c: curved From Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 165. # c: curved location: 2-75.5. phenotype: Wings thin textured, divergent, uplifted at base, and curved downward throughout their length. RK1. alleles: allele origin discoverer synonym ref ( __________________________________________________ c1 spont Bridges, 11l24 1,3 c2 Erlich, 62i c62i 4 c3 EMS Davis 2 c4 EMS Davis 2 c5 EMS Davis 2 c6 EMS Davis 2 c7 EMS Davis 2 ( 1 = Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 164 (fig.); 2 = Davis and MacIntyre, 1988, Genetics 21: 755-66; 3 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 211 (fig.); 4 = Nelsen, 1967, DIS 42: 37. cytology: Placed in 52D3-9 based on its inclusion in Df(2R)KL9 = Df(2R)52D3;52D7-9 (Davis and MacIntyre). # CK: see C-K # C-abl: see Abl # C-erb: see Egfr #*C-K: Curved of Krivshenko location: 2- or 3- (rearrangement). origin: X ray induced. discoverer: Krivshenko, 55l3. references: 1956, DIS 30: 74. synonym: CK. phenotype: Wings are thin textured, slightly divergent, uplifted basally, and then curved downward. Homozygous lethal. RK2A. cytology: Associated with T(2;3)C-K = T(2;3)52;76;81;86. other information: Probably allele of Rev. # C-myb: see Myb # C-ras1: see Ras1 # C-ras2: see Ras2 # C-ras3: see Ras3 # C-src1: see Src1 # C-src2: see Src2 # C( ): Crossover suppressor The terminology originally used for dominant suppressors of crossing over. These effects were found to be rearrangements and are so treated here. The symbol C in this context has been dropped except where included under synonymy. #*c(1)a: crossover suppressor for chromosome 1 location: One factor in X and probably several autosomal modif- iers. origin: Spontaneous. discoverer: Bridges, 1916. references: Bonnier, 1923, Hereditas 4: 81-110. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 220. phenotype: Reduces recombination between v and f from 23 to 15% and between we and v from 31% to 10%. c(1)a was probably the cause of a secondary nondisjunction frequency of 15-30%. RK3. other information: Validity of phenotypic description seems dubious. Probably an inversion. # C(2)R: see In(2R)NS # C(2;3): see In(2L)t # C(2L)HR: see In(2L)t # C(2L)T: see In(2L)t # c(3)G: crossover suppressor in chromosome 3 of Gowen location: 3-57.4 (1.0 to the left of sbd2, 4.0 to the right of cv-c). phenotype: Eliminates meiotic crossing over in homozygous females. First-division nondisjunction and chromosome loss frequent (30% for X, 2, and 3; 20% for 4); second division normal; exceptions more frequent at 25 than at 19. Production of triploids and intersexes 300-500 times normal. Egg hatch very low. Synaptonemal complexes absent from oocytes (Meyer), and both duration of meiotic prophase and number of 16-cell cysts per germarium reduced in c(3)G/c(3)G females (Smith and King, 1969, Genetics 60: 335-51). Meiotic loss of ring chro- mosomes increased in c(3)G females (Sandler, 1961, Nat. Cancer Inst. Monogr. 18: 243-73). No meiotic effects in homozygous males. In c(3)G/+ females, both intergenic recombination (Hinton, 1966, Genetics 53: 157-64) and the subset of intragenic recombination accompanied by recombination of flanking markers (Carlson, 1972, Genet. Res. 19: 129-32) increased. Somatic pairing (Semjenov, 1979, Tsitologiya 21: 1353-55) and somatic crossing over (Le Clerc, 1946, Science 103: 553-54) normal in c(3)G homozygotes; however, reported to be deficient for one of two X-ray-induced reac- tions leading to mitotic exchange (Handle, 1974, Molec. Gen. Genet. 128: 233-39). Heterochromatic interchanges inducible in oocytes of homozygous females by X irradiation (Roberts, 1969, Genetics 47: 387-408; Wurgler, Graf, Ruch, Beck, and Steiner, 1978, Arch. Genet. 51: 217-42). Oocytes of homozy- gous females show increased sensitivity to X irradiation and lack the normally observed fractionation effect (Watson, 1969, Mutat. Res. 8: 91-100; 1972, Mutat. Res. 14: 299-307); Wat- son (1972) also reports increased sensitivity of c(3)G-bearing sperm from c(3)G/+ males to translocation induction. RK3. allele origin discoverer synonym ref ( comments | _________________________________________________________________________ c(3)G1 spont Gowen cx, c(3)G17 1, 2, 3 c(3)G68 EMS Sandler, 1968 mei-W22 3, 5 > c(3)G1 c(3)GOR28 / EMS R.F. Grell 4 < c(3)G1 ( 1 = Gowen, 1922, Am. Naturalist 56: 286-88; 2 = Gowen, 1933, J. Exp. Zool. 65: 83-106; 3 = Hall, 1972, Genetics 71: 367-400; 4 = McKinley, Generoso, and Grell, 1979, Genetics 92: s79. 5 = Sandler, 1971, DIS 47: 48. | Severity of phenotype vis-a-vis c(3)G. / Fourteen other alleles recovered in same experiment. cytology: Placed in region 89A2-5 on the basis of its inclusion in Df(3R)c3G2 = Df(3R)89A2-3;89B4-5 (Hughes, Nelson, Yanuk, and Szauter). # c(3)G68 phenotype: Effects slightly more severe than in c(3)G. Meiotic recombination absent; first-division nondisjunction and loss high (40% for X, 2, and 3; 30% for 4). Low level of nondis- junction in second meiotic division. Oocytes of homozygous females lack synaptonemal complex (Carpenter). # c(3)GOR28 phenotype: Hypomorphic allele. Homozygous females show polar- ized reduction of recombination to 4.3% between y and f with greatest reduction distally. X-chromosome nondisjunction tem- perature sensitive; 16.7% at 25; reduced to 10.2% in oocytes exposed to 17 during metaphase I and anaphase I; no X- chromosome loss at either temperature. Synaptonemal complex reduced in quantity and abnormal in structure. c(3)GOR28/Df(3R)sbd105 females exhibit no recombination and 32% X-chromosome nondisjunction. # C2L: see In(2L)NS # C3: see In(3R)C # C4: see RpIIC4 # CIIL: see In(2L)NS # CIIIRE: see In(3R)C # ca: claret location: 3-100.7. references: Sequeira, Nelson, and Szauter, 1989, Genetics 123: 511-24. Yamamoto, Komma, Shaffer, Pirrotta, and Endow, 1989, EMBO J. 8: 3543-52. phenotype: Eye color ruby. With cn, eye color is deep reddish yellow; with bw, translucent brownish yellow (Mainx, 1938, Z. Indukt. Abstamm. Vererbungsl. 75: 256-76). Larval Malpighian tubes colorless (Beadle, 1937, Genetics 22: 587-611). Eye color autonomous when larval optic disk from ca is transplanted into wild type or v. Wild-type disk in ca not entirely autonomous (Beadle and Ephrussi, 1936, Genetics 21: 230); ca flies produce less v+ substance than wild type (Clancy, 1942, Genetics 27: 417-40). Uptake of radio-labeled kynurenine by larval Malpighian tubules greatly reduced; uptake by developing eyes nearly normal (Sullivan and Sul- livan, 1975, Biochem. Genet. 