivided into four components based on the sites of lesions causing mutant phenotypes by Garcia-Bellido (1979); they are, from left to right, ac, sc(, l(1)sc, and sc|; a fifth component, sc/, has been identified by Dambly-Chaudiere and Ghysen (see also Ghysen and Dambly- Chaudiere). Four genes that function in neurogenesis, and thus comprise ASC, are ac, sc (in the sc( region), l(1)sc, and ase (in the sc/ region); some lesions in sc affect sex deter- mination and are currently denoted sis-b. ac, and ase function in the genesis of both larval and adult peripheral nervous- system elements; l(1)sc functions in central-nervous-system development. Hw alleles are dominant gain-of-function muta- tions in ASC; unlike loss of function mutations, at least two Hw mutations have foreign sequences inserted into structural genes of ASC (Campuzano, Balcells, Villares, Carramolino, Garcia-Alonzo, and Modolell, 1986, Cell 44: 303-12). Defi- ciencies for most regions of the complex are hemizygous and homozygous viable; however, deficiency for l(1)sc is lethal. Interestingly, sc rearrangements with breakpoints in the sc( region have their second breakpoints in pericentric hetero- chromatin, whereas those broken in the sc| region have euchromatic second breakpoints (Garcia-Bellido, 1979). Dif- ferent segments of ASC tend to affect different subsets of bristles in the adult, as will be described in entries to fol- low; detailed descriptions of these bristle patterns are given by Dubinin (1933, J. Genet. 27: 446) and Garcia-Bellido (1979). ASC deficiencies also result in absences of campani- form and trichoid sensilla (Garcia-Bellido and Santamaria, 1978, Genetics 88: 469-86). In larvae, ASC specifies neurons innervating peripheral sensory organs plus another class of neurons of uncertain (perhaps proprioceptive) function, but not chordotonal-organ-innervating neurons; here too, different components of ASC specify different and sometimes overlapping subsets of pattern elements (Dambly-Chaudiere and Ghysen). Double hemizygotes for ASC and da [Df(1)260-1/+; Df(2L)J27/+] or ASC and Df(4)M101-62f show loss of macrochaetae, which none of the single hemizygosities does (Dambly-Chaudiere, Ghysen, Jan, and Jan, 1988, Roux's Arch. Dev. Biol. 197: 419-23). Homozygous ASC deficiencies tend to counteract the embryonic effects of deficiencies for the neurogenic loci; i.e., they cause a partial return to epidermigenesis (Brand and Campos- Ortega, 1988, Roux's Arch. Dev. Biol. 197: 447-56). In the following treatment of ASC, ac, ase, Hw, l(1)sc, sc, and sis-b are discussed in turn; a general discussion of phenotype of each element is followed by a table of alleles, after which specific aspects of various alleles are described. cytology: Placed in 1B1-7 based on its being positioned to the right of the left breakpoint of In(1)y3P = In(1)1B1-2;20F and to the left of the left breakpoint of Tp(1;2)sc9 = Tp(1;2)1B1-2;1B4-7;25-26. The region has been subdivided by rearrangement breakpoints in the following order: In(1)y3P, In(1)y4, ac, In(1)sc8, sc(, In(1)scL8, In(1)scS1, In(1)sc4, l(1)sc, In(1)sc9, sc|, Df(1)sc19, sc/, Df(1)260.1. molecular biology: Most of the complex has been cloned and res- triction mapped in a chromosome walk of over 100 kb (Campuzano et al.); insertions and rearrangement breakpoints associated with different sc mutations located on restriction map. The coordinate system designates 0 as an arbitrarily chosen EcoRI site in the sc| region with positive values extending to the left (Carramolino, Ruiz-Gomez, Guererro, Campuzano, and Modolell, 1982, EMBO J. 1: 1185-92). Sequence variation in ASC region of chromosomes isolated from natural populations investigated by Aguade, Miyashita, and Langley (1989, Genetics 22: 607-15). Nine different transcription units, originally designated T1 to T9, identified in the ASC region. Four of these, T5, T4, T3, and T8 (formerly T1a), appear to be respon- sible for the neurogenic functions of the complex and correspond to ac, sc, l(1)sc, and ase, respectively; they are transcribed from left to right and encode members of the helix-loop-helix class of proteins, which are able to bind, as dimers, to DNA. In addition, the ac, sc, and l(1)sc tran- scripts share a 15-nucleotide acidic C-terminal sequence (Vil- lares and Cabrera, 1987, Cell 50: 415-24; Alonso and Cabrera, 1988, EMBO J. 7: 2585-91; Gonzalez, Romani, Cubas, Modolell, and Campuzano, 1989, EMBO J. 8: 3553-62). Transcription unit T2 is found in the sc| region; its protein product and spatial pattern of expression rule out a neurogenic function and therefore membership in ASC. ac: achaete From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 12. # ac: achaete phenotype: ac specifies the formation of the anterior and pos- terior dorsocentral, the posterior supra-alar (as does sc), the anterior vertical bristle, and in addition the acrostichal rows of microchaetae on the notum. Absence of bristles accom- panied by absence of associated socket and underlying cen- trally projecting neuron (Stern, 1938, Genetics 23: 172-73). In addition mutant alleles of ac tend to remove the interocel- lar hairs and the hairs on the surface of the eye and a res- tricted subset of the campaniform sensilla on the wing blade (Leyns, Dambly-Chaudiere and Ghysen, 1989, Roux's Arch. Dev. Biol. 198: 227-32). Trichomes are not affected. ac defi- ciencies, e.g., In(1)y3PLsc8R, survive as fully mobile and fertile adults (Garcia-Bellido, 1979, Genetics 90: 491-529). A series of terminal deficiencies approaching the ac coding sequence from the left a few hundred base pairs at a time, when tested in heterozygotes with In(1)y3PLsc8R or Df(1)sc19, cause, with few exceptions, progressive loss of chaetae as the amount of deleted material increases; response of anterior verticals erratic. First effects of deficiencies noted with chromosomes broken 10 kb upstream of the transcription start site. Despite loss of most of the DNA upstream from the tran- scribed region, the phenotypes associated with these deletions still suppressed by emc and h (Ruiz-Gomez and Modolell, 1987, Genes Dev. 1: 1238-46). Deficiencies for ac act as suppres- sors of h (Sturtevant, 1970, Dev. Biol. 21: 48-63), whereas extra doses of ac+ enhance expression of h (Moscoso del Prado and Garcia-Bellido, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 242-51). Longitudinal stripes of expression on either side of the midline during gastrulation become internalized and segmented into four longitudinal rows of clusters of expressing cells at half-segment intervals. ac RNA undetect- able in germ band at time of germ-band shortening. Several regions of high expression seen in cephalic region. Also expressed in posterior midgut rudiment (Romani, Campuzano, and Modolell, 1987, EMBO J. 6: 2085-92; Cabrera, Martinez-Arias, and Bate, 1987, Cell 50: 425-33). In third-instar larvae, expression in wing imaginal disks restricted to regions where precursors of cuticular organs specified by ac are known to reside (Romani, Campuzano, Macagno, and Modolell, 1989, Genes Dev. 3: 997-1007). alleles: allele origin discoverer synonym ref ( comments _____________________________________________________________________ ac1 spont Weinstein, sc11 8 deletion for kb 84 16b3 to 64; includes y *ac2 X ray Dubinin, 2, 6 induced with sc3 1928 ac3 X ray Dubinin, sc10, sc11 3, 4, 5 In(1)1B2-3;1B14-C1; 1929 kb 59.6 to 58.8 ac3B 1 gypsy at kb +63.7 *ac4 X ray Dubinin, 1929 ac3 3, 4, 5 ac54e X ray W. K. Baker with y54e in y+Y *ac260-28 X ray Sutton, 7 39l26 ( 1 = Campuzano, Carramolino, Cabrera, Ruiz-Gomez, Villares, Boronat, and Modolell, 1985, Cell 40: 327-38; 2 = Dubinin, 1929, Biol. Zentralbl. 49: 328-39; 3 = Dubinin, 1930, Zh. Eksperim. Biol. 6: 300-46; 4 = Dubinin, 1932, J. Genet. 25: 163-81; 5 = Dubinin, 1933, J. Genet. 27: 443-64; 6 = Serebrovsky and Dubinin, 1930, J. Hered. 