#*cr: crisp location: 1- (not located). discoverer: Agol. references: 1936, DIS 5: 7. phenotype: Bristles like forked. RK2. other information: Not an allele of f or sn. # CR: Compensatory Response (K. Tartof) location: 1-{66}. CR is located in the centric heterochromatin of the X chromosome distal to the tandem array of ribosomal RNA genes (rDNA). It lies between the heterochromatic break- points of sc4 (distally) and wm4 and rst3 (proximally). origin: Absence or dysfunction of this otherwise wild-type locus is detected by deletions or rearrangements of the heterochromatic interval indicated above. references: Tartof, 1971, Science 171: 294-97. Spear and Gall, 1973, Proc. Nat. Acad. Sci. USA 70: 1359-63. Procunier and Tartof, 1978, Genetics 88: 67-79. synonym: cr+. phenotype: In females there are about 250 tandemly arrayed rRNA genes in each of the two X chromosome. However, when only a single X is present, as in X/O males or X/In(1)sc4Lsc8R females, there are appoximately 400 rRNA genes per X. This phenomenon, referred to as "compensation", results from the disproportionate replication of rDNA in somatic cells of adults and is controlled by the CR locus. CR is novel in that it exhibits both trans and contiguous-cis acting properties. It acts in trans to detect the presence of its partner locus in the homologue, and if that partner locus is absent, it acts in cis to drive the disproportionate replication of those rRNA genes that are contiguous with it. The observed dispropor- tionate rDNA replication may occur primarily in polytene nuclei. CR is not required for the "magnification" or "reduc- tion" of germ line rDNA. cytology: Placed in 20F based on its location between the prox- imal breakpoints of In(1)sc4 to the left and In(2)rst3 and In(1)wm4 to the right. This places CR in h26-29 on the heterochomatic map of Gatti and Pimpinelli. #*Cr-2: Cream in chromosome 2 location: 2- (not located). origin: Spontaneous. discoverer: Bridges, 13i15. references: 1919, J. Exp. Zool. 28: 337-84. Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 239 (fig.). phenotype: Specific dilutor of we. we; Cr-2/Cr-2 has a pale- cream eye color. we; Cr-2/+ has eye color between eosin and cream. RK3. #*cr-3: cream in chromosome 3 location: 3-36.5. origin: Spontaneous. discoverer: E. M. Wallace, 14b27. references: Bridges, 1919, J. Exp. Zool. 28: 337-84. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 112 (fig.). phenotype: Homozygote has slightly diluted eye color. Eye color of we; cr-3 cream. Larval Malpighian tubes of we; cr-3 white, those of cr-3 bright yellow (Brehme and Demerec, 1942, Growth 6: 351-56). RK3. #*cr-a: cream-a location: Autosomal, not located. origin: Spontaneous. discoverer: Bridges, 13g15. references: 1916, Genetics 1: 147. 1919, J. Expt. Zool. 28: 337-84. phenotype: Strong specific dilutor of we. RK3. #*cr-b location: 2-24. origin: Spontaneous. discoverer: Bridges, 14c10. references: 1916, Genetics 1: 149. 1919, J. Exp. Zool. 28: 337-84. Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 245 (fig.). phenotype: Specific dilutor of we. RK3. #*cr-c location: 2- (near S). origin: Spontaneous. discoverer: Bridges, 16g13. phenotype: Weak specific dilutor of we. RK3. # cra: crack (C. Nusslein-Volhard) location: 2-77. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. phenotype: Embryonic lethal. Defect in head involution. Shows abdominal transformations in combination with Pc-like mutants. alleles: Two. # cramped: see crm # cramped-like: see crm2 # crb: crumbs location: 3-82. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). phenotype: Homozygous lethal; many small holes in cuticle. alleles: Six; one weak. cytology: Placed in 95E-96A; covered by YP3D element from T(Y;3)H173 = T(Y;3)Xhy+;95E but not T(Y;3)G73 = T(Y;3)YL;96A. molecular biology: Tentatively identified as a putative neuro- genic gene based on hybridization of a cDNA clone with partial homology to N and Dl to 95F (Knust, Dietrich, Tepass, Bremer, Weigel, Vassin, and Campos-Ortega, 1987, EMBO J. 6: 761-66). # CRB: see T(1;4)A1 # crc: cryptocephal location: 2-55. origin: Spontaneous. discoverer: Hadorn, 1942. synonym: l(2)crc. references: Hadorn and Gloor, 1943, Rev. Suisse Zool. 50: 256-61. Gloor, 1945, Arch. Julius Klaus-Stift. Vererbungsforsch. Sozi- alanthropol. Rassenhyg. 20: 209-56. Fristrom, 1965, Genetics 52: 297-318. Sparrow and Chadfield, 1985, Dev. Genet. 5: 103-14 (fig.) phenotype: Homozygotes frequently die as larvae; failure to eliminate chitinous mouthparts at the larval molt frequently results in larvae with suspernumerary mouth parts; homozygotes undergo pupation but rarely eclose from puparia. Imaginal head is not everted from thorax. Except for slightly reduced eyes and shortened legs, wings, and thoracic bristles, the head and thorax are fully differentiated; frequently fail to pass gas bubble to anterior retro-opercular position, thus failing to provide space for head eversion. Head eversion is inhibited by integument being more rigid than normal. Mutant integument contains more glucosamine than normal; Sparrow and Chaddfield unable to confirm (1982, Dev. Genet. 3: 235-45). Feeding glucosamine to wild-type larvae produces a phenocopy very similar to l(2)crc. Abdomen often shows no differentia- tion, and internal organ development is arrested at pupal stage. Lethality suppressed by su(crc)1 (Sparrow, 1981, Genet. Res. 38: 297-314). RK3. cytology: Placed in 39C2-D12 based on its inclusion in Df(2L)TW12 = Df(2L)37E2-F4;39D12 but not in Df(2L)TW1 = Df(2L)38A7-B1;39C2-3 or Df(2L)TW2 = Df(2L)37D2-E1;38E6-9 (Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85). # cream: see cr- # Cream: see Cr-2 # Cream: see bwV291 # cream underscored: see cru # creased: see cs # creeper: see rk4 # crib: cribble (T. Schupbach) location: 2-{57}. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Maternal-effect lethal mutant; Embryos from homozy- gous females cellularize irregularly at the blastoderm stage. Further development is very abnormal; at final differentiation embryos form only fragmented pieces of cuticle. alleles: cribHD = crib1, cribPA, cribRS cytology: Placed in 42C1-43F8, since uncovered by Df(2R)pk78s = Df(2R)42C1-7;43F5-8. # cricklet: see clt # Crimp: see Cm # crinkled: see ck #*crip: cripple location: 2- (between pr and cn). discoverer: Komai, 1924. references: 1926, Genetics 11: 280-93. 1927, Mem. Coll. Sci. Univ. Kyoto, Ser. B 2: 211-57. phenotype: Middle and hind legs twisted and shortened. Thirty percent penetrance. RK3. # cripA: crippled-A (J.C. Hall) location: 1-1.8. origin: Induced by ethyl methanesulfonate. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. phenotype: Adults walk slowly in uncoordinated manner, dragging one or more legs; legs weak and unable to support normal pos- ture; flies weak; males court feebly and move wings up and down slowly instead of vibrating them. cytology: Proximal to 2B11 owing to its not being deleted by Df(1)RA19 = Df(1)1E3-4;2B11-12 nor carried by the terminal duplication y2Y67g = Dp(1;Y)2B6-7 (Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbertova, Kramers, and Zhimulev, 1982, DIS 58: 184-90). # cripB (J.C. Hall) location: 1-8.8. origin: Induced by ethyl methanesulfonate. references: Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. phenotype: Adults walk in uncoordinated manner; normal jumping difficult to induce; legs move to abnormal position during tethered flight; roughened eye phenotype. # cripC (J.C. Hall) location: 1-57 (approximate). origin: Induced by ethyl methanesulfonate. references: Homyk, Szidonya, and Suzuki, 1980, Mol. and Gen. Genet. 