13: 603-13). Presence of 4-0- glucosyl-N-acetyldopamine, possibly a detoxification product of dopamine, reported by Okubo (1958, Med. J. Osaka Univ. 9: 327-37). Slightly narrow body and pointed wing. RK1. alleles: Some alleles are mutant for two closely spaced genes and are ncd ca double mutants; these alleles are designated cand in the following table. allele origin discoverer synonym ref ( comments ______________________________________________________________________________ ca1 spont Bridges, 19l12 1, 2 ca2 spont Bridges, 32f22 2 in In(3R)P ca3 ca572jIIIa3 ca4 / ray 8 ca5 / ray 8 ca6 / ray 8 ca7 / ray 8 ca8 / ray 8 ca9 / ray 8 ca10 / ray 8 ca11 / ray 8 ca12 / ray 8 ca13 / ray 8 ca14 / ray 8 ca15 / ray 8 ca16 / ray 8 hypomorphic allele; Malpighian tubes pale yellow ca17 / ray 8 ca18 / ray 8 ca19 / ray 8 ca20 / ray 8 ca21 X ray ca5 4 in Dp(3;1)B152 ca22 X ray ca15 4 in Dp(3;1)B152 ca23 X ray ca17 4 in Dp(3;1)B152 ca24 X ray ca31A 4 in Dp(3;1)B152 ca25 X ray ca50 4 in Dp(3;1)B152 ca26 X ray ca92 4 in Dp(3;1)B152 ca27 X ray ca129P 4 in Dp(3;1)B152 ca28 X ray ca148P 4 in Dp(3;1)B152 ca29 X ray ca166P 4 in Dp(3;1)B152 ca30 X ray caR16 4 in Dp(3;1)B152 ca31 X ray caG 4 in Dp(3;1)B152 ca32 HD caP1 9 no P insert ca33 HD caP2 9 no P insert ca34 HD caP6 9 P insert at 99B8-10 *ca35 X ray E. L. Smith, 34f bw-b 2 *ca36 X ray caG, bwnG 5,6 cand1 X ray cand 3,7 mutant for ncd cand3 / ray cand2 8 T(2;3)44B-C;100B mutant for ncd cand4 / ray cand3 8 mutant for ncd; also lethal rearranged in 99B cand5 HD ca3-1 9 mutant for ncd; no P insert cand6 HD ca22-8 9 mutant for ncd; no P insert cand7 spont caCm 9 mutant for ncd cand8 HD caP3 9 mutant for ncd; no P insert cav X ray cav 2 T(2;3)59D;81F;94;99C-E ( 1 = Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 219 (fig.); 2 = CP627; 3 = Davis, 1969, Genetics 61: 577-94; 4 = Frisardi and MacIntyre, l984, Mol. Gen. Genet. 197: 403-13; 5 = Gossi and Moree, l971, DIS 46: 40; 6 = Gossi, Kreisman, and Moree, DIS 48: 15; 7 = Lewis and Gencarella, l952, Genetics 37: 600-01; 8 = Sequeira, Nel- son, and Szauter, 1989, Genetics 123: 511-24; 9 = Yamamoto, Komma, Shaffer, Pirrotta, and Endow, 1989, EMBO J. 8: 3543-52. cytology: Placed in region 99B5-9 based on its inclusion in both Df(3R)ca46 = Df(3R)98F14;99B5-9 and Df(3R)L127 = Df(3R)99B5-6;99E4-F1 (Frisardi and MacIntyre, 1984, Mol. Gen. Genet. 197: 403-13). Placed in 99B8-10 by in situ hybridiza- tion (Yamamoto et al.). molecular biology: Region cloned in a 160-kb chromosome walk from 99C6-8 to 99B8-10 (Yamamoto et al.). A 7.4 kb mRNA detected on Northern blots with sequence from this region is the putative ca transcript; it is reduced or absent in ca1, ca34, cand1, and cand7, but present in ncd RNA. The 7.4-kb RNA is transcribed from left to right and its 5 end is very close to that of a transcription unit on the opposite strand that generates a 2.2-kb mRNA thought to encode the ncd product. All five ncd ca chromosomes tested have the same or similar 2.6-kb deletions for the 5 region shared by the two transcription units; the P element insert of ca34 resides in this segment. # cav: claret-variegated origin: X ray induced. discoverer: E. B. Lewis. phenotype: cav/ca slightly variegated. Can be confused with wild type. cav/cand1 females produce normal progeny. Homozy- gous lethal. RK3A. cytology: Associated with T(2;3)cav = T(2;3)59D;81F;94;99C-E (Craymer, 1980, DIS 55: 199). # cab: cabbage (J.C. Hall) location: 1-(not localized). origin: Induced by ethyl methanesulfonate. discoverer: Sziber. references: Aceves-Pi~a and Quinn, 1979, Science 206: 93-96. phenotype: Blocked or impaired in learning, with respect to several types of conditioning tests used on groups of flies or on individuals, including those involving electric shocks (Booker and Quinn, 1981, Proc. Nat. Acad. Sci. USA 78: 3940- 49) or exposure to flies (mated females, immature males) that in wild type induce poor courtship subsequently (Gailey, Jack- son, and Siegel, 1982, Genetics 102: 771-82). cab flies may be generally debilitated, and tests involving habituation or sensitization to sugar stimuli gave unreliable results (Duerr and Quinn, 1982, Proc. Nat. Acad. Sci. USA 79: 3646-50). # cac: cacophony (J.C. Hall) location: 1-36.6. origin: Induced by ethyl methanesulfonate. references: Schilcher, 1976, Behav. Biol. 17: 187-96. 1977, Behav. Genet. 7: 251-59. Hall, Siegel, Tompkins, and Kyriacou, 1980, Stadler Genet. Symp. 12: 43-82. Kulkarni and Hall, 1987, Genetics 115: 461-75. Wheeler, Kulkarni, Gailey, and Hall, 1989, Behav. Genet. 19: 503-28. phenotype: Males court abnormally with poor mating success and aberrant courtship song, which includes pulses of tone that are polycyclic, rather than monocyclic or tricyclic, within wild-type pulses and have increased amplitude. Some cac pulses, however, are quasi-normal in their cycle numbers (Wheeler et al., 1989); these, as well as many of the polycy- clic pulses, have essentially normal intra-pulse frequencies; other cac pulses exhibit anomalous modulations, and these show multiple peaks in the intra-pulse spectra, unlike wild type. Mating success of wingless mutant males is still worse than that of wingless wild-type males, which is correlated with genetic separability of song abnormalities from deficit in mating performance. Female courtship appears to be unaffected by cac; but general locomotor activity of males or females is subnormal. cac is recessive for generally abnormal behavior and for courtship song defects in tra/tra flies (Kulkarni, Hall, and Schilcher). cytology: Placed in 11A2 based on the failure of Df(1)HF368 = Df(1)11A2;11A9 to complement cac in Df(1)HF368/cac; tra/tra flies, and the normal courtship song of cac males carrying Dp(1;3)v+74c = Dp(1;3)9E2;11B1-2. other information: l(1)11Aa fails to complement both cac and nbaA; however cac and nbA complement, and cac flies exhibit normal visual behavior and visual system physiology (Kulkarni and Hall, 1987). Chromosome rearrangements with breakpoints in 11A and which are lethal in combination with l(1)11Aa also fail to complement cac and nbA [In(1)A78, In(1)A97, In(1)N66, and Tp(1;1)A101]. Complementation tests for cac carried out in diplo-X individuals transformed into phenotypic males by tra. # cact: cactus (T. Schupbach) location: 2-52 (between b and pr). origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal mutant; embryos from homozy- gous mothers appear "ventralized"; at differentiation they form only a narrow strip of dorsal cuticle, whereas ventral setal belts are expanded and encircle in irregular fashion most of the embryonic periphery. At gastrulation the germband hardly extends at all, and the posterior midgut invaginates close to the posterior pole. Cephalic furrow is more pro- nounced than in wildtype. alleles: allele origin synonym comments _______________________________________________________________ cact1 EMS cact99 zygotic lethal cact2 EMS cactD12 zygotic lethal cact3 EMS cactD13 zygotic lethal cact4 EMS cactG8 zygotic lethal cact5 EMS cactS1 zygotic lethal cact6 EMS cactU7 zygotic lethal cact7 EMS cactA2 very strong allele cact8 EMS cactF11 very strong allele cact9 EMS cactIIIG very strong allele cact10 EMS cactH4 very strong allele cact11 EMS cactO9 very strong allele cact12 EMS cactO11 very strong allele cact13 EMS cactPD very strong allele cact14 EMS cactSG very strong allele cact15 EMS cactH8 weak allele; temperature sensitive cact16 EMS cactHE weak allele; temperature