21: 259-65 7 = Sutton, 1943, Genetics 28: 210-17; 8 = Weinstein, 1918, Genetics 3: 133-72. cytology: Placed in 1B1-2 based on its position between left breakpoints of In(1)y4 = In(1)1A8-B1;18A3-4 and In(1)sc8 = In(1)1B2-3;20F. molecular biology: The ac transcription unit, designated T5 by Campuzano et al. is located from kb 59 to 58, and transcrip- tion is from left to right. cDNA and genomic sequences of the putative ac transcribed region determined by Villares and Cabrera (1987, Cell 50: 415-24); the transcription unit of 911 nucleotides is without introns and specifies a 201-amino- acid polypeptide of 22.7 kd. # ac1 phenotype: Hypomorphic; phenotype of homozygous females weaker than in hemizygous females (Garcia-Bellido, 1979, Genetics 91: 491-520). Posterior dorsocentral bristles missing; also posterior supra-alar and anterior vertical bristles frequently missing. Anterior dorsocentrals displaced anteriorly (Claxton, 1969, Genetics 63: 883-96). Garcia-Bellido (1979) finds anterior dorsocentral bristles more strongly decreased than posterior dorsocentrals. Hairs usually fewer near position of posterior dorsocentrals; interocellar hairs invariably fewer, typically absent. Eyes partly devoid of hairs. Trichomes unaffected. Limited nonautonomy near the borders of somatic spots with respect both to numbers and positions of bristles and hairs (Stern, 1954, Am. Sci. 42: 212-47; Roberts, 1961, Genetics 46: 1241-43; Claxton, 1976, Genet. Res. 27: 11-22). ac partially suppresses h; Hw/ac = Hw/+ (Sturtevant, 1969). molecular biology: A deficiency extending from a point between kb 64.9 and 63.5, which is approximately 5 kb upstream from the presumptive ac transcription unit, to the left to approxi- mately kb 82. (Campuzano, Carramolino, Cabrera, Ru'z-G'mez, Villares, Boronat, and Modolell, 1985, Cell 40: 327-38). #*ac2 phenotype: Since ac2 and sc3 were for practical purposes inseparable by crossing over, the effect of ac2 alone could not be assessed. The double mutant removed all bristles except scutellars and postdorsocentrals. ac2/ac2 and ac2/+ suppress h (Sturtevant). Viability of males low; females nearly inviable. RK2. cytology: Salivary chromosomes normal (Schultz). # ac3 synonym: Called ac2 by Dubinin, the earlier ac2 with sc3 having been omitted from the series, sc10, sc11 (Sturtevant and Schultz, 1931, Proc. Nat. Acad. Sci. USA 17: 265-70). phenotype: Posterior and usually anterior dorsocentrals lack- ing; other bristles wild type. Hairs removed from areas across rear and front edges of thorax, through mid-dorsal area, and between ocelli. ac3 even in ac3/+ heterozygotes exerts strong suppression on h (Sturtevant, 1970, Dev. Biol. 21: 48-61). RK2A. cytology: Inseparable from In(1)ac3 = In(1)1B2-3;1B14-C1 (Muller, Prokofyeva, and Raffel, 1935, Nature (London) 135: 253-55). molecular biology: Left breakpoint of In(1)ac3 at DNA coordi- nate +59 near the transcription start site of the ac tran- script; transcript levels substantially reduced in both embryos and pupae; the l(1)sc transcript but not the sc tran- script also reduced (Campuzano, Carramolino, Cabrera, Ru'z- G'mez, Villares, Boronat, and Modolell, 1985, Cell 40: 327- 38). # ac3B phenotype: Low level of absence of dorsocentral bristles as well as microchaetae. Bristles normally removed by sc muta- tions not missing. molecular biology: A gypsy insert in the ac region of ASC at +63.7; in addition there is a 0.5 kb insert in the sc| region at approximately -5.0 to -6.5, which shows sequence homology with the gypsy LTR. other information: ac3B is a derivative of sc3B, which origi- nally displayed a sc1-like phenotype. The original phenotype is no longer present and a weak achaete phenotype appears instead. Apparently a gypsy element originally inserted between -5.0 and -6.5 has excised, leaving a 0.5 kb remnant and resulting in reversion of the sc phenotype, and a new gypsy has inserted at 63.7, about 4 kb upstream from the ac transcription unit, to produce the present ac phenotype. Level of ac transcript reduced. ac3B complements ac1 (Garcia- Bellido, 1979, Genetics 91: 491-520). # ase: asense location: 1-0.0. references: Ghysen and Dambly-Chaudiere, 1988, Genes Dev. 2: 495-501. Gonzalez, Romani, Cubas, Modolell, and Campuzano, 1989, EMBO J. 8: 3553-62. phenotype: ase1 (formerly sc2) shown to be a molecular deletion including the ase transcription unit. ase embryos lack a sub- set of peripheral neurons (Dambly-Chaudiere and Ghysen, 1987, Genes Dev. 1: 297-306); third-instar larvae show disrupted optic-lobe development; in adults almost all abdominal chaetae are removed as are the extra chaetae induced by Tft. Abdomen tends to be swollen; wings poorly expanded; viability of homozygous and hemizygous females low (Garcia-Bellido, 1979, Genetics 91: 491-520). Gene expression first detectable in the neural primordium, presumably in the neuroblasts. In later embryos, RNA is detected in most cells of the CNS pri- mordium as well as in the labrum, optic lobe rudiment, pro- cephalic neurogenic region, and the posterior midgut rudiment. Expression lasts into germ-band retraction. Also expressed sparsely in third-instar larvae; scarce in imaginal disks except for one large cell cluster in each leg disk; strong in the CNS, especially in a cap of cells over each optic lobe, which are destined to generate ganglion mother cells of the lamina and medulla; expression also seen in inner anlagen of optic lobes, which give rise to cells of the medulla and lobula complex. Otherwise expression in brain and ventral ganglion occurs in isolated clusters of cells and single cells. Expression thought to identify actively proliferating cells (Gonzalez et al.). cytology: Placed in 1B4-7, the 22-kb region defined as sc/ by Dambly-Chaudiere and Ghysen (1987), based on its being included in the apparently terminal deficiency Df(1)260.1 = Df(1)1B4-6 but in neither Df(1)sc19 = Df(1)1B1-2;1B4-5 nor in the terminal duplication afforded by the 4PXD element of T(1;4)scH. molecular biology: Both cDNA and genomic clones isolated and sequenced (Gonzalez et al.); 1596 ORF encodes a protein of 486 amino acids; in addition to the helix-loop-helix motif, it contains a centrally located acidic region and a proline-rich region near the N terminus; it lacks the N-terminal acidic domain characteristic of the other three ASC transcripts. The protein also contains PEST and opa sequences. The genomic sequence is without introns. ase1 mutation is a small dele- tion from coordinates -11.5 to -30 kb that includes the ase transcription unit, which is located at approximately coordi- nate -25 kb. # Hw: Hairy wing references: Campuzano, Balcells, Villares, Carramolino, Garcia-Alonzo, and Modolell, 1986, Cell 44: 303-312. Garcia-Alonzo and Garcia-Bellido, 1986, Wilhelm Roux's Arch. Dev. Biol. 193: 259-64. Balcells, Modolell, and Ruiz-Gomez, 1988, EMBO J. 7: 3899- 3906. phenotype: Gain of function alleles of ASC, which lead to the development of supernumerary bristles and hairs in all seg- ments of the fly: in the prefrons, postfrons, postgena, and occipital regions of the head; in the preepisternum, epister- num, anepisternum, scutum, scutellum, postnotum, wingblade, legs, humerus, and halteres of the thorax; and in the ter- gites, pleura, and sternites of the abdomen. Phenotype suppressed by three doses of h+ (Botas, Moscoso del Prado, and Garcia-Bellido, 1982, EMBO J. 1: 307-10) and enhanced by h, emc, and pyd (Neel, 1941, Genetics 26: 52-58; Moscoso del Prado and Garcia-Bellido, 1984, Wilhelm Roux's Arch Dev. Biol. 193: 242-45). Numbers of super numerary bristles reduced in da+ hemizygotes (Dambly-Chaudiere, Ghysen, Jan and Jan, 1988, Roux's Arch Dev. Biol. 97: 419-23). alleles: allele origin discoverer ref ( comments ___________________________________________________________ Hw1 spont Bridges, 23c12 1, 3, 6 in y Hw2 spont Nichols-Skoog, 35a9 2 derivative of Hw1 Hw49c 32P King, 49c21 4, 8 with sc49c Hw59g X ray Green 5, 7 in sc1; In(1)1B;2B3-4 Hwbap Cline 9 T(1;2)1B;21B HwBS spont Garcia-Bellido 1 derivative of Hw1 HwUa spont Garcia-Bellido 1, 3 in y2 sc1 ( 1 = Campuzano, Balcells, Villares, Carramolino, Garcia- Alonzo, and Modolell, 1986, Cell 44: 303-312; 2 = CP627; 3 = Garcia-Alonzo and Garcia-Bellido, 1986, Wilhelm Roux's Arch. Dev. Biol. 193: 259-64; 4 = Gottleib, 1964, Genetics 49: 739-60; 5 = Green, 1961, Genetics 46: 671-82; 6 = Neel, 1941, Genetics 26: 52-58; 7 = Lee, 1972, DIS 48: 18-19; 8 = Poulson and King, 1949, DIS 23: 62-63; 9 = Roseland and Schneiderman, 1979, Wilhelm Roux's Arch. Dev. Biol. 186: 235-65. Hw: Hairy wing Edith M. Wallace, unpublished. # Hw1 phenotype: Males and heterozygous females have extra