177: 553-65. phenotype: Running, climbing, jumping are uncoordinated and generally abnormal; all such defects seemingly caused by stiffness of legs (nonbending at tibia-tarsal joints); mutant males court in uncoordinated manner with abnormal wing display, e.g., extension of both wings simultaneously; wing beat abnormal in tethered flight, as is position of legs. # crisp: see cr #*crk: crooked setae location: 1-60.1. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1953. references: 1958, DIS 32: 69. phenotype: Bristles thin and slightly shortened; occasional missing scutellar. Acrostichals deranged. Abdominal hairs of female frequently missing; tergites occasionally abnormal. Classification difficult. Viability and fertility good. RK3. other information: One allele induced by L-p-N,N-di-(2- chloroethyl)amino-phenylalanine. #*crm: cramped location: 1-1.48 (based on crmsa mapping 0.02 unit to the left of w). origin: Induced by P32. discoverer: Bateman. synonym: staP: stubarista from P32; cramped-like (crm2). references: 1951, DIS 25: 78. 1953, DIS 27: 55. phenotype: Antennae swollen, aristae short, and branches fewer than in wild type. Wings slightly divergent and in some alleles nicked. Males have small extra sex combs on second tarsal segment of prothoracic legs and less frequently on basitarsal segments of mesothoracic and rarely metathoracic legs. crmsa;Pc/+ males have large sex combs on all six basi- tarsi and small sex combs on all second tarsal segments in many flies. One or both postverticals lacking and other bris- tles occasionally missing or doubled. Body slightly darkened. Fertility of both males and females reduced, females more severely than males. Strength of sterilizing effect allele dependent. Females generally sterile; surviving crml females have rudimentary ovaries with no oocytes beyond stage 7 (Shan- non, Kaufman, Shen, and Judd, 1972, DIS 48: 92); males of crm2 and crm7 partially fertile, other alleles male sterile. Viability variably reduced depending on crowding in culture; crm4, crm7 are semilethal alleles, crm6 die in late third instar; survivors eclose on days 11-13; rarely survive in com- bination with a deficiency (Judd, Shen, and Kaufman, 1972, Genetics 71: 139-56; Shannon et al., 1972). alleles: Independently discovered and named mutants with the same phenotype and map position have been designated l(1)zw9, sa: sparse arista, and swa: swollen antennae. These are now designated alleles of crm. Designated alleles are tabulated below. allele origin discoverer synonym ref ( comments ______________________________________________________________________ crm1 32P Bateman staP 1 *crm2 CB3025 Fahmy, 1953 1 crm3 | X ray l(1)3C165g 2 in In(1)wm51bLwmJR crm4 | X ray l(1)3C165l 2 in In(1)wm51bLwmJR crm5 X ray l(1)zw9lf4 6 crm6 X ray l(1)zw9lk17 6 crm7 X ray l(1)zw9lk18 6 crm8 spont Schalet l(1)17-15 l(1)zw9S1 crm9 EMS Lefevre l(1)DA670 3 crm10 EMS Lefevre l(1)VA54 3 crmsa spont sa 4, 5 crmsa2 spont sa2 4, 5 crmswa CB1506 | Fahmy, 1956 swa 1 ( 1 = CP627; 2 = Gersh, 1967, Genetics 56: 309-19; 3 = Lefevre; 4 = Rayle, 1968, DIS 43: 62; 5 = Rayle and Green, 1969, Genetica 39: 497-507; 6 = Shannon, Kaufman, Shen, and Judd, 1972, DIS 48: 92. | Allelism inferred from missing-bristle