sensitive cact17 EMS cactQ6 weak allele; temperature sensitive cact18 EMS cactP2 weak allele; temperature sensitive cact19 P cactUK cact20 P cactUL cact21 P cactUW cact22 P cactVQ cytology: Placed in 35E6-36A9 between the right break of Df(2L)osp29 = Df(2L)35B1-3;35E6 and the left break of Df(2L)H20 = Df(2L)36A8-9;36E1-2. # cad: caudal location: 2-{55}. references: Mlodzik, Fjose, and Gehring, 1985, EMBO J. 4: 2961-69 (fig.). Levine, Harding, Wedeen, Doyle, Hoey, and Radomska, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 209-33 (fig.). Macdonald and Struhl, 1986, Nature 324: 537-456 (fig.). Hoey, Doyle, Harding, Wedeen, and Levine, 1986, Proc. Nat. Acad. Sci. USA 83: 4809-13. Mlodzik and Gehring, 1987, Cell 48: 465-78. phenotype: Homozygous lethal; homozygous cad embryos from cad/+ mothes develop into nearly normal first-instar larvae, which, however, lack cuticular structures of the external terminalia, e.g., the anal tuft, parts of the anal pads and the terminal sense organs. Distribution of cad+ gene product in such embryos indistinguishable from that in their cad/+ and +/+ sibs, evidently maternally derived. cad/+ offspring from cad/cad oogenic cysts indistinguishable from those from cad/+ cysts; larvae lack portions of the eighth abdominal segment and sometimes parts of the fourth and less frequently other even-numbered abdominal segments; frequently they develop into normal adults. cad/cad embryos from homozygous cad cysts display variably abnormal segmentation; head and anterior thorax normal; many posterior segments deleted with T2 and odd-numbered abdominal segments more resistant to deletion; most of eighth abdominal segment and terminalia (but not some parts of posterior spiracles) deleted; replaced by small plates of sclerotized cuticle resembling mouth hooks. Mater- nal germ-line transciption of the cad/+ gene demonstated by the detection of transcript in oocytes and nurse cells; tran- scripts uniformly distributed in early embryos; in the syncy- tial blastoderm transcripts disappear from the anterior end of the embryo and an anterior-posterior gradient develops with heaviest concentration posteriorly. The cellular blastoderm shows a band of hybridization three to five cells wide encir- cling the embryo .13 to .19 of the distance from posterior to anterior end; label is internalized during gastrulation and is seen in hind gut, midgut, and Malpighian tubules. Immunocyto- chemical observations detect no cad polypeptide until the stage 5 or 6 embryo. In the syncytial blastoderm there is dramatic accumulation of cad polypeptide in the same antero- posterior gradient as observed for transcript; the polypeptide localizes strongly to nuclei during interphase. The same gra- dient develops over time in unfertilized eggs. Subsequent collapse of the gradient into a posteriorly disposed circum- ferential band follows the behavior of transcript. Embryos produced by homozygous BicD or bcd females display an uniform distribution of cad+ product, which subsequently becomes res- tricted to symmetrically disposed anterior and posterior rings of cad polypeptide. During gastrulation cad+ polypeptide per- sists in a position suggesting a fifteenth parasegment, in the posterior midgut and Malpighian tubules, in six narrow bands at double segment intervals, in pairs of neuromeres initially in parasegments 1-14, later in thorax and anterior abdomen, and in portions of the genital disc, possibly precursors of the analia. In third instar larvae transcripts are also found in germ cells of both sexes and in the presumptive hind gut and analia of the genital disc. The cad gene product can increase the level of ftz transcription in the posterior half of the embryo by interacting with multiple copies of a TTTATG consensus sequence located in the zebra-stripe element of the ftz promoter (Dearolf, Topol, and Parker, 1989, Nature 341: 340-42). alleles: Four ethyl-methanesulfonate-induced alleles described by Macdonald and Struhl: cad1, cad2 cad3, and cad4. cytology: Localized to 38E5-6 by in situ hybridization. molecular biology: Locus initially identified and gene isolated on basis of homeobox homology. Genomic clones isolated and sequenced; two exons separated by an intervening sequence of 10.5 kb. The homeobox begins 14 base pairs from the beginning of the 3' exon. 2.4 kb maternal mRNA detected in 0-4 hr embryos and a 2.6 kb zygotic mRNA at cellular blastoderm. mRNA's differ in both initiation and termination sites; exons identical in the two. The polypeptide is characterized by a number of homopolymeric repeats: 10/10 His/Ala, 6/7 His, 10/12 Ser, 15/20 gly/val and 20/27 Asn in the 5' exon and 11/11 Arg in the 3' exon. #*cal: coal location: 3-59.5. origin: Spontaneous. discoverer: Grout, 47l20. references: Ives, 1948, DIS 22: 53. phenotype: Black body color similar to e4. Viability reduced slightly. RK2. # Cal: Calmodulin location: 2-{67}. discoverer: Yamanaka. references: Yamanaka, Sangstad, Hanson-Painton, McCarthy, and Tobin, 1987, Nucleic Acids Res. 15: 3335-48. Smith, Doyle, Maune, Munjaal, and Beckingham, 1987, J. Mol. Biol. 196: 471-85. phenotype: The structural gene of the calcium-binding protein, calmodulin (148 amino acids, 17000 daltons). cytology: Located in region 49A by in situ hybridization (E.B. Lewis). molecular biology: Genomic clone isolated from library using electric eel cDNA probe. Gene comprises four exons separated by three introns of 3400 to 4300 base pairs in length, exon 1 consists of 5' untranslated region and the initiator ATG; exon 2 encodes amino-acid residues 1 to 58.3; exon 3 residues 58.3 to 139.3 and exon 4 residues 139.3 to 148 plus the 3' untranslated region. Sequence highly conserved among eukaryotic species. Transcripts of 1.65 and 1.9 kb found at intemediate levels in embryos, high levels in larvae, and low levels in adults. # Calcium dependent protein kinase: see Pkc # Calmodulin: see Cal # calyx bulging: see cxb # camel: see iab5 under BXC # canoe: see cno # canopy wing: see cpw # capu: cappucino (T. Schupbach) location: 2-8. origin: Induced by ethyl methanesulfonate. references: Manseau and Schupbach, 1989, Genes Dev. 3: 1437- 52. Schupbach and Wieschaus, 1989, Genetics 121: 101-17. phenotype: Maternal-effect lethal. Homozygous females lay eggs which sometimes (5-10%) have a "pointed cap" (cappucino) of dorsal appendage material sitting over the anterior end of the egg, instead of two distinct dorsal appendages. Such eggs are similar to eggs formed by the female-sterile mutation fs(1)K10 but the extent of dorsal appendage material on capu eggs is much more variable than that of fs(1)K10 eggs. No polar granules are found in such eggs. Mutant females produce embryos lacking polar granules, pole cells, and normal abdomi- nal segmentation. In combination with Bic-D, however, abdomi- nal segmentation does develop in the anterior half of the embryo. Improper localization of abdominal determinants also indicated by the lack of posterior localization of vasa pro- tein. Cellularization of the blastoderm irregularly defec- tive, with nuclei of different sizes and densities. Resemble embryos formed by other grandchildless-knirps-like mutations, such as vasa or tudor, but in addition, some of the embryos from capu also appear dorsalized. Mosaic studies demonstrate germ-line function of capu. alleles: Four, capu1 to capu4 isolated as RK, G7, H3, and H8, respectively. # car: carnation location: 1-62.5. origin: X ray induced. discoverer: Patterson, 28c20. references: 1934, DIS 1: 31. phenotype: Eye color dark ruby. Body shape and proportions seem rounded. With st, eye color is yellow-brown; with bw, brownish yellow to brown (Mainx, 1938, Z. Indukt. Abstamm. Vererbungsl. 