bristles on the head (especially occipitals), the notum and the meso- pleurae; also extra bristles, including sensory ones and cam- paniform sensilla (Palka, Schubiger, and Hart, 1981, Nature 294: 447-49), along longitudinal veins and in membrane of wing. Classifiable in a single dose in triploids (Schultz, 1934, DIS 1: 55). Homozygous females more extreme; 110 extra chaetae on wing vs. 49.5 for Hw1/+; 11 on scutellum and post- notum vs. 0.7 in Hw/+ (Garcia-Bellido and Merriam, 1971, Proc. Nat. Acad. Sci. USA 68: 2222-26). Number of extra bristles inversely correlated with temperature (Ohn and Sheldon, 1970, Genetics 66: 517-40). Hw1/Hw1 females exhibit 40-80% wild- type viability and are agametic steriles; clones of homozygous germinal cells in Hw/+ females capable of producing progeny (Garcia-Bellido and Robbins, 1983, Genetics 103: 235-47); however, Garcia-Alonzo and Garcia-Bellido claim that their strain is no longer homozygous female sterile. Viability and fertility of Hw1/Y males and Hw1/+ females good. Hw1/Hw1 and _ autonomous in somatic clones until 8 hr before puparium forma- tion; altering cellular genotype after that time is without effect owing to perdurance (Garcia-Bellido and Merriam). X- ray-induced full and partial revertants are frequently mutant for ac (Garcia-Alonzo and Garcia-Bellido). RK1 as male or heterozygous female. cytology: Claimed by Demerec and Hoover (1939, Genetics 24: 68) to be associated with duplication for the 1B1-2 doub- let; however restriction mapping of ASC fails to confirm this claim (Campuzano et al.). Many rearrangements with break- points in distal portion of sc complex have a weak Hw effect, especially as indicated by microachaetae on the mesopleurae; duplications for rearranged scute loci have enhanced effects; duplications of Hw+ without phenotypic effects except that they suppress h (Botas et al.). molecular biology: Carries a gypsy insert near the midpoint of the ac structural gene (T5) as well as a 2.6 kb insert (Sancho 2) located 8.5 kb to the left of the gypsy. Transcript 5 shortened from 1.1 kb seen in wild type to 0.9 kb; initiation normal; termination takes place in insert. Developmental Northern blots show peak accumulations in early embryos and early pupae; this transcript, which contains only the 5' half of the normal T5, is still functional in that no ac bristles are removed; it is present in many fold excess at all develop- mental stages examined (Campuzano et al.). The distribution of expressing cells in the wing disk is much less localized than in wild type (Balcells et al.). # Hw2 phenotype: Females homozygous for Hw2 show only occasional extra hairs along wings. Overlaps wild type. RK3A. cytology: Salivary chromosome analysis by Schultz (Morgan, Schultz, and Curry, 1941, Year Book - Carnegie Inst. Washing- ton 40: 284) shows small inversion of the region from 1A3 through 1B1 i.e., associated with In(1)Hw2 = In(1)1A2-3;1B1-2. # Hw49c phenotype: More extreme than Hw1. Homozygous female has dou- bling and tripling of many bristles, three or four extra dor- socentral bristles per side, extra wing veins, gap in poste- rior crossvein, and extra hairs on vein L2 and in wing cells. Width of mesonotum in region between dorsocentral bristles increased leading to increased numbers of acrostichal rows as well as extraneous extra microchaetae (Gottlieb, 1964, Genet- ics 49: 739-60); many lack one or more ocellar or postverti- cal macrochaetae (Stoddard, 1972, DIS 48: 137-38). Heterozy- gous female has normal bristles, extra hairs on L2 and L3 and in wing cells, and often an extra free vein from posterior crossvein; also extra acrostichal rows. Hw49c male much like homozygous female but bristle duplication less extreme. Low degree of non autonomy reported at junction between Hw49c/Hw49c and +/+ twin spots (Gottlieb). Male and heterozy- gous female fertile; homozygous female sterile. Revertants of Hw49c lose their dominant phenotypes; however they remain sc and may exhibit a weak ac phenotype or be lethal in combina- tion with Df(1)sc19 (Garcia-Alonzo and Garcia-Bellido). Not suppressed by su(Hw). Hw49c and Oce act synergistically in removing head bristles but cancel each others effects on thorax in Hw/Oce females (Stoddard). ac, sc, and l(1)sc tran- scripts considerably more abundant than in wild type; also more generally expressed in wing disks than normal (Balcells et al.). RK1. cytology: Associated with In(1)1B;2B3-4, with one breakpoint between 14.8 kb and 13.5 kb in the walk of Campuzano et al. and the other between 111 kb and 122 kb in the walk of Chao and Guild (Balcells et al.). other information: Three X-ray-induced revertants of Hw49c, all of which lack ectopic chaetae, characterized by Balcells et al.; Hw49c-rv1 is associated with T(1;3)1B;95A; its breakpoint in region 1B is in the same restriction fragment as that of In(1)Hw49c. Hw49c-rv4 is associated with T(1;2)1B;21A; its 1B breakpoint is between sc and l(1)sc in 26.8 kb to 25.0 kb. Hw49c-rv5 is associated with an eight-base-pair deletion in the sc coding region; it produces a polypeptide containing the first 114 amino acids of the sc translation product followed by 53 nonsense amino acids; the truncated polypeptide retains the basic region but not the helices of the helix-loop-helix motif. A null allele of sc. # Hw59g phenotype: Extra vertical, dorsocentral, and scutellar bris- tles. Suppression of sc with su(Hw)2 does not suppress Hw59g. # Hw685 references: Ruiz-Gomez and Modolell, 1987, Genes Dev. 1: 1238-46. Balcells, Modolell, and Ruiz-Gomez, 1988, EMBO J. 7: 3899- 3906. phenotype: Df(1)Hw685/Df(1)sc19 generates lateral clusters of microchaetae on the scutellum and promotes differentiation of extra sensilla campaniformia on the dorsal radius of the wing, of microchaetae or other sensilla on wing vein 3, and occasional microchaetae on wing vein 2. Slight increases in numbers of microchaetae on notum as well. Displays a very weak achaete effect despite presumed homozygous deficiency for ac. cytology: Claimed to be associated with terminal deficiency, Df(1)yT1b-685, which was broken at 45.4 kb to 43.9 kb. That this determination may be in error is suggested by the obser- vation: (1) that no other terminal Df(1)yT1b, including two others broken in the same restriction fragment, shows a hairy-wing effect; (2) terminal deficiencies induced in mu2 females are unstable losing about 75 base pairs per generation (Biessman and Mason, 1988, EMBO J. 7: 1081-86); yet Hw685 appears to be stable, and (3) Hw685 does not appear to be com- pletely deficient for ac. # Hwbap: Hairy wing-bristly abdominal pleura phenotype: Nearly all abdominal segments have on the pleurae two rows of bristles, which are the same size as those on the sternites. Mutant-bearing flies have a row of bristles aris- ing immediately posterior to each pigment band that are shorter than other tergite bristles. cytology: Associated with the 2PXD element of T(1;2)Hwbap = T(1;2)1B;21B. # HwBS phenotype: Spontaneous derivation of Hw1 with slightly weaker phenotype. molecular biology: Contains an 8 kb insert near the distal LTR in the gypsy element that is inserted in T5, the presumptive ac transcript, in Hw1. The identity of this sequence is unk- nown, but its internal 1.7 Pst1 fragment is repeated fifteen times in the genome of HwBS and Oregon R. The developmental profile of the HwBS T5 transcript is similar to that of Hw1 (Campuzano et al.). # HwUa phenotype: Weak Hw phenotype in heterozygous females. Pheno- type only slightly enhanced by suppressing the pre-existing sc1 allele with su(Hw)2 (Garcia-Alonzo and Garcia-Bellido). molecular biology: Complete copia element inserted into T4, the presumed sc structural gene, about one third of the distance from termination of the transcription unit. The HwUa tran- script, which carries the 5' two-thirds of the presumptive sc and terminates in copia, is present in excess in early larvae but not in crawling larvae or early pupae (Campuzano et al.). # l(1)sc: lethal at scute synonym: l'sc. references: Muller, 1935, Genetica 17: 237-52. Garcia-Bellido, 1979, Genetics 91: 491-520. Jimenez and Campos-Ortega, 1987, J. Neurogenet. 