phenotype of escapers; could be allelic to l(1)3Bf instead. cytology: Placed in the left edge of or to the left of 3C1 based on the failure of Df(1)wr-J1 = Df(1)3A1-2;3C2-3 but not Df(1)X2 = Df(1)2F6-3A1;3B5-C1 to complement crml (Judd, Shen, and Kaufman, ibid.) and the failure of Df(1)w70e7 = Df(1)3B5- C1;3C1-2 [Sorsa, Green, and Beermann, 1973, Nature (London) New Biol. 245: 34-37] to delete crm. # crn: crooked neck location: 1-{0.95}. synonym: l(1)2Fa. references: Gvozdev, Gerasimova, Kovalev, and Ananiev, 1977, DIS 52: 67-68. Perrimon, Engstrom, and Mahowald, 1984, Genetics 111: 23-41 (fig.). phenotype: Hemizygous embryos from heterozygous mothers show twisted phenotype; crn3/Df(1)64c18 and crn4/Df(1)64c18 exhibit a similar but more extreme phenotype, suggesting that they are hypomorphic. Both alleles lethal in female germ-line clones. alleles: allele origin discoverer synonym ref ( comments ___________________________________________________________ crn1 X ray Lefevre l(1)A35 4 crn2 X ray Lefevre l(1)HC208 4 crn3 X ray Lefevre l(1)RC63 2, 4, 6 2.5 kb insert at coordinate +66 crn4 EMS Lefevre l(1)EA130 5, 6 heterochromatic rearrangement crn5 EMS Gvozdev l(1)N72 1 crn6 EMS Gvozdev l(1)N78 1 crn7 EMS Gvozdev l(1)N730 1 crn8 EMS Gvozdev l(1)N751 1 crn9 EMS Gvozdev l(1)N759 1 crn10 EMS Gvozdev l(1)N766 1 crn11 EMS Gvozdev l(1)N776 1 crn12 EMS Gvozdev l(1)N783 1 crn13 EMS Gvozdev l(1)N785 1 crn14 EMS Gvozdev l(1)N791 1 crn15 EMS Gvozdev l(1)N792 1 crn16 / ray Gvozdev l(1)N7106 1 crn17 HMS | l(1)HM23 3 crn18 HMS l(1)HM27 3 crn19 HMS l(1)HM433 3 ( 1 = Gvozdev, Gerassimova, Kovalef, and Ananiev, 1977, DIS 52: 67-68; 2 = Haenlin, Steller, Pirrotta, and Mohier, 1985, Cell 40: 827-37; 3 = Kramers, Schalet, Paradi, and Huiser-Hoogteyling, 1983, Mutation Res. 107: 187-201; 4 = Lefevre, 1981, Genetics 99: 461-80; 5 = Lefevre; 6 = Perrimon, Engstrom, and Mahowald, 1984, Genetics 108: 559-72. | HMS = hycanthon methanesulfonate. Failure of HMS-induced mutants to complement both crn3 and crn7 established allelism among the three series. cytology: Placed in 2F1 based on its inclusion in Df(1)278.4B1 = Df(1)2E3-F3;3A5-B4 but not Df(1)2F1-3A4. molecular biology: Localized by transformation to a subclone of a component cosmid of a 200 kb walk initiated from micro- dissected polytene chromosomes. crn 65-70 kb to the right of the arbitrarily chosen initiation point of the walk; probes from the region identify a 2.1 kb transcript on Northern blots (Haenlin, Steller, Pirrotta, and Mohier, 1985, Cell 40: 827- 37). # Crn: Crown location: 3-46.8 (0.1 map unit to left of in). origin: Induced by ethyl methanesulfonate. discoverer: E.H. Grell phenotype: Dark trident pattern in heterozygote. Homozygous lethal. # cro: see ptg3 # crooked: see fwc # crooked neck: see crn # crooked setae: see crk # Crossover suppressor: see C( ) # crossveinless: see cv # crown: see ptg3 # crs: cru sterile location: 2- (between px and bw). discoverer: Muller. references: 1951, DIS 25: 119. 1955, DIS 29: 146. phenotype: Male sterile. RK2. cytology: Located between 58E3 and 59A2 on basis of sterility in combination with Df(2R)P + Dp(2;Y)bw+ = Df(2R)58E3- F1;60D14-E2 + Dp(2;Y)YL;58F1-59A2;60D14-E2 (Muller, 1955). other information: Male sterility formerly associated with but separable from cru. # crt: crumpled tips location: 1-40.3 (7.3 units from v, based on 3035 flies). origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1952. references: 1959, DIS 33: 84. phenotype: Wing tips frequently shriveled, pleated, or crumpled and often turned up or down. Wings vary from completely unex- panded to wild type. Viability and