75: 256-76). Malpighian tubes pale yellow in mature larva (Beadle, 1937, Genetics 22: 587-611) but hard to distinguish from wild type before third instar. Eye color autonomous in transplant into wild-type host (Beadle and Ephrussi, 1936, Genetics 21: 230). car dor is pupal lethal and shows reduced recovery in gynandromorphs with male parts car dor (Nash, 1971, DIS 47: 73). car lt also lethal, dies as larva when mother car;lt/+ or car/+;lt and as pupa when mother car/+;lt/+ (Nickla, 1977, Nature 268: 638-39); lethal focus domineering; fate maps to ventral nervous system (Nickla, Lilly, and McCarthy, 1980, Experientia 36: 402-05). Brain histology abnormal [McCarthy and Nickla, 1980, Experien- tia 36: 1361-63 (fig.)]. alleles: *car2 and car26-48 (CP627). cytology: Shown to lie in doublet 18D1-2 by deficiency analysis (J.I. Valencia). # caramel: see cml # cardinal: see cd # carmine: see cm # carminoid: see cmd # carnation: see car # Casein kinase: see CkII # cast: ojos castanos location: 1-36. origin: Spontaneous in dysgenic cross. references: Valde del Rio and Costas, 1982, DIS 58: 210. phenotype: Eye color chestnut brown in both sexes. cast- bearing strain reverts with low frequency and generates muta- tions at other loci as well. # Cat: Catalase location: 3-47.0 (assuming that strain differences in catalase level represent allelic differences at the Cat locus). references: Lubinski and Bewley, 1977, Genetics 86: s39. 1979, Genetics 91: 723-42. Bewley, Nahmias, and Cook, 1983, Dev. Genet. 4: 49-60. Mackay and Bewley, 1989, Genetics 122: 643-52. phenotype: The structural gene for catalase [CAT(EC 1.11.1.6)]. Two peaks of activity, the smaller in late third instar larvae just prior to puparium formation and the larger during metamorphosis; coincident with the two major peaks of ecdysone titer. High specific activity in larval Malpighian tubules, gut, and fat body; higher in adult abdomen than in thorax or head. Purification and characterization of enzyme by Nahmias and Bewley (1984, Comp. Biochem. Physiol. 77B: 355-64). Amorphic and hypomorphic mutants are hemizygous viable on nor- mal medium; however those with the lowest levels of catalase activity exhibit severely reduced viability (i.e., less than 2% normal levels). All mutants show increased sensitivity to the presence of hydrogen peroxide in the medium. alleles: No electromorphs detected among 50 inbred laboratory strains. Bewley, MacKay, and Cook (1986, Genetics 113: 919- 38) describe two strains that differ from the majority of strains in their levels of catalase; one exhibits a reduction in activity to 0.47 X normal, with a disproportionate reduc- tion during third instar, and the other displays a 1.5 fold increase in activity; the differences are attributable to differences in the rates of enzyme synthesis. The difference maps between st and cu at 3-47.0, which is within or near the 75D-F interval within which Cat resides. Thus these activity differences may be attributable to allelic variation at the Cat locus. allele origin ref ( comments _____________________________________________________ Cat+lo spont 1 47% wild type activity Cat+hi spont 1 150% wild type activity Catn1 EMS 2 amorphic allele; no CRM Catn2 EMS 2 hypomorphic allele; low CRM Catn3 EMS 2 hypomorphic allele; low CRM Catn4 EMS 2 amorphic allele; no CRM Catn5 EMS 2 hypomorphic allele; low CRM Catn6 EMS 2 hypomorphic allele; low CRM ( 1 = Bewley, Mackay and Cook, 1986, Genetics 113: 919-38. 2 = Mackay and Bewley, 1989, Genetics 122: 643-52. cytology: Located in region 75D1-F1 based on specific activity of segmental hyperploid produced from T(Y;3)L131 = T(Y;3)75D and T(Y;3)B132 = T(Y;3)76A, and the segmental hypoploid pro- duced from T(Y;3)L131 and T(Y;3)L14 = T(Y;2)76B, and on Df(3L)Cat = Df(3L)75B8;75F1. other information: Catn6 complements Catn, partially comple- ments Catn2 and Catn3, and displays nearly wild-type activity levels in combination with Cat+. CAT is a tetrameric enzyme (Nahmias and Bewley). # Cat: see Cha and spaCat # Catalase: see Cat # cau: cauliflower location: 1-4.2. origin: Induced by ethyl methanesulfonate. references: Eberl and Hilliker, 1988, Genetics 118: 109-20. phenotype: Hemizygous lethal; midgut poorly developed; dense yolk plug; poor cuticle differentiation. cytology: Located in 2A2-B18. # caudal: see cad # cauliflower: see cau #*cb: club location: 1-16.5. origin: Spontaneous. discoverer: Morgan, 13e. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 69 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet 2: 78 (fig.). phenotype: Wings unexpanded in about half the flies. Sterno- pleural bristles absent from all flies. RK3. # cb8: see ogre #*Cb: Curled blistered location: 1-13. origin: Spontaneous. discoverer: Villee, 40b. references: 1945, DIS 19: 47. phenotype: Heterozygous or homozygous Cb give curled and blistered wings only in presence of homozygous pxCb. RK3. # cbd: central body defect (J.C. Hall) location: 1-41. origin: Induced by ethyl methanesulfonate. references: Heisenberg, Borst, Wagner, and Byers, 1985, J. Neu- rogenet. 2: 1-30. phenotype: Entire central complex of brain (with exception of protocerebral bridge) dissociated into two fiber masses of variable shape; some of dorsal brain's mushroom body lobes reduced in size; inter-hemispheric commissure of brain reduced in size (in white pupae); abnormal learning in adult and lar- vae tests using olfactory stimuli; subnormal locomotor activity. alleles: cbd1, cbd2, and cbd3 (formerly cbdKS96, cbdKS171, and cbdKS188). #*cbf: clubfoot location: 1-45. origin: X ray induced. discoverer: Cantor, 46d20. references: 1946, DIS 20: 64. phenotype: Leg segments greatly shortened; abnormally shaped tarsi and metathoracic legs. Wings slightly warped, wide in center, and tapering at ends. All flies emerging show both wing and leg effects but expression variable. Only about 3% of cbf flies eclose. RK3. other information: Not tested for allelism to pl (1-47.9). # Cbx: see BXC # cc: see svr # ccb: central complex broad (J.C. Hall) location: 1-56. origin: Induced by ethyl methanesulfonate. references: Heisenberg, Borst, Wagner, and Byers, 1985, J. Neu- rogenet. 