4: 179-200. phenotype: Deficiency from which existence of l(1)sc inferred, i.e., In(1)sc4Lsc9R, embryonic lethal. Volume of embryonic ventral nerve cord slightly reduced; posterior commisures thinner than in wild type; longitudinal connectives virtually lacking. Concomitant deletions for sc( or sc( and ac cause more severe CNS disruptions, although by themselves these deletions have no observable CNS effects; simultaneous dele- tion of the sc/ region also enchances the CNS disruptions (Jimenez and Campos-Ortega). Transiently expressed at peri- phery of syncytial blastoderm; late blastoderm shows paired dorsolateral and ventrolateral longitudinal stripes of expres- sion, the latter being coincident with the presumptive neuro- genic ectoderm. During germ-band expression, l(1)sc expres- sion seen in many cell clusters over most of the ectoderm; segmental distribution becomes apparent both internally and externally. l(1)sc expression seen in many foci in the head region and in the posterior midgut rudiment (Romani, Cam- puzano, and Modolell, 1987, EMBO J. 6: 2085-92; Cabrera, Martinez-Arias, and Bate, 1987, Cell 50: 425-33). Little if any expression in later stages, except in the central nervous system (Romani, Campuzano, Macagno, and Modolell, 1989, Genes Dev. 3: 997-1007). molecular biology: The gene encodes a 258-amino-acid, 29-kd polypeptide with a helix-loop-helix motif in the N-terminal end and a 15-residue C-terminal acidic domain (Alonso and Cabrera, 1988, EMBO J. 7: 2585-91). Transcription unit between coordinated 19.9 and 17.8 kb. other information: Inferred from the inviability of In(1)sc4Lsc9R = In(1)1B3-4;19F-20C1L1B2-3;18B8-9R [left break of In(1)sc9 in doubt], except in the presence of Dp(1;2)sc19. No mutant recovered (Garcia-Bellido). # sc: scute phenotype: Specifies the differentiation of numerous macrochae- tae on the head and thorax as well as microchaetae on the ter- gites: anterior, medial, and posterior orbital, posterior vertical, ocellar, and postvertical bristles on the head plus humeral, presutural, anterior and posterior notopleural, ante- rior supra-alar, sternopleural, anterior and posterior pos- talar, and anterior and posterior scutellar bristles on the mesothorax; also participates with ac in specifying the ante- rior vertical, posterior supra-alar, and anterior dorsocen- tral bristles; specifies the majority of the campaniform sen- silla on the wing blade (Leyns, Dambly-Chaudiere and Ghysen, 1989, Wilhelm Roux's Arch. Dev. Biol. 198: 227-32). Males deficient for sc, i.e., In(1)sc8Lsc4R, are poorly viable and catatonic; homozygous deficient females lethal; males defi- cient for both ac and sc, i.e., In(1)y3PLsc4R, are lethal (Garcia-Bellido, 1979, Genetics 91: 491-520). sc deficien- cies suppress the phenotype of emc; extra doses of ASC enhance the emc phenotype (Moscoso del Prado and Garcia-Bellido, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 242-51). alleles: Numerous alleles described, all but one of which are associated either with chromosome rearrangements with one breakpoint in region 1B or with inserts of foreign DNA. All but two chromosomal lesions with sc effects map proximal to the presumptive sc transcription unit; two inversions with breakpoints just distal to the transcription unit have slight effects; proximal lesions map to either side of l(1)sc, and strength of expression is inversely correlated with the molec- ular distance between the lesion and the scute transcription unit. Proceeding from right to left, lesions remove bristles from the mesonotum in a roughly hierarchical fashion in the following order: scutellars, (postverticals, ocellars, ster- nopleurals, anterior and medial orbitals, postalars), anterior notopleurals, (posterior orbitals, postverticals, anterior supra-alars) (presuturals, orbitals), with those enclosed in parentheses tending to be removed together (see Ghysen and Dambly-Chaudiere, 1988, Genes Dev. 2: 495-501). Transcrip- tion first observed in early gastrula in regions with neuro- genic potential, but before any overt evidence of neurogenesis apparent. As development proceeds, a complex temporal and spatial program of expression, mostly in neurogenic precursor cells ensues; expression ceases during the period of germ band shortening (Cabrera, Martinez-Arias, and Bate, 1987, Cell 50: 425-33; Romani, Campuzano, and Modolell, 1987, EMBO J. 6: 2085-92). In third-instar larvae, expression in wing disks is confined to restricted subsets of cells known to correspond to regions giving rise to precursors of cuticular sense organs that are under control of sc (Romani, Campuzano, Macagno, and Modolell, 1989, Genes Dev. 3: 997-1007). allele origin discoverer synonym ref ( comments | ________________________________________________________________________________________ sc1 spont Bridges, 16a22 ase1 12, 20 gypsy at 1.9 to 2.4 sc2 X ray Dubinin, 1928 7, 12 17-19 kb deletion between -11.5 and -30 *sc3 X ray Dubinin, 1928 7, 35 sc3-1 X ray Sturtevant 12, 39 partial reversion of sc3 sc3B spont Bridges, 26d26 12 sc4 Agol, 1928 1, 2, 34, 35 In(1)1B3-4;20F; in y; kb 25.8 to 24.0 sc5 X ray Gaissinovitsch, 1923 12, 13, 35 in wa; 1.2 kb deletion around -17 sc6 X ray Serebrovsky, 29a21 12, 34, 35 17.4 kb deletion in 7.4 to -10.8 kb sc7 X ray Dubinin, 1929 8, 10, 35, 41 In(1)1B3-4;6D-E; in y; kb -1.8 to -5.9; -2.4 to -4.9 kb fragment deleted sc8 X ray Sidorov, 1929 29, 37, 38 In(1)1B2-3;20F; kb 47.9 to 46.8 sc9 X ray Levit, 1929 18 In(1)1B3-4;18C1; kb 5.6 to 4.7 sc10 ac3 sc10-1 X ray Sturtevant, 1930 39, 40 derivative of In(1)ac3; nonsense mutation in sc transcript sc11 ac3 *sc12 X ray Shapiro, 1929 36 *sc13 Dubinin, 1929 8, 9, 10 with ac4; derivative of sc1 *sc15 X ray Muller scutex 30 Df? sc19 X ray League 24 Tp(1;2)1B1-2;1B4-5;25A5; kb -12.2 to -13.2 sc28 17 sc29 Agol, 1930 In(1)1B;13A2-5; kb -6.1 to -6.4 sc49c 32P Lewis, 1965 with Hw49c sc52c spont Green, 52c 15 with su(s)52c sc60d19 33 sc67b5 17 *sc90 X ray Goldat 14 derivative of sc6; In(1)1B4-7;1D2-E1 sc115 X ray Goldat 14 derivative of sc6; T(1;2)1A6-B1;25F sc260-14 X ray Sutton, 39b 43 In(1)1B2-3;11D3-8; kb 17.6 to 16.4 sc260-15 X ray Demerec, 38l 43 T(1;3)1B4-5;71C-D; kb 25.8 to 24.0 *sc260-16 X ray Sutton, 1938 43 *sc260-17 X ray Sutton, 39d 43 T(1;2)1B2-3;31C *sc260-18 X ray Sutton, 39d 43 T(1;2)1A6-B1;41D-E *sc260-20 X ray Sutton, 39e 43 T(1;3)1A8-B1;61A1-2 sc260-22 X ray Sutton, 39f 43 In(1)1B2-3;1E2-3; kb -10.9 to -11.5 *sc260-23 X ray Sutton, 1939 43 T(1;?) sc260-25 X ray Sutton, 39k 42 In(1LR)1B2-3 *sc260-26 X ray Sutton, 39l 43 T(1)2)1B4-5;41F2-3;58B2-3 + In(2LR)27D2-3;41A *sc260-27 X ray Sutton, 39l 43 T(1;2)1A8-B1;15E;19F; 33-34;57B-C *sc260-29 X ray Sutton, 40a 43 T(1;2;3)1A6-B1;22A-B; 34A-B;75C-E sc1744 Schalet, '85 insert in -6.1 to -7.2 *scA Agol 3 In(1)? scA spont Capdevila insert in -13.2 to -16.8 *scB X ray Brande, 37g In(1)y4 scB57 4 scC 17 scD1 X ray Dobzhansky, 1930 6, 19 gypsy at 2.4 to 1.9; with a y allele scD2 spont Dobzhansky, 1931 6, 12 gypsy at 2.4 to 1.9; in y scdr 17 scFah CB3007 Fahmy, 1954 11 Df(1)1A8-B1;1B2-3 scH / ray Hackett, 46a 28 T(1;4)1B4;101D-E; kb 6.5 to 6.0 scJ1 X ray Jacobs-Muller 21, 25 In(1)1A4-5;1B4-5, with l(1)1Ac1 scJ4 X ray Jacobs-Muller 22, 25 T(1;3)1B;3A3-C2;61A; kb 26.1 to 20.9 *scK Krivshenko 3 T(1;3)? *scK3 X ray Krivshenko, 53j29 16 T(1;3)1B2-3;61A1-2 scKA8 T(1;3)1B4-5;98; kb 16.3 to 14.9 scL3 Levy, 1932 12 gypsy at 2.4 to 1.9 scL6 17 scL8 Levy, 1932 26, 27, 31 In(1)1B3-4;20F; kb 30.9 to 28.8 *scP1 Panshin, 1934 T(1;2;3)scP1 scR 17 scS1 Sinitskaya, 34c 23, 26, 31, 5 In(1)1B3-4;20F; kb 28.2 to 26.9 scS2 Sinitskaya, 1934 T(1;2)1B4-7;60C-E; kb 1.2 to -3.2; 0.3 to -2.7 fragment deleted scSJ X Ray 32 In(1)1B3-4;2E3 *scSo Sytko 3 scV1 / ray J. I. Valencia, 46h23 28 In(1LR)1A8-C3 scV2 / ray J. I. Valencia, 46h23 28 In(1)1B2-3;20F ( 1 = Agol, 1929, Zh. Eksperim. Biol. 5: 86-101 (fig.); 2 = Agol, 1931, Genetics 16: 254-66; 3 = Agol, 1936, DIS 5: 7; 4 = Bier, Ackerman, Barbel, Jan and Jan, 1988, Sci- ence 240: 913-16; 5 = Crew and Lamy, 1940, J. Genet. 30: 273-83; 6 = Dobzhansky, 1935, DIS 3: 16; 7 = Dubinin, 1929, Biol. Zentralbl. 49: 328-39; 8 = Dubinin, 1930, Zh. Eksperim. Biol. 6: 300-24; 9 = Dubinin, 1932, J. Genet. 26: 37-58 10 = Dubinin, 1933, J. Genet. 