fertility good in both sexes. Failure of crt2 to produce homozygous germ-line clones reported by Perrimon, Engstrom, and Mahowald (1989, Genetics 121: 333-52). RK2. alleles: crt2, induced by ethyl nitrosourea by Scott (PhD Thesis, 1987, University of California, San Diego), considered to be allelic based on similarity in phenotype and genetic position. Twelve other alleles: One each induced by X rays, triethylenemelamine, 2-fluoroethyl methanesulfonate, and L-p- N,N-di-(2-chloroethyl)amino-phenylalanine; two induced by p- N,N-di-(2-chloroethyl)amino-phenylethylamine; three each induced by S-2-chloroethylcysteine, and DL-p-N,N-di-(2-chloro- ethyl)amino-phenylalanine. cytology: Placed in region 11F2 through 12A2 based on its inclusion in Df(1)C246 = Df(1)11D1-2;12A1-2 but not Df(1)wy2 = Df(1)11A6-12;11F2-4 (Scott). # cru: cream underscored location: 2-52.5. origin: Spontaneous. discoverer: Bridges, 20a5. phenotype: Specific dilutor of we and P. Slight dominant but used as a recessive. Originally thought to be male sterile, but this was caused by a factor in 2R, crs. Larval Malpighian tubes of we; cru colorless; those of +; cru bright yellow (Brehme and Demerec, 1942, Growth 6: 351-56). RK3. cytology: Not uncovered by Df(2L)64j = Df(2L)34D1-2;35B9-C1, Df(2L)75c = Df(2L)35A1-2;35D4-7, or Df(2L)fn1 = Df(2L)34F4- 35A1;35D5-7. Presumably proximal to 35D5 (Woodruff and Ash- burner, 1979, Genetics 92: 117-32). # crumbs: see crb # crumpled: see cmp # crumpled tips: see crt # crumpled wings: see cwi # cru sterile: see crs # cryptocephal: see crc # cs: creased location: 1-56. origin: X ray induced. discoverer: K. C. Atwood, 41i. references: 1942, DIS 16: 47. phenotype: Wings longitudinally creased in first posterior cell from distal end of L3 virtually to anterior crossvein. Fer- tility and viability good. RK1. alleles: cs53 (CP627). # csk: costakink location: 1-33.0. phenotype: Most alleles are lethal; originally described on basis of a single surviving semilethal allele which displayed smaller eyes, with wings slightly reduced in size and abnor- mally held, with the costal vein frequently kinked near L2. Not fully penetrant; male viability and fertility good; female fertility reduced to about 50% wild type. Survivors of other semilethal or nearly lethal alleles display similar phenotype (Zhimulev, Pokholkova, Bgatov, Umbetova, Solovjeva, Khudyakov, and Belyaeva, 1987, Biol. Zentralbl. 106: 699-720). Lethal allele csk33, functions in homozygous germ-line clones, but has no maternal effect (Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52). Fate maps, as a bilateral dom- ineering mutant, to a broad region of the neurogenic ectoderm posterior to the metathoracic ganglion; in addition a nonauto- nomous focus in the wing disc gives rise to crumpled turned up wings (Bgatov, Zharkikh, and Zhimulev, 1984, Mol. Gen. Genet. 196: 110-16). allele origin discoverer synonym ref ( comments _________________________________________________________________________ *csk1 TEM Fahmy, 1953 1 viable allele *csk2 X ray Fahmy, 1953 1 viable allele csk3 EMS Belyaeva l(1)162 6, 7, 8 heat-sensitive semilethal csk4 EMS Belyaeva l(1)166 6, 7, 8 heat-sensitive semilethal csk5 EMS Belyaeva l(1)E109 6, 7, 8 heat-sensitive semilethal csk6 EMS Belyaeva l(1)E115 6, 7, 8 csk7 EMS Belyaeva l(1)E128 6, 7, 8 csk8 EMS Belyaeva l(1)E143 6, 7, 8 csk9 EMS Belyaeva l(1)E147 6, 7, 8 csk10 Pokholkova l(1)F57 9 heat-sensitive semilethal csk11 Pokholkova l(1)F69 9 heat-sensitive semilethal csk12 Pokholkova l(1)F97 9 heat-sensitive semilethal csk13 Pokholkova l(1)F98 9 heat-sensitive semilethal csk14 Pokholkova l(1)F101 