2: 1-30. phenotype: Ellipsoid body and central body of central brain abnormally flat and broad; learning abnormal in tests using olfactory stimuli. alleles: ccb1 and ccb2 (formerly ccbKS127 and ccbKS145). # ccd: central complex deranged (J. Hall) location: 1-15. origin: Induced by ethyl methanesulfonate. references: Heisenberg, Borst, Wagner, and Byers, 1985, J. Neu- rogenet. 2: 1-30. phenotype: Ellipsoid body of central brain abnormally flat and broad; fiber number in inter-hemispheric commissure of brain reduced (in white pupae); abnormal larval and adult learning in tests using olfactory stimuli; activity in open-field locomotor test reduced. # ccw: concave wing location: 1-23.4. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 68. phenotype: Wings shorter and narrower with L3 and L4 shifted toward each other, occasionally truncated. Wing membrane depressed in center into slight concavity, giving slight scooped effect. Not easily classified. RK3. other information: One allele induced by L-p-N,N-di-(2- chloroethyl)amino-phenylalanine. # cd: cardinal location: 3-75.7. origin: Spontaneous. discoverer: Johnson, 19k24. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 217 (fig.). phenotype: Eye color yellowish vermilion, changing toward wild type with age. Drosopterin content of eyes about 85% normal (Gearhart and MacIntyre, 1970, Anal. Biochem. 37: 21-25). Phenoxazinone synthetase activity about 39% wild type; accumu- lates 3-hydroxykinurenine (Phillips, Forrest, and Kulkarni, 1973, Genetics 73: 45-56; Sullivan, Grillo, and Kitos, 1974, J. Exp. Zool. 188: 225-34). Ocelli white, showing no effect of age. Accumulates a blue-fluorescent compound termed cardi- nalic acid (xantherenic acid 8-O-|-O-glucoside) (Ferre, Men- sua, and Jacobson, 1985, DIS 61: 71). Eye color autonomous in transplant of larval optic disk into wild type, ca, cn, st, or v larval host (Beadle and Ephrussi, 1936, Genetics 21: 230). Larval Malpighian tubes bright yellow; not distin- guishable from wild type. RK2. alleles: cd3 [persistant allele in Amherst population (Ives, 1970, Evolution 24: 507-18)]; cd79i and cd81d isolated from a natural population by Najera (1985, DIS 61: 215) and *cd63 (CP627). cytology: Placed in 94A-E based on segmental hypoploid from T(Y;3)D100 = T(Y;3)94A and T(Y;3)B27 = T(Y;3)94E (Jones, 1971, DIS 47: 90). # cdwo: cardinal-white ocelli discoverer: Bridges, 12f21. synonym: wo. references: 1920, Biol. Bull. 38: 231-36. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 66. phenotype: Ocelli colorless. Eye color wild type. Modifies we to a lighter and less yellow tone. cd/cdwo has normal eye color but white ocelli (Jones, 1971, DIS 47: 90). RK2. # Cd: see Cu # Ce: Cell origin: Spontaneous. location: 4- (not located). discoverer: Green. references: 1952, DIS 26: 63. phenotype: Ocelli reduced or absent; ocellar and scutellar bristles absent; interocellar microchaetae disrupted but fron- tals normal; postverticals short, thick, often with an adven- titious pair between the normally placed postvertical bris- tles. Wing veins L3 and L4 converge, giving wing phenotype much like fu although wing phenotype variable. Homozygous lethal; lethality occurs during embryonic period (Hochman). Shown to be a segment polarity gene; homozygous embryos exhi- bit loss of the naked cuticle in the posterior half of each segment plus the anterior margin of the adjacent segment; most dorsal pattern elements also eliminated, leaving a lawn of fine hairs. Engrailed-antibody staining fails to detect a subset of CNS neurons in Ce homozygotes that are normally stained in wild-type embryos (Patel, Schafer, Goodman, and Holmgren, 1989, Genes Dev. 3: 890-904). No maternal require- ment of Ce+ for either oogenesis or embryonic phenotype (Orenic, Chidsey, and Holmgrern, 1987, Dev. Biol. 124: 50- 56). Lethal phenotype of Ce not complemented by l(4)17 or by induced revertants of the wing phenotype of ciD (Orenic et al.); pupal lethal in combination with ciD [Hochman, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 902-28]. RK3. alleles: l(4)17 renamed Cer: Cell recessive; homozygous and heterozygous with Ce2 has the same phenotype as Ce2/Ce2. Scn may also be allelic to Ce (Hochman). allele origin discoverer ref ( comments ________________________________________________________________ *Ce1 Glass, 39a28 1, 2 Ce2 spont Green 1, 3 *Ce3 X ray Green, 59c11 1, 4 Cer1 X ray 1, 5, 6 no dominant phenotype Cer2 X ray 1, 5, 6 no dominant phenotype ( 1 = CP627; 2 = Glass, 1939, DIS 12: 47; 3 = Green, 1952, DIS 26: 63; 4 = Green, 1959, DIS 33: 94; 5 = Hochman, Goor, and Green, 1964, Genetica 35: 109-26; 6 = Orenic, Chidsey, and Holmgren, 1987, Dev. Biol. 124: 50-56. cytology: Placed in salivary chromosome region 101E through 102B16, based on the inclusion of both Ce1 and Ce2 within Df(4)M = Df(4)101E-F;102B6-17. other information: Based on (a) position, (b) homozygous pheno- type, and (c) complementation results, Ce and ciD postulated to be part of a single complex (Orenic et al.). # ceb: central brain deranged (J.C. Hall) location: 1-23. origin: Induced by ethyl methanesulfonate. discoverer: Heisenberg. phenotype: Extra lobe, in adult brain, of approximately 400 coiled Kenyon-cell fibers next to calyx of mushroom bodies; olfactory learning in adults slightly reduced; memory is nor- mal. cytology: Located in 7F1-8A5. # Cec: Cecropin location: 3-{101}. references: Kylsten, Samakovlis, and Hultmark, 1990, EMBO J. 9: 217-24. phenotype: Three structural genes for three very similar cecro- pin proteins (cecropin A1, A2, and B), bacteriacidal proteins that are induced in adults in response to bacterial infection. All three cecropin genes are coordinately induced by injection of bacteria, although the B gene is expressed at a much lower level. Levels appreciable within one hour, peak at 6 hours and have generally returned to base line by 24 hours. Cecro- pins also induced by ingested bacteria. cytology: Placed in 99E by in situ hybridization. molecular biology: Isolated from genomic library using homolo- gous cloned sequence from Sarcophaga peregrina. Two neighbor- ing clones found to encode three functional cecropin genes and two apparent pseudogenes, the order being A1, |1, A2, |2, and B. Each gene is interrupted by a short intron in the coding sequence; CecA1 and CecA2 encode the same peptide and differ from Sarcophaga sarcotoxin 1A at five residues in the signal sequence; CecB differs from A1 and A2 by ten amino acid replacements, five in the signal sequence. cDNA's from all three genes recovered indicating that all are transcribed. CecA1 and CecA2 are transcribed off of the same strand and CecB is transcribed off the other. # cel: celibate (J.C. Hall) location: 1-48.5. origin: Induced by ethyl methanesulfonate. discoverer: Lindsley. references: Hall, Siegel, Tompkins, and Kyriacou, 1980, Stadler Genet. Symp. 12: 43-82. phenotype: Males court females vigorously but rarely attempt to copulate and even less frequently achieve genital contact; females apparently unaffected by the mutation. # central body defect: see cbd # central brain deranged: see ceb # central complex broad: see ccb # central complex deranged: see ccd #*cf: cleft location: 1-65.6. origin: Spontaneous. discoverer: Bridges, 14j28. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 55 (fig.). phenotype: Wings smaller and somewhat spread. L3 split just beyond first crossvein; extra crossveins and branches. Gap in L4 beyond second crossvein. Males sterile. Viability good. RK2. # cf: see cff # Cf: see Pxcf # cf1: Chorion factor 1 location: 1-{0.5}. references: Shea, King, Conboy, Mariani, and Kafatos, 1990, Genes Dev. 4: 1128-40. phenotype: Encodes a protein that binds the promoter region of Cp15. cytology: Placed in 2C4-8 by in situ hybridization. molecular biology: Gene cloned and sequenced. # cf2 location: 2-{13}. references: Shea, King, Conboy, Mariani, and Kafatos, 1990, Genes Dev. 4: 1128-40. phenotype: Encodes a protein that binds the promoter region of Cp15. cytology: Placed in 25A5-8 by in situ hybridization. molecular biology: Gene cloned and sequenced. # Cf-3: see DlCf-3 # cff: control of female fertility location: 1-39.09 (0.09 unit to the right of dnc). origin: Spontaneous. synonym: cf (preoccupied). references: Salz and Kiger, 1984, Genetics 108: 377-92. phenotype: cff is a specific cis-acting enhancer of the female-sterile phenotype of dnc1, without effect on phospho- diesterase activity. The number of progeny per female meas- ured as 0 in dnc1 cff/dnc1 cff, 2.3 in dnc1 cff/dncM14 cff+, and 30 in dnc1 cff+/dncM14 cff. # cg: comb gap location: 2-71.1. origin: Spontaneous. discoverer: Bridges, 25k16. phenotype: Sex combs of male extremely large. Number of sex comb teeth increased from 10 to 18; number of bractless bris- tles increased; width of distal portion of basitarsus increased 1.6 fold; total number of bristles on basitarsus increased in both sexes (Datta and Mukherjee, 1968, Proc. XII Int. Congr. Genet. 1: 146; 1971, Genetics 68: 269-86). Some distortion and shortening of legs. Wings show gap in vein L4 between posterior crossvein and margin. Wings slightly curved. Effects result from a combination of overgrowth and irregular folding of imaginal rudiments during the pupal period. Strong exaggeration in compound homozygotes with genes such as d, fj, ds, and ssa. Double heterozygote for cg and ci often shows gap in L4 (Waddington, 1952, J. Genet. 51: 243-58). Double heterozygote en cg/++ has slight degree of L4 interruption and thinning at low temperature. Triple heterozygote en cg/++; ci/+ has L4 interruption in half the flies (House, 1961, Genetics 46: 871). ciW interacts strongly with cg. cg/+; ciW/+ resembles ciW/ciW (House, 1953, Genetics 38: 669-70). Sex-comb phenotype enhanced by sn or Pc/Scx (Datta and Mukherjee, 1968, Proc. XII Int. Congr. Genet. 1: 146). Females sterile. Oogenesis highly irregular (Beatty, 1949, Proc. Roy. Soc. Edinburgh B 63: 249-70). RK2. cg: comb gap From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 40. # Cg: Collagen Fifteen of thirty clones, isolated from a genomic library using a chicken-derived pro(2I collagen clone, define at least ten different sequences that can be differentiated by (1) their positions in the genome, (2) their restriction maps, (3) the numbers and sizes of mRNA's with which they hybridize on Northern blots, and (4) the developmental profiles of the various mRNA's (LeParco, Cecchini, Knibiehler, and Mirre, 1986, Biol. Cell 56: 217-26). The genes tabulated below are differentiated according to their estimated position on the polytene map based on in situ hybridization. Two of these loci (Cg19-20 and Cg25C) had been identified previously and are described in more detail following the table. genetic locus location synonym mRNA sizes (kb) _______________________________________________ Cg9E 1-{32} 1.3, 6.3 Cg10AB 1-{34} 1.3, 2.3 Cg16-17 1-{58} 0.7, 1.6, 2.7 Cg19-20 1-{65} 3.8, 4.3 Cg25C 2-{15} DCg1 6.4 Cg42DE 2-{57} Cg63-64 3-{15} 1.6 Cg98F99A 3-{101} Cg-C ( ( At least five separable sequences in the chromocenter; the probe that identifies these sequences does not contain rDNA sequences. # Cg19-20 location: 1-{65}. references: Natzle, Monson, and McCarthy, 1982, Nature 296: 368-71. phenotype: Encodes a type IV collagen, the major component of basement membrane. Transcripts accumulate during ecdysis in wandering hematocytes, indicating that hematocytes contribute to extra cellular matrix deposition (Knibiehler, Mirre, Cec- chini, and LeParco, 1987, Dev. Biol. 196: 243-47). cytology: In situ hybridization 3HcRNA from pDCg2 to polytene chromosomes identifies complementary sequences in region 19E- 20B. molecular biology: Identified by means of a genomic clone (pDCg2) selected from a Drosophila melanogaster \ library using a cDNA probe for chicken pro(2(I) collagen. Developmen- tal profile of RNA hybridizing to pDCg2 shows peak during lar- val stage; little hybridization at other stages. # Cg25C location: 2-{15}. synonym: DCg1. references: Natzle, Monson, and McCarthy, 1982, Nature 296: 368-71. Monson, Natzle, Friedman, and McCarthy, 1982, Proc. Nat. Acad. Sci. USA 79: 1761-65. LeParco, Knibiehler, Cecchini, and Mirre, 1986, Exp. Cell. Res. 163: 405-12 (Fig.). phenotype: Structural gene for a type IV basement-membrane col- lagen. Expression first detected following germ-band shorten- ing in cells of both somatic and visceral mesodermal origin, specifically in mesoblasts (hemocytes) and fat-body cells (Mirre, Cecchini, LeParco, and Knibiehler, 1988, Development 102: 369-76). Translation takes place in embryonic mesob- lasts and larval fat-body cells, and is deposited extracellu- larly in basement membranes surrounding skeletal and visceral muscles (LeParco, Bevic, Knibiehler, Mirre, and Cecchini, 1989, Insect Biochem. 19: 789-802). cytology: Placed in 25C by in situ hybridization. molecular biology: Identified by means of a genomic clone selected from a Drosophila melanogaster \ library using a cDNA probe for chicken pro(2(I) collagen. Drosophila probe hybri- dizes to a 6.4 kb mRNA which shows peak during larval stages preceded by a small peak in late embryonic stages; cDNA and genomic sequence studies (Cecchini, Knibiehler, Mirre, and LeParco, 1987, Eur. J. Biochem. 