27: 443-64; 11 = Fahmy, 1958, DIS 32: 74; 12 = Garcia-Bellido, 1979, Genetics 91: 491-520; 13 = Gassinovitsch, 1930, Eksperim. Biol. 6: 15-14; 14 = Goldat, 1936, Biol. Zh. 5: 803-12; 15 = Green, 1952, DIS 26: 63; 16 = Krivshenko, 1959, DIS 33: 95-96; 17 = Lee, 1973, Aust. J. Biol. Sci. 26: 903- 909; 18 = Levit, 1930, Wilhelm Roux's Arch. Entwick- lungsmech. Organ. 122: 770-83; 19 = Morgan, Bridges, and Schultz, 1935, Carnegie Inst. Wash. Year Book 34: 290; 20 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 211, 235 (fig.); 21 = Muller, 1932, Proc. Intern. Congr. Genet., 6th., Vol. 1: 225; 22 = Muller, 1934, DIS 2: 60; 23 = Muller, 1935, DIS 3: 50; 24 = Muller, 1935, Genetica 17: 237-52; 25 = Muller, Prokofyeva, and Raffel, 1935, Nature, 135: 253-55; 26 = Muller and Raffel, 1938, Genetics 23: 160; 27 = Muller, Raffel, Gershenson, and Prokofyeva- Belgovskaya, 1937, Genetics 22: 87-93; 28 = Muller and Valencia, 1947, DIS 21: 69-70; 29 = Noujdin, 1935, Zool. Zh.14: 317-52; 30 = Patterson and Muller, 1930, Genetics 15: 495-577 (fig.); 31 = Raffel, and Muller, 1940, Genetics 25: 541-83; 32 = Rowan, 1968, DIS 43: 61; 33 = Scowcroft, 1973, Heredity 30: 289-301; 34 = Serebrovsky, 1930, Wilhelm Roux Arch Entwicklungsmech. Organ. 122: 88-104;. 35 = Sere- brovsky and Dubinin, 1930, J. Hered. 21: 259-65 (fig.); 36 = Shapiro, 1930, Zh. Eksperim. Biol. 6: 347-64; 37 = Sidorov, 1931, Zh. Eksperim. Biol. 7: 28-40; 38 = Sidorov, 1936, Biol. Zh. 5: 3-26; 39 = Sturtevant, 1935, DIS 3: 15; 40 = Sturtevant, 1936, Genetics 21: 444- 66; 41 = Sturtevant, 1969, Dev. Biol. 21: 48-61; 42 = Sut- ton, 1940, Genetics 25: 628-35; 43 = Sutton, 1943, Genetics 28: 210-17; | DNA coordinates from Carramolino, Ruiz-Gomez, Guerrero, Cam- puzano, and Modolell (1982, EMBO J. 1: 1185-91) and Cam- puzano, Carramolino, Cabrera, Ruiz-Gomez, Villares, Boronat, and Modolell (1985, Cell 40: 3227-38). 0 defined as the more distal EcoRI site within the scS2 molecular deficiency; positive values extend to the left. Where known, restriction fragment interrupted by the 1B breakpoint of sc rearrange- ments indicated. cytology: Placed in 1B3 based on its location between the left breakpoints of In(1)sc8 = In(1)1B2-3;20F and In(1)sc4 = In(1)1B3-4;20F. molecular biology: sc assigned to transcript T4 of Campuzano, Carramolino, Cabrera, Ruiz-Gomez, Villares, Boronat, and Modolell (1985, Cell 40: 3227-38); the sc transcription unit is transcribed from left to right and occupies DNA coordinates approximately 34 to 32 kb. A series of terminal deletions approaching the sc transcription unit from the left were placed in heterozygous combination with In(1)sc8Lsc4R, among other sc deficiencies, and the phenotypes assessed (Ruiz-Gomez and Modolell, 1987, Genes Dev. 1: 1238-46). The majority of deficiencies between coordinates 55 and 38 kb showed signifi- cant but weak sc phenotypes; those ending within 4-5 kb of the transcription start caused stronger phenotypic effects, remov- ing first posterior supra-alar, and then posterior notopleural bristles (see also Ghysen and Dambly-Chaudiere, 1988, Genes Dev. 2: 495-501). cDNA and genomic sequences of the sc tran- scribed region determined by Villares and Cabrera (1987, Cell 50: 415-24); the transcription unit of 1430 nucleotides is without introns; the longest open reading frame encodes a 345-amino-acid polypeptide of 38.1 kd. Contains both the helix-loop-helix motif and the C-terminal acidic region characteristic of ac and l(1)sc. # sc1 phenotype: Causes loss or marked reduction in number of scutel- lar, coxal, ocellar, first and second orbital, anterior noto- pleural, postvertical, tergital, and sternal bristles. Bristle sockets missing; bristle cells absent 19 hr after pupation, when normally present [Lees and Waddington, 1942, DIS 16: 70-70a; 1943, Proc. Roy. Soc. (London), Ser. B 131: 87- 110]. Suppressed by su(Hw) and su(Hw)2. RK1. other information: Revertable by X rays (Green, 1961, Genetics 46: 671-82). # sc2: see ase #*sc3 phenotype: Most bristles affected, principally ventrals, orbi- tals, verticals, postverticals, ocellars, humerals, presutur- als, notopleurals, supra-alars, postalars, sternopleurals, abdominals, and anterior dorsocentrals; scutellars and post- dorsocentrals usually present. Viability of male low; female virtually lethal. RK2. cytology: Salivary chromosomes appear normal (Morgan, Bridges, and Schultz, 1935, Year Book - Carnegie Inst. Washington 34: 290). # sc3-1 phenotype: Partial reversion from sc3. Homozygous females show reduced viability; hemizygous females lethal (Garcia-Bellido, 1979, Genetics 91: 491-520). RK2. #*sc3B: scute-3 of Bridges phenotype: Like sc but does not affect anterior notopleurals. Suppressed by su(Hw)2 (Lee, 1973, Aust. J. Biol. Sci. 26: 903-09). RK1. other information: Some stocks currently labelled sc3B are reverted for sc but are now ac3B. # sc4 phenotype: Extreme scute. Bristles of head, except anterior verticals, absent. Only posterior notopleurals and alars remain on sides of mesothorax; abdominals, ventrals, coxals, and scutellars also missing. Slight variegation for Hw. RK1A. # sc5 phenotype: Sternital and scutellar bristles reduced in number; others rarely affected. sc5/sc6 is practically wild type. RK1. # sc6 phenotype: Slight sc; removes coxals, ocellars, first and second orbitals, postverticals, and anterior notopleurals. Scutellars and sternitals not affected. RK1. cytology: No inversion. # sc7 phenotype: Like sc but anterior notopleurals not affected. sc7 tends to suppress expression of h (Steinberg, 1942, DIS 16: 68). RK1A. other information: wa separable from sc7 by exchange in tri- ploid female. # sc8 phenotype: Slight sc; supra-alars, sternopleurals, or other bristles sometimes affected. Extra bristles may be present. Shows Hw effect and may be recognized in heterozygote, homozy- gote, or male by presence of one or more hairs on anterior mesopleural region. The Hw effect interacts strongly with h to produce extremely hairy wings (Steinberg, 1942, DIS 16: 68). sc8/0 male nearly lethal; survivors show variega- tion for y and ac; lethality suppressed by a Y chromosome, partially suppressed by parts of the Y (Hess, 1962, DIS 36: 74-75; 1963, Verhandl. Deut. Zool. Ges., Zool. Anz. Suppl. 26: 87-92). RK2A. # sc8c.o. X: see Df(1)sc8 # sc8ENc.o. X: see Df(1)sc8 # sc9 phenotype: Like sc but scutellars always absent. Abdomen swol- len and wings poorly expanded, like sc2. RK2A. # sc10: see ac3 # sc10-1 phenotype: Like sc3 but more extreme; most extreme viable sc allele. Viability low. RK2A. cytology: Originally thought to be associated with a minute deficiency (Schultz); not confirmed by molecular analysis. molecular biology: Sequence data reveal a silent C->T transi- tion at nucleotide 669, a C->G transversion at nucleotide 1143 causing ser161->arg161, and a C->T transition in nucleotide 1147 resulting in a stop codon; (first nucleotide of initial ATG codon at nucleotide 660) (Villares and Cabrera, 1987, Cell 50: 415-29). # sc11: see ac3 #*sc12 phenotype: First and second orbitals reduced or absent; other head bristles, posterior scutellars, and coxals also affected. Also shows achaete effect. Viability of homozygous female low. RK2. #*sc13 phenotype: Like sc but scutellars invariably absent and ocel- lars, postverticals, and first and second orbitals less fre- quent. Anterior and posterior dorsocentrals also absent, as are thoracic hairs, because of ac4. Viability low. RK2. #*sc15 phenotype: Originally allelic to sc and semilethal in male. Subsequently, allelic to y, ac, and sc, and male lethal. Lethal form exaggerates other ac and sc alleles in heterozy- gote. RK2A. cytology: Presumably associated with Df(1)sc15; breakpoints unknown. other information: Apparently, y+ and ac+ were inserted else- where in the genome (as in sc19 or scV1), became separated from the left end of X, and were lost. # sc19 phenotype: Scutellar bristles absent and sternitals reduced. RK1A. # sc28 phenotype: Strong scute; not suppressed by su(Hw)2. # sc29 phenotype: Similar to sc7. Viable and fertile. RK2A. # sc49c other information: Overlooked at the time Hw49c was described. Possibly of subsequent spontaneous origin. # sc52c other information: Association with In(1)sc52c (breakpoints unknown) inferred, since sc52c has been inseparable from ras v. # sc67b5 phenotype: Strong scute; not suppressed by su(Hw)2. # sc260-14 phenotype: Both