165: 587-93; Blumberg, MacKrell, Olson, Kurkinen, Monson, Natzle, and Fessler, 1987, J. Biol. Chem. 262: 5947-50; Blumberg, MacKrell, and Fessler, 1988, J. Biol. Chem. 263: 18328-37) reveal that the gene comprises nine relatively large exons interrupted by eight relatively small introns (unlike mammalian homologues, which have numerous small exons separated by large introns). The complete cDNA sequence encodes an 1775 amino-acid protein including a signal peptide. Both N-terminal and C-terminal nonhelical domains involved in intermolecular junctional com- plexes share homology with mammalian type IV collagens, whereas the triple helical region shows little homology. The triple helical region comprises repeating sequences of Gly X Y tripeptides typical of such regions; similarly to other type IV collagens, the Y residues of the Gly X Y tripeptides show preference for lysines and prolines; furthermore, the posi- tions of 11/22 interruptions of the tripeptide-repeat sequences in the Drosophila protein correspond nearly exactly to those of such nonhelical segments of the mammalian triple- helical domain, although there is no conservation of length or sequence of such interruptions. The C-terminal nonhelical domain displays 58% amino-acid identity and 76% similarity to its counterparts in human and mouse type IV collagen. In all three sequences this region is composed of two homologous halves, A and B; all six segments each contain six completely conserved cysteins. Intraspecific homology between the A and B segments is considerably less than interspecific homology between A segments or B segments, indicating an ancient origin of the duplication. # cgd: congested location: 1-40 (37.6 and 41.7 in two determinations). origin: Induced by ethyl methanesulfonate. references: Eberl and Hilliker, 1988, Genetics 118: 109-20 (fig.). phenotype: Hemizygous lethal; first instar larvae unable to escape egg shell. Gut often poorly differentiated; cuticle phenotype variable - some normal, some with abnormal (e.g. fused) segments. Frequent holes in cuticle or absence of regions of cuticle. alleles: Two. cytology: Placed in 11B12-12C7. ch: chubby Left: wild-type larva. Right: chubby larva. From Dobzhansky and Duncan, 1933, Wilhelm Roux' Arch. Entwickslungmech. Organ. 130: 109-30. # ch: chubby location: 2-73.8 (based on mapping of ch76F; Rizki and Rizki, 1981, J. Hered. 72: 78-81). origin: Spontaneous. discoverer: Bridges, 17j26. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 222. phenotype: Adults, pupae, and larvae thickset and short. Dif- ficult to distinguish from wild type. Chubby larvae shorter than wild type at hatching [Dobzhansky and Duncan, 1933, Wilhelm Roux's Arch. Entwicklungsmech. Organ. 130: 109-30 (fig.)]. RK3. alleles: ch76f, spontaneous (Rizki and Rizki, 1981). # ChV: see KgV #*ch-b: chilblained-b location: 1-23.8. discoverer: Moriwaki, 39e22. references: 1939, DIS 12: 50. phenotype: Tarsi conglutinated. RK3. # cha: chaff (T. Schupbach) location: 2-84. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal mutant; embryos from homozygous mothers form a fragmented cuticle with variable holes and head defects. alleles: chaHB = cha1. # Cha: Choline acetyltransferase (J.C. Hall) location: 3-64.6. synonym: Cat. references: Hall, Greenspan, and Kankel, 1979, Soc. Neurosci. Symp. 4: 1-42. Greenspan, 1980, J. Comp. Phys. 137: 83-92. phenotype: Probable structural gene for choline acetyl transferase [ChAT, acetyl CoA-choline-O-acetyltransferase (EC 2.3.1.6)], which has been purified and whose molecular weight approximates 67 kilodaltons (Slemmon, Salvaterra, Crawford and Roberts, 1982, J. Biol. Chem. 257: 3847-52); monoclonal anti- bodies prepared and inhibit enzyme (Crawford, Slemmon, and Salvaterra, 1982, J. Biol. Chem. 257: 3853-56); homozygotes and hemizygotes for either of the original two non- conditionally mutant alleles, Chal1 or Chal2, show no detect- able enzymatic activity as late embryos, which is when the mutants die; other non-conditional lethals at the locus not tested for lethal stage or ChAT activity; either of two tem- perature sensitive alleles, Chats1 or Chats2, causes a variety of phenotypic defects when hemizygous or homozygous: reduced viability at 25 and death at 29 (Chats1), reduced viability at 18 and death at 22 or above (Chats2) plus gradual but reversi- ble decline of enzymatic activity and of acetylcholine levels following transfer of low-temperature reared Chats adults to 29-30 or above (Greenspan, 1980; Salvaterra and McCaman, 1985, J. Neurosci. 5: 903-10); correlated with decrements in these biochemical parameters (reversible on lowering temperature), are heat-induced abnormalities of general mobility, male courtship ability, plus electroretinogram (Greenspan, 1980), landing response (Gorczyca and Hall, 1985, Neurosci. Abstr. 11: 512), and of several elements of physiological responses made by thoracic indirect flight muscles following stimulation of giant fiber pathway, implying that certain interneuronal synapses in this pathway are cholinergic (Gorczyca and Hall, 1984, J. Neurogenet. 1: 289-313); whereas wild type exhibits two molecular forms of ChAT activity after isoelectric focus- ing, homogenates of Chats1 lead to a single form, and of Chats2 to two forms shifted to higher-than-normal pI (Salva- terra and McCaman, 1985); these two conditional Cha mutations also cause ChAT activity to have accentuated thermolability in vitro (Greenspan, 1980; Salvaterra and McCaman, 1985). Immu- nohistochemical staining of ChAT reveals wide distribution in CNS; this staining is strong in Chats1 at permissive tempera- ture but diminishes after in-vivo heat treatment (Gorczyca and Hall, 1987, J. Neurosci. 7: 1361-69); Chats2 staining is poor even at permissive temperature and diminishes after heating the flies (Gorczyca and Hall, 1987). In situ hybridization to tissue sections detected transcriptional activity in most neu- ronal elements of the cell-rich areas of the cortical regions of the cerebrum and optic lobes; however, some cells in the lamina including the amacrine neurons showed no label. Highest expression is seen in laminar monopolar-cell region, and the cerebral cortical rind, and to a lesser degree, over cortical cells of medulla-lobula, the antennal sensory neu- rons, and the retinular-cell layer of the compound eye (Barber, Sugihara, Lee, Vaughn, and Salvaterra, 1989, J. Comp. Neurol. 280: 533-43). Immunolocalization of ChAT in the adult cephalic ganglion reveals weak staining in the lamina corresponding to the synaptic layer of photoreceptor cells 1-6 of the ommatidia, three layers of strong reaction correspond- ing to the synaptic layers in the medulla, and labeling of four layers in the lobula (Ikeda and Salvaterra, 1989, J. Comp. Neurol. 280: 283-90). In Chats1 staining seen at 19 but disappears by 120 hours after shift to 30; Chats2 shows reduced staining at 19 and none after 80 hours at 30. alleles: allele origin synonym ref ( cytology ___________________________________________________ Chal1 EMS Chal9 1, 2 + | Chal2 EMS Chal28 1, 2 Chal3 X ray 3 T(H;3)91C Chal4 / ray 3 In(3R)91C;93B-D Chal5 X ray 3 + Chal6 / ray 3 + / Chal7 / ray 3 Tp(2;3)41;91C Chal8 / ray 3 + Chal9 EMS 3 Chal10 EMS 3 Chal11 EMS 3 Chal12 EMS 3 Chal13 EMS 3 Chal14 EMS 3 Chats1 EMS Chal16 1, 2 Chats2 EMS Chal43 1, 2 ( 1 = Hall, Greenspan, and Kankel, 1979, Soc. Neurosci. Symp. 4: 1-42; 2 = Greenspan, 1980, J. Comp. Physiol. 137: 83- 92; 3 = Myers and Gelbart. | Fails to complement l(3)91Ca, l(3)91Cb, Cha, and l(3)91Cd. / Fails to complement both Cha and l(3)91Cb. cytology: Placed in 91C7-D2 based on common breakpoints of Chal rearrangements and on its absence from Df(3R)Cha9 = Df(3R)91C7;92A8-9 and from Df(3R)Cha12 = Df(3R)91A;91D1-2. molecular biology: 3' end of coding sequence recovered as a cDNA clone prepared from mRNA isolated from adult heads; sequence determined (Itoh, Slemmon, Hawke, Williamson, Morita, Itakura, Roberts, Shively, Crawford, and Salvaterra, 1986, Proc. Nat. Acad. Sci. USA 83: 4081-85). The Drosophila enzyme produced from complete Cha cDNA expressed in Xenopus oocytes, leads to active Chat (McCaman, Carbini, Maines, and Salvaterra, 1988, Mol. Brain Res. 3: 107-14). # chaeta: see cht # chaetelle: see chl # chaff: see cha # chal: chalice (T. Schupbach) location: 2-37. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female sterile; homozygous females show abnormali- ties in late oogenesis. Follicle cells do not migrate cen- tripetally between nurse cells and oocyte. They do synthesize a chorion which remains open ended (like a chalice, or cup). Such eggs are usually not laid and remain unfertilized. alleles: chal1 to chal3 isolated as WP, HC, and QC, respec- tively. chal2 produces eggs of normal morphology which remains unfertilized. # chaoptic: see chp #*che: cherub location: 2-62.0. origin: Ultraviolet induced. discoverer: Meyer, 48g. references: Meyer and Edmondson, 1951, DIS 25: 71. phenotype: Wings short, papery, and downcurved with short, broad alulae. Males sterile. Homozygotes short lived; bal- anced stock cn che bw sp/In(2L+2R)Cy, al2 Cy cn2 L4 sp2 has a generation time 30% longer than normal. RK3. alleles: *che2 and *che3 in CP627. # chic: chickadee (T. Schupbach) location: 2-23. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female sterile; nurse cell contents are not tran- sported into the egg, and homozygous females lay tiny eggs, which remain unfertilized. alleles: chic1 to chic3 recovered as WC, WF, and WK. # chif: chiffon (T. Schupbach) location: 2-53 (between b and pr). origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female sterile, homozygous females lay eggs which have thin, fragile chorions and remain unfertilized. alleles: chif1 to chif4, recovered as WD, QV, QW, and WF respectively. cytology: Placed in 35E6-A9 between the right break of Df(2L)osp29 = Df(2L)35B1-3;35E6 and the left break of Df(2L)H20 = Df(2L)36A8-9;36E1-2. # chilblained-b: see ch-b # chl: chaetelle location: 2-60.8. discoverer: Bridges, 33a4. references: Beatty, 1949, Proc. Roy. Soc. Edinburgh B 63: 249-70. phenotype: Bristles very small. Wing venation slightly plexus- like, exaggerates px when combined with it. Body size small. Rotated genitalia in many males. Blunt-tipped abdomen. Females infertile, but ovary and oocytes appear normal. RK2. # chlorotic: see svr # cho: chocolate location: 1-5.5 [right of ec; (Lefevre, 1970, DIS 45: 40)]. origin: X ray induced. discoverer: Weigle, 1955. references: Sturtevant, 1955, DIS 29: 75. phenotype: Eye color brown with whitish highlights. Paler than se, less purplish than pn. In cho2 2-amino-4-hydroxypterine absent; isoxanthopterin II present in excess (McKay, 1972, DIS 48: 62). Malpighian tubes of larvae and adults contain brown pigment like red. Larvae easily distinguished from wild type. Malpighian tube color autonomous in mosaic larvae [Falk, Orevi, and Menzel, 1973, Nature (London) New Biol. 246: 19- 20]. Brown pigment of Malpighian tubes absent when cho is combined with v, cn, or st, mutations which prevent formation of brown eye pigment. Eye color of cho v is yellowish, but cho g cannot be distinguished from g. Separability, viabil- ity, and fertility excellent. RK1. alleles: cho2 (CP627). cytology: Placed in 3F on the basis of being included in Df(1)GA102 = Df(1)3D5;3F7-8, but not Df(1)w64d = Df(1)3C2;3E8. # Choline acetyltransferase: see Cha # Chorion factor: see Cf # Chorion protein: see Cp # chp: chaoptic location: 3-{103}. references: Fujita, Zipursky, Benzer, Ferrus, and Shotwell, 1982, Proc. Nat. Acad. Sci. USA 79: 728-33. Zipursky, Venkatesh, Teplow, and Benzer, 1984, Cell 36: 15- 26. Zipursky, Venkatesh, and Benzer, 1985, Proc. Nat. Acad. Sci. USA 82: 1855-59. VanVactor, Krantz, Reinke, and Zipursky, 1988, Cell 52: 281- 90. Reinke, Krantz, Yen, and Zipursky, 1988, Cell 52: 291-301. phenotype: The structural gene encoding chaoptin, a 160 kd glycoprotein localized to the extracellular membrane surface of photoreceptor cells and their axonal projections to the optic ganglia. Protein first identified by a monoclonal anti- body (MAb24B10). Antigen first appears behind the morpho- genetic furrow during differentiation of the eye imaginal disk. Defective alleles, chp1 and chp2, recognized by reduced levels of antigen. Rhabdomeres of mutant photoreceptor cells highly deranged or nearly absent in homozygotes and hemizy- gotes for chp1 or chp2, respectively; also close apposition of adjacent retinular cells partially disrupted. Gene product postulated to play role in cell surface interactions necessary for correct alignment of the microvilli that form the rhab- domeres. cytology: Located in 100B6-9 by in situ hybridization, uncovered by Df(3R)tll-e = Df(3R)10A5;100C1 but not by Df(3R)ca48 = Df(3R)98F14;100B7-8. molecular biology: Genomic clone isolated using synthetic oli- gonucleotide probe; clone hybridizes to a 4.3 kb polyadenylated transcript in head-derived RNA, which is absent from body RNA. Same sequence isolated by Levy and Manning (1982, Dev. Biol. 94: 465-76) using poly-A+ head RNA. Both cDNA and genomic sequences determined; eleven introns, eight of which are in the translated region, varying from 509 (intron 1) to 49 (intron 6) base pairs. Two CATT boxes but no TATA box found 5' to the transcription initiation site. Open reading frame with conceptual amino sequence of 1134 amino acids; first 29 amino acids have features of signal sequences; otherwise there is no membrane spanning domain, although chaoptin shown to be an integral membrane protein. Mature polypeptide of 127 kd with fourteen potential N-linked glycosylation sites. 90% of the sequence comprises 41 tan- demly arranged repeats of average residue number 24, with periodically disposed hydrophobic amino acids separated by hydrophilic ones; repeats occur in three large blocks separated by short unique regions; homologous to repeats occurring in three other known polypeptides including the Toll gene product in Drosophila. #*chr: chrome location: 1- (not located). origin: Spontaneous. discoverer: Bridges, 13l15. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 74. phenotype: Body color brownish yellow or tan. Abdominal bands clear yellow. RK3. # cht: chaeta location: 2-65.6 (located in relation to po, sca, and vg). origin: Isolated from a line selected for high scutellar- bristle number. references: MacBean, McKenzie, and Parsons, 1971, Theor. Appl. Genet. 41: 227-35. phenotype: cht/cht averages 1.64 scutellar bristles more than cht/+ (6.04 vs. 4.40). # chubby: see ch # chy: chunky location: 2- (between 8 and 28). origin: Spontaneous. discoverer: Bridges, 38b10. phenotype: Body short and heavy set. Wings shorter than wild type. Difficult to classify. RK3.