sexes viable and fertile. RK2A. # sc260-15 phenotype: Male sterile. Viability reduced. RK2A. #*sc260-16 phenotype: sc260-16/sc overlaps wild type. Lethal homozygous and hemizygous. RK2. cytology: Salivary chromosomes normal. #*sc260-17 phenotype: Male and homozygous female viable and fertile. RK2A. #*sc260-18 phenotype: Male sterile. RK2A. #*sc260-20 phenotype: Male and homozygous female viable and fertile. RK2A. # sc260-22 phenotype: Both sexes viable and fertile. RK2A. #*sc260-23 phenotype: Both sexes viable. RK3A. # sc260-25 phenotype: Variegates for y, ac, and probably l(1)1Ac but not for svr; more extreme than scV1. Homozygous lethal. RK2A. #*sc260-26 phenotype: Viability reduced in male. Male fertile. RK2A. #*sc260-27 phenotype: Male viable but sterile. RK2A. #*sc260-29 phenotype: Male viable but sterile. RK2A. #*scA: scute of Agol phenotype: Similar to sc. Viability low. RK2A. #*scB1: scute of Brande phenotype: Similar to sc. Viability good. RK2A. # scB57 phenotype: Embryo displays reduced numbers of CNS and PNS neu- rons. # scD1: scute of Dobzhansky phenotype: Weak sc. RK2. cytology: Salivary chromosomes apparently normal (Schultz). # scD2 phenotype: Slight sc. RK2. # scFah: scute of Fahmy phenotype: Bristles (principally orbitals, verticals, postvert- icals, and ocellars) missing. Scutellars and postdorsocen- trals left nearly intact. Male viable and fertile; female homozygous lethal. scFah/sc has only occasional absence of postvertical or ocellar bristles. RK2A. # scH: scute of Hackett phenotype: Similar to sc but more extreme. RK2A. # scJ4 phenotype: Scute and achaete effects. RK3A. #*scK: scute of Krivshenko phenotype: Similar to sc but semilethal in male and lethal in homozygous female. RK2A. # scL3: scute of Levy phenotype: In addition to scute, it has a spoon-like wing caused by a mutation to the right of sc. Viable. Suppressed by su(Hw)2 (Lee, 1973, Aust. J. Biol. Sci. 26: 903-09). RK2. # scL6 phenotype: Moderate scute; suppressed by su(Hw)2 (Lee, 1973, Aust. J. Biol. Sci. 26: 903-09) # scL8 phenotype: Similar to sc4 but more extreme. Homozygous female sterile. RK2A. # scS1: scute of Sinitskaya phenotype: Rather extreme sc allele; slight Hw effect; hairs often removed from abdomen and wings. Homozygous female sterile and low in viability. Male fertile and fairly viable. RK2A. # scS2 phenotype: Similar to sc7. RK1A. #*scSo: scute of Sytko phenotype: Like sc; viability of homozygous female low. RK2. # scV1: scute of Valencia phenotype: Extreme scute and achaete. Viability low. RK2A. # scV2 phenotype: Both achaete and scute variably affected. Some ten- dency for extra or twin bristles. Abdominal bristles markedly fewer both dorsally and ventrally. Male and homozygous female viable and fertile. RK2A. # sis-b: sisterless b (T. W. Cline) location: 1-0.0. synonym: sc3-1. references: Cline, 1988, Genetics 119: 829-62. Torres and Sanchez, 1989, EMBO J. 8: 3079-86. Cline, 1989, Cell 59: 231-34. phenotype: Original hypomorphic allele recovered as a reversion of sc3 to nearly wild-type ac and sc phenotype in hemizygote and homozygote; originally designated sc3-1 by Sturtevant, renamed sis-b by Cline. Locus also characterized by dominant effects of deficiencies and duplications of the ASC region, and later by mutant alleles sc10-1 and Hw49c that affect ASC functions more than sis-b functions. sis-b reduces viability of homozygous females and hemizygous females are lethal; yet hemizygous males fully viable. Dominant synergistic female- specific lethal interactions with loss-of-function alleles of Sxl, sis-a, and/or maternal da; magnitude of viability effects depends on genetic background and inversely correlates with background effects on male-lethal effects; interactions tem- perature dependent, generally more extreme at higher tempera- tures. Female viability effects suppressed by gain-of- function SxlM1 allele, and by duplications of Sxl+ or sis-a+. Duplication of sis-b+ male-lethal in combination with duplica- tion of Sxl+ and/or sis-a+, more so at lower temperatures. Male lethality of duplication combinations suppressed by Sxl-. Phenotype of 2X;3A intersexes strongly dependent on dose of sis-b+. The dose-dependent interactions of this gene identify it as a positive regulator of Sxl+ and part of the numerator of what is referred to as the X/A balance, the primary sex- determination signal. This is a character it shares with sis-a. cytology: Located in 1B3, based on its location between the left breakpoints of In(1)sc8 = In(1)1B2-3;20F and In(1)sc4 = In(1)1B3-4;20F. molecular biology: Activity mostly (but not entirely) confined to a region of approximately 24 kb as determined by Cline (1988), which includes the scute-alpha member of the ASC, and is known to encode one (T4) or possibly two (also T7) tran- scripts. Location refined further by Torres and Sanchez (1989) to the 8.3 kb fragment between the breakpoint of In(1)scL8 distally and the breakpoint of Df(1)yT2-650 proxi- mally, a region containing only transcription unit T4; how- ever, there are uncertainties connected with this assignment: Df(1)yT rearrangements are reported to be highly unstable, losing 75 base pairs per generation (Biessmann and Mason, 1988, EMBO J. 7: 1081-86), the assay used to assess sis-b function was not always sufficient to establish whether wild- type levels of sis-b activity were present. Molecular charac- terization of sc10-1 and Hw49c indicates that sis-b function requires protein encoded by the sc transcription unit; nevertheless, it seems worthwhile to retain both gene names for the time being, since different regulatory information, and perhaps even somewhat different protein activities, are involved in sex determination versus neurogenesis. # ascutex: see asx # asense: see ase under ASC # ash1: absent, small, or homeotic discs location: 3-46. references: Shearn, 1974, Genetics 77: 115-25. Shearn, Hersperger, and Hersperger, 1987, Roux's Arch. Dev. Biol. 196: 231-42 (fig.). phenotype: Most alleles homozygous lethal; stage of lethality variable. Surviving and pharate adults display transforma- tions including haltere to wing, first and third legs to second leg, genitalia to leg or antenna; ash18 and ash110 show transformation of posterior to anterior wing margin. Homeotic transformations also seen in clones of homozygous cells in otherwise heterozygous flies. Larvae homozygous for ash112, a severe allele, displays a high incidence of failure to form imaginal disks, especially antennal, genital, haltere, and wing disks. alleles: allele origin synonym comments _________________________________________________ ash11 ICR170 III-10 prepupal-pupal lethal ash12 ICR170 XVI-18 pupal lethal ash13 EMS RD317 pharate-adult lethal ash14 EMS RE418 L2 lethal ash15 EMS RF327 L2 lethal ash16 EMS RF605 L1 lethal ash17 EMS RL031 adults eclose ash18 EMS RZ426 adults eclose ash19 EMS RZ606 L1 lethal ash110 EMS SP1017 pharate-adult lethal ash111 / ray TK117 L1 lethal ash112 / ray TN402 L2-to-prepupal lethal cytology: Placed in 76B5-E based on its position between the 3L breakpoints of T(Y;3)L14 = T(Y;3)h3;76B5-10 and T(Y;3)A112 = T(Y;3)h11;76E. # ash2 location: 3-{85} (distal to aor). references: Shearn, 1974, Genetics 77: 115-25. Shearn, Hersperger, and Hersperger, 1987, Roux's Arch. Dev. Biol. 196: 231-42 (fig.). phenotype: Most alleles homozygous lethal; stage of lethality variable. Surviving and pharate adults display transforma- tions similar to those indicated for ash1. alleles: allele origin synonym comments _________________________________________________ ash21 NNG 703 L2-L3 lethal ash22 NNG 1803R prepupal lethal ash23 EMS R0631 pupal-adult lethal ash24 EMS SE420 ash25 EMS SH536 prepupal-pupal lethal cytology: Placed in 96A1-25 based on its inclusion in Df(3R)96A1-7;96A20-25 associated with In(3R)Ubx7LatsR (Gon- zalez, Molina, Casal, and Ripoll, 1989, Genetics 123: 371- 77). # asp: abnormal spindle location: 3-85.2 (based on 64 hh1-tx recombinants). origin: Induced by ethyl methanesulfonate. references: Ripoll, Pimpinelli, Valdivia and Avila, 1985, Cell 41: 907-12. Gonzalez, Molina, Casal, and Ripoll, 1989, Genetics 123: 371-77. phenotype: Cold-sensitive recessive semilethal; 12% survive to adulthood at 25; most larvae with small or absent imaginal discs; delayed development; survivors with nicked wings and rough eyes. Males sterile at 18 and fertile at 25; produce abundant MI nondisjunction; females sterile. Larval neurob- lasts frequently polyploid, especially when held at 18. Phenotype enhanced by duplication for 97B, i.e., the YP3D ele- ment of T(Y;3)B158 = T(Y;3)BSXh;97B, but not that of T(Y;3)R71 = T(Y;3)h1-2;97B cytology: Localized to 96A21-B10 between third chromosome breakpoints of T(Y;3)A117 = T(Y;3)h24;96A21-25 and T(Y;3)B197 = T(Y;3)h3;96B1-10. L-aspartate: 2-oxyglutarate aminotransferase: see Got # ast: asteroid location: 2-1.3 (0.02 unit to right of S). origin: Spontaneous. discoverer: E. B. Lewis, 38b. synonym: Sr: Star-recessive. references: 1938, DIS 10: 55. 1942, Genetics 27: 153-54. 1945, Genetics 30: 137-66. 1951, Cold Spring Harbor Symp. Quant. Biol. 16: 159-74 (fig.). phenotype: Eyes small and rough. Veins L2, L3, L4, and L5 do not always extend to margin. Overlaps wild type rarely. S +/+ ast has very small eyes with fused facets; veins L2 to L5 incomplete at tip. S ast/+ ast has slightly larger eye than S +/+ ast. S ast/+ + resembles S +/+ +. S +/+ ast and ast/ast partially suppress px and net. Eyes of ast/E(S) rough. RK2. alleles: *ast2 and ast3 show eye but not wing effect of ast (CP627). ast4, *ast5, and astX homozygotes look normal but enhance expression of S in heterozygotes (Lewis, 1951). Three reversions of ast superscripted *rv1, *rv2, and *rv3 (Lewis, 1951). astv is variegating allele associated with T(2;4)21E2-3;101 (Lewis, 1951). cytology: Placed in the 21E1-2 doublet on the basis of its being included in the synthetic deficiency derived by combin- ing the Y-centric portion of T(Y;2)21E = T(Y;2)21D4-E1 and the 2-centric portion of T(2;4)astv = T(2;4)21E2-3;101 (Lewis, 1945). See also Roberts, Brock, Rudden, and Evans-Roberts, 1985, Genetics 109: 145-56. #*asx: ascutex location: 1-26. origin: Spontaneous. discoverer: Bridges, 24b14. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 218. phenotype: Furrow between scutellum and thorax much shallower; scutellum inflated. Body color pale. Legs have blackened leaky joints. Character less extreme in old dry cultures. Viability 60% wild type. RK3. # Asx: Additional sex combs location: 2-72. origin: Induced by ethyl methanesulfonate. discoverer: Jurgens. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Jurgens, 1985, Nature 316: 153-55. Breen and Duncan, 1986, Dev. Biol. 118: 442-56 (fig.) phenotype: Asx/+ males have extra sex-comb teeth on meso- and metathoracic legs (e.g., Asx6 -> 11.8 sex-comb teeth per prothoracic, 0.5 per mesothoracic, and 0.2 per metathoracic leg). Homozygote embryonic lethal. Abdominal denticles in head and thoracic segments; abdominal segments 1-7 transformed into more posterior segments. With respect to the degree of transformation to more posterior structures, Df(2R)trix/Df(2R)trix > Df(2R)trix/Asx5 > Asx5/Asx5, indicat- ing that Asx5 is hypomorphic mutation. Similar genotypes derived from Df(2R)trix/Asx5 oocytes achieved by means of pole-cell transplantatiton display more severe transformation than their counterparts above derived from mothers carrying one dose of Asx+ (Breen and Duncan). In double mutant combi- nations with Pcl, Psc, or Scm shows strong posterior transfor- mation of all segments and failure of head involution. The presence of BXC+ required for expression of phenotype. allele origin discoverer synonym ref ( comments ________________________________________________________________________ Asx1 EMS AsxIIF 3 Asx2 EMS AsxET21 3 Asx3 X ray AsxXT129 3 Asx4 HD AsxP2 2, 3 recovered as dominant enhancer of Pc Asx5 EMS Duncan AsxD1 1 recovered as suppressor of Pc Asx6 / rays Tiong, 1982 AsxT1 T(2,3) ( 1 = Breen and Duncan, 1986, Dev. Biol. 118: 442-56 (fig.); 2 = Dura, Brock, and Santamaria, 1985, Mol. Gen. Genet. 198: 213-20; 3 = Jurgens, 1985, Nature 316: 153-55. cytology: Placed in 51A1-B4 based on its being deleted by both Df(2R)trix = Df(2R)51A2-4;51B3-6 and Df(2R)L+48 = Df(2R)51A1;51B4. # Asy: see A-p # Asymmetric: see A-p #*at: arctus oculus location: 2-60.l. origin: Spontaneous. discoverer: Fernandez Gianotti, 42g28. synonym: bar eye; arctops. references: 1943, DIS 17: 48. 1944, DIS 18: 45. 1945, Rev. Inst. Genet. Fac. Agron. Vet. Univ. Buenos Aires 2(14): 171-77. 1948, DIS 22: 53. phenotype: Eyes similar to B but with more facets. Classifica- tion, fertility, and viability excellent. RK1. # At: Attenuated location: 1- (in the B region). origin: Induced with soft X rays in In(1)scS1Lsc8R+d1-49, scS1 sc8 B; associated with loss of B phenotype. discoverer: Valencia and Valencia, 1949. references: 1949, DIS 23: 64. phenotype: In At/+ females, wings incised medially and laterally, usually have one large central blister. At/At females have badly crumpled, blistered, and sometimes poorly developed wings. Wings of At males tend to be more like those of At/+ females, although many fall somewhere between At/+ and At/At in phenotype. Thus there is evidence for only a slight dosage compensation for At. This mutant is similar to some Beadex alleles, but allelism not tested. Both males and homozygous females viable and fertile. RK1A. cytology: Associated with In(1)At = In(1)16A4-5;18C4-6;20A2-3. # Ata: Arista location: Not located. origin: X ray induced. discoverer: Krivshenko, 1949. synonym: At (symbol preoccupied). references: 1954, DIS 28: 74-75. 1955, DIS 29: 73. phenotype: Lateral branches of aristae reduced, especially branches extending upward from central axis and situated at base of arista. Axis of arista often abnormal. Wings have small transparent spots distally. Homozygous lethal. Hetero- zygous viability and fertility comparatively high. RK2A. cytology: Associated with T(2;3)Ata = T(2;3)40;66F-67A + T(2;3)47;81. # athrin: see Act88F # atn: see ems # Atp(: (Na+ + K+) ATPase ( subunit location: 3-{70}. references: Lebovitz, Takeyasu, and Fambrough, 1989, EMBO J. 8: 193-202. phenotype: Structural gene for the ( or catalytic subunit of Na+ K+ ATPase (ouabain sensitive). Immunofluorescence micro- scopy with a monoclonal antibody demonstrates high concentra- tions of (ATPase in adult muscle, nervous tissue, and Malpig- hian tubules; strong immunofluorescence observed in brain, optic lobes, photoreceptor cells of retina, and ventral tho- racic neuromere. Flies heterozygous for Df(3R)r1-G6 which lacks Atp(, are sluggish and less tolerant of physical stress than normal. cytology: Placed in 93B by in situ hybridization. Included in Df(3R)r1-G6 = Df(3R)93A2-B1;93E-F. molecular biology: cDNA clones isolated by probing a late-pupal and six-hour embryonic cDNA libraries with probes from the homologous gene from chicken. All tissues and all stages tested produce three homologous transcripts of 3.6, 3.8, and 4.8 kb, with the 4.8-kb species being the most abundant, except in the adult thorax where all are equally abundant. The sequence reveals an open reading frame encoding a polypep- tide of 1038 amino acids; the conceptual sequence is 75-80% homologous to other ( subunits. Genomic clones contain more than 10 kb of intron sequence. # atrophie gonadique: see agq # ats: abnormal tarsi location: 3- (not localized). origin: Spontaneous in a third chromosome carrying three non- overlapping paracentric inversions. references: Sierra and Comendador, 1984, DIS 60: 244-45(fig.) phenotype: Homozygotes exhibit different degrees of tarsal aplasia; most frequently second, third, and fourth tarsal joints missing; less frequently the fifth tarsal joint arises from tibia; often a rudimentary tarsal appendage arises from tibia or the fifth tarsal joint. Homozygous males and females sterile. Adult and preadult survival reduced; more than 50% of imagos die during the first day. # Attenuated: see At # aub: aubergine (T. Schupbach) location: 2-39. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female sterile; homozygous females lay eggs which are of variable shapes; in the most extreme cases, the eggs are longer than the normal, more pointed at the posterior end, and lack dorsal appendages, resembling eggs produced by the dominant female-sterile mutation Fs(2)G. alleles: aubOC = aub1, aubAHN, aubHN. # augenwulst: see awu # aur: aurora location: 3-53. synonym: early-A; fruhe2. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal-effect lethal. Embryos abnormal from nuclear cycle 9 onward. Multiple spindles assemble in long arrays with shared centrosomes. Polyploid nuclei develop with multiple centrosomes. Larval mitosis not investigated (Glover and Nusslein-Volhard). alleles: Three ethyl-methanesulfonate-induced alleles, aur1, aur2, and aur3 recovered as 074, 175, and 287. cytology: Placed in 87A7-B2 based on inclusion in the region of overlap of Df(3R)E229 = Df(3R)86F6-7;87B1-2 and Df(3R)kar-D1 = Df(3R)87A7-8;87D1-2. #*aw: awry location: 1-32 (not allelic to wy). origin: Induced by ingested radiophosphorus. discoverer: Bateman, 1949. references: 1950, DIS 24: 54. 1951, DIS 25: 77. phenotype: Wings upcurled, slightly wavy, convex, opaque, or vestigial-like. Variable; overlaps wild type. Viability about 50% wild type. Not enhanced in presence of y, as is dvr (1-28.1). RK3. #*aw-b: awry-b location: 1-38 to 39. origin: Induced by ingested radiophosphorus. discoverer: Bateman, 1950. synonym: aw2. references: 1950, DIS 24: 54. 1951, DIS 25: 77. phenotype: Like aw. Good expression at 25. Viability 10% that of wild type. Most males fail to eclose. RK3. # awd: abnormal wing disc (A. Shearn) location: 3-102.9 (based on mapping of awdK). origin: P mutagenesis. discoverer: Dearolf, 1983. references: Dearolf, Hersperger, and Shearn, 1988, Dev. Biol. 129: 159-68. Dearolf, Tripoulas, Biggs, and Shearn, 1988, Dev. Biol. 129: 169-78. Biggs, Tripoulas, Hersperger, Dearolf, and Shearn, 1988, Genes Dev. 2: 1333-43. phenotype: Homozygotes die in late third larval instar; wing discs variably hypoplastic; other discs appear grossly normal. Trypan blue staining reveals cell death in wing disc, either in area of presumptive wing blade, or scattered throughout disc; other discs reveal lesser amounts of cell death later in development than in wing discs. Extensive lipid vacuolization in larval ventral ganglion, brain lobes, and proventriculus. Mutant discs exhibit slow growth when transplanted into wild- type hosts; normal discs in mutant hosts grow normally. Metamorphosis of eye-antennal, wing, and leg discs when tran- splanted into normal larvae severely restricted; few or no adult structures develop; mutant ovaries do not survive tran- splantation to wild-type hosts; however, transplanted awd pole cells capable of producing both awd/+ and awd/awd progeny. Epidermal clones nearly lethal and with thin, short, bent bristles and hairs when induced early; survive in reduced numbers and size when induced late. alleles: Five P-induced alleles and twelve revertants of awdK reported but only a subset of them identified in publications; some revertants listed under Df(3R)awd. allele origin discoverer synonym ref ( comments ____________________________________________________________________ awdb3 P Dearolf, 1983 2, 3 amorphic allele P element in exon 1 awdK Sturtevant, 54a Kpn 1, 4, 5, Killer of prune; 6, 7 description follows awdKrv14 / ray Biggs awdKR14 1 hypomorph; lesion in 5' untranslated region; 20% normal protein awdKrv17 / ray Biggs awdKR17 1 0.8-kb deletion; mutates awd and adjacent downstream gene ( 1 = Biggs, Tripoulas, Hersperger, Dearolf, and Shearn, 1988, Genes Dev. 2: 1333-43; 2 = Dearolf, Hersperger, and Shearn, 1988, Dev. Biol. 129: 159-68; 3 = Dearolf, Tripoulas, Biggs, and Shearn, 1988, Dev. Biol. 129: 169-78; 4 = Orevi and Falk, 1974, Arch. Genet. 47: 172-83; 5 = Orevi and Falk, 1974, Mutat. Res. 33: 193-200; 6 = Sturtevant, 1955, DIS 29: 75; 7 = Sturtevant, 1956, Genetics 41: 118-23. cytology: Placed in 100C-D by in situ hybridization. molecular biology: Locus cloned by transposon tagging and res- triction mapped. 850 base pair transcript detected by north- ern analysis. Rescue of mutant phenotype achieved by germ- line transformation. Transcript detected by northern analysis, abundantly in larval and less abundantly in adult tissues as well as in cultured cells. Sequencing shows exon 1 = ~130 nucleotides, intron 1 = ~250 nucleotides, and exon 3 = ~300 nucleotides. Sequence determined by Biggs et al. indi- cates a protein of 153 amino acid residues and 16-17 kd in molecular weight. Gel-filtration experiments of embryonic extracts indicate that the AWD protein is present in cells in a 100 kd species. The conceptual amino acid sequence shows 78% identity and 95% similarity to that of the human metas- tasis inhibiting factor, NM23 (Rosengard, Krutzsch, Shearn, Biggs, Barker, Inger, Margulies, King, Liotta, and Steeg, 1989, Nature 342: 177-80). Both sequence and activity (Shearn) indicate that the protein is a nucleoside diphosphate kinase. # awdK phenotype: An antimorphic allele; no phenotypic effects, either when homozygous or heterozygous; however, it is a dominant conditional lethal, which is lethal in combination with pn, i.e., pn/Y; awdK/+ males or pn/pn; awdK/+ females. awdK does not interact with any other eye-color mutant. Interacts lethally with all standard alleles of pn tested; however, pnts-ek insensitive to awdK at permissive temperatures, whereas nine other temperature-sensitive alleles of pn are insensitive under all conditions. Lethal phase of pn;awdK genotypes begins in early second larval instar and lasts until after the time that normal larvae pupate. Using pnts-ek, the temperature-sensitive period of the pn component of the lethal interaction determined to begin in second instar and last until eclosion. pn;awdK sons of pn mothers appear to die ear- lier than those of pn/+ mothers, suggesting a maternal effect of pn+, which is revealed in the presence of awdK (Hackstein, 1971, Mol. Gen. Genet. 111: 371-76). Fate mapping in pn//pn/+;awdK/+ gynandromorphs places the focus of the lethal interaction in the midventral part of the blastoderm, not a focus of pteridine biosynthesis. awdK eye disks transplanted into pn hosts develop autonomously as do the reciprocal tran- splants (Grell, 1958, DIS 32: 123-24). The levels of awd transcript are normal in (1) pn, (2) awdK/+, and (3) pn;awdK/+ flies; however, only the first two genotypes accumulate normal levels of the AWD polypeptide, the last having little or none, despite the presence of one copy of awd+. pn;awdK/+ larvae die in early third instar, whereas those that are pn;awdK/+/+ die at the end of L3. other information: Allelism of awdK demonstrated by two obser- vations. First induced revertants of awdK, as recovered on the basis of their failure to interact lethally with pn, are lethal in all pairwise combinations (Lifschytz and Falk, 1969, Genetics 62: 353-58) and in combination with awdb3. Second transformants carrying an awd homologous sequence isolated from homozygous awdK DNA are able to rescue awdb3 lethality and are able to kill pn in the presence of homozygous awd+ (Biggs et al.). # awry: see aw # awu: augenwulst location: 2-53.7 (based on mapping of awu2 by Carfagna and Melen). origin: Spontaneous. discoverer: Rosin, 1951. references: Volkart, 1959, DIS 33: 100. phenotype: Eyes deformed; in most extreme expression, deeply indented at middle of anterior margin where invaginating integument forms a pad-like swelling with bristles. Expres- sion variable, often asymmetrical. Overlaps wild type. Heterozygote occasionally has minor effects. Good viability. RK3. alleles: *awu1; awu2, spontaneous (1971, Carfagna and Melen, DIS 47: 38). Shows more dominance than awu. # Ax: see under N # Axs: Aberrant X segregation (A.E. Zitron and S. Hawley) location: 1-56 (not separated from f in 80 recombinants between v and car). origin: Induced by ethyl methanesulfonate. references: Zitron, and Hawley, 1989, Genetics 122: 801-21. phenotype: Dominant meiotic mutant that affects distributive pairing; disrupts meiotic segregation of non-exchange chromo- somes in females. Has no effect on the frequency of exchange. Loss of function mutation at a dosage sensitive locus; Axs+ duplication can rescue mutation in trans. Specific to female meiosis. In Axs/Axs/Y females, X-chromosomes nondisjunction is accompanied by random disjunction of the Y rather than directed disjunction from the X's as observed in +/+/Y females. Axs homozygotes increase X nondisjunction many fold; parallel but lesser effects observed on autosomal disjunction. cytology: Associated with a small chromosome aberration at 15D1.