9 heat-sensitive semilethal csk15 Pokholkova l(1)F124 9 heat-sensitive semilethal csk16 Pokholkova l(1)F128 9 heat-sensitive semilethal csk Pokholkova l(1)F305 9 csk Pokholkova l(1)F404 9 csk Pokholkova l(1)F407 9 csk Pokholkova l(1)F411 9 csk Pokholkova l(1)F436 9 heat sensitive semilethal csk17 EMS Pokholkova l(1)G50 6, 7, 8 csk18 EMS Pokholkova l(1)G92 6, 7, 8 heat sensitive semilethal csk19 EMS Pokholkova l(1)G99 6, 7, 8 csk20 EMS Pokholkova l(1)G130 6, 7, 8 csk21Y EMS Pokholkova l(1)dpG1 6, 7, 8 on v+Yy+ csk22 EMS Khudyakov l(1)J20 6, 7, 8 csk23 EMS l(1)v88 2 larval lethal csk24 EMS l(1)v301 2 csk25 EMS l(1)v318 2 csk26Y EMS l(1)v370 2 on v+BS-Yy+ csk27 X ray Lefevre l(1)GA54 3 csk28 X ray Lefevre l(1)HF319 3 hetab, sev mutant csk29 X ray Lefevre l(1)L68 3, 5 l(1)RC68 csk30 X ray Lefevre l(1)N43 3 euchab csk31 EMS Lefevre l(1)DA651 4 csk32 EMS Lefevre l(1)DC835 4 csk33 EMS Lefevre l(1)DF923 4 P/NME csk34 EMS Lefevre l(1)EA46 4 csk35 EMS Lefevre l(1)VA28 4 csk36 EMS Lefevre l(1)VE710 4 csk37 EMS Lefevre l(1)VE793 4 ( 1 = Fahmy, 1958, DIS 32: 69; 2 = Geer, Lischwe, and Murphy, 1983, J. Exp. Zool. 225: 107-18; 3 = Lefevre, l981, Genet- ics 99: 161-80; 4 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 5 = Lefevre and Wiedenheft, l974, DIS 51: 83; 6 = Zhimulev, Belyaeva, Pokholkova, Kotchneva, Fomina, Bga- tov, Khudyakov, Patzevich, Semeshin, Baritcheva, Aizenzon, Kramers, and Eeken, 1981, DIS 56: 192-96; 7 = Zhimulev et al., 1981, Chromosoma 82: 25; 8 = Zhimulev, Belyaeva, Pokholkova, Kochneva, Fomina, Bgatov, Khudyakov, Patzevich, Semeshin, Baricheva, Aizenson, Kramers, Eeken, 1982, DIS 58: 210-14; 9 = Zhimulev, Pokholkova, Bgatov, Umbetova, Solovjeva, Khudyakov, and Belyaeva, 1987, Biol. Zentralbl. 106: 699-720. cytology: Allelism inferred from observation that both samples of alleles map to the region of overlap between Df(1)v-L1 and Df(1)v-L2. Survivors carrying semilethal alleles exhibit csk phenotype. Some surviving heteroallelic combinations display late eclosion and small pale bristles. # csw: corkscrew location: 1-{0.55}. synonym: l(1)2Db. references: Perrimon, Engstrom, and Mahowald, 1985, Genetics 111: 23-41 (fig.). phenotype: Hemizygotes die at the larval-pupal transition; dissected third-instar larvae display small imaginal disks. Larval neuroblast cells show low mitotic index, but chromosome morphology appears normal. Homozygous germ-line clones pro- duce inviable embryos with U-shaped or twisted phenotypes, which are unaffected by paternal genotype or developmental temperature. csw6 is viable and fertile with rough eyes. alleles: allele origin discoverer synonym ref ( comments ________________________________________________________________ csw1 X ray Lefevre l(1)C114 2, 4 euchromatic rearrangement csw2 X ray Lefevre l(1)GA113 2 T(1;2)2C;49A (complex) csw3 X ray Lefevre l(1)KC16 2 T(1;2)2D5;52F csw4 X ray Lefevre l(1)S53 2 T(1;2;3)2D5;57E;86B csw5 EMS Lefevre l(1)VA199 3, 4 csw6 l(1)15086 viable and fertile csw7 spont Schalet l(1)19-106 csw8 X ray 1 csw9 X ray 1 csw10 X ray 1 csw11 EMS 1 csw12 EMS 1 csw13 EMS 1 viable ( 1 = Dura, Randsholt, Deatrick, Erk, Santamaria, Freeman, Freeman, Weddell, and Brock, 1987, Cell 51: 829-39; 2 = Lefevre, 1981, Genetics 99: 461-80; 3 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 4 = Perrimon, Engstrom, and Mahowald, 1985, Genetics 111: 23-41. cytology: Placed in 2D3-4 based on its inclusion in Df(1)pn38 = Df(1)2D3-4;2E3 but not Df(1)Pgd-kz = Df(1)2D3-4;2F5. # ct: cut location: 1-20.0. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 35, 223 (fig.). Lefevre and Johnson, 1973, Genetics 74: 633-45. Johnson and Judd, 1979, Genetics 92: 485-502. Jack, 1985, Cell 42: 869-76. phenotype: ct mutations fall into three nonoverlapping pheno- typic classes: kinked femur, cut wings, and lethal. Kinked- femur mutants are small with slightly dark, dull, red eye color; femurs kinked; wings seldom expand following eclosion, or when they do expand they are opaque and abnormal in shape; flies seem unable to move normally and die on the food soon after eclosion. Cut-wing mutants variably affect wing shape and head capsule development; phenotypic effects include incised wing margins with the tips usually cut to points, missing or ventrally displaced vibrissae, deformed antennae, e.g., flattened and embedded with aristae concave forward, smaller kidney-shaped eyes, warped abdominal bands, and fine bristles. Most lethal alleles survive as clones of homozygous epidermal cells (Demerec). Developmental study of ct6 by Wad- dington [1939, Proc. Nat. Acad. Sci. USA 25: 299-308; 1940, J. Genet. 41: 75-139 (fig.)] shows wing bud narrower than wild type as early as just after eversion of wing in early pupa. Cell death observed in prepupal wing bud (D. Fristrom, 1969, Mol. Gen. Genet. 103: 363-79). Clones of ct6 cells in internal areas of wing blade normal in size; marginal clones much reduced in size indicating cell death. Homozygous clones in either dorsal or ventral membrane must reach margin in order to produce incision, 100/127 marginal clones unassoci- ated with gaps; when gaps are produced, they affect both wing surfaces even though clone confined to a single surface. Both dorsal and ventral chaetal elements at the edges of such gaps may show the markers of such clones (Santamaria and Garc'a- Bellido, 1975, Wilhelm Roux's Arch. Entwicklungsmech. Org. 178: 233-45). Lethal alleles fall into three groups, based on their complementation characteristics: cutless, group I, and group II. Lethal alleles ctC145, ctJA124, and ctl49 exhibit polyphasic lethality from late embryo to pharate adult (John- son and Judd, 1979). Lethal embryos characterized by posterior defects in spiracles; no Keilin's organs, and abnormal maxil- lary complex (Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307). Group II and to a slightly lesser degree group I lethals fail to differen- tiate external sensory neurons in the peripheral nervous sys- tem; the presumptive external sensory neurons of the embryonic peripheral nervous system and their support cells are transformed into chordotonal neurons with their support cells; the transformed organs are chordotonal both in morphology and antigenic specificity. Same effect seen in the adult sensory organs in mosaics; embryonic effect differs from that seen in adults in that embryos lack peripheral sensory structures, e.g., Keilin's organs, whereas such structures persist, though reduced in size, in adult tissue. The numbers and positions of peripheral neurons is normal. CNS structure and function appear normal. No discernable effect of absence of ct func- tion in the maternal germ line. Effect of ct mutations on PNS differentiation cell autonomous. [Bodmer, Barbel, Sheperd, Jack, Jan, and Jan, 1987, Cell 51: 293-307 (fig.).] Antibo- dies to ct protein specifically bind to nuclei of presumptive external sensory organ cells including those of the anten- namaxillary organ and external sensory organs in spiracles, but not to nuclei of chordotonal organs; antibody staining also seen in some neurons with multiple dendritic arborizations and in cells lining the Malpighian tubules (Blochlinger, Bodmer, Jack, Jan, and Jan, 1988, Nature 333: 629-35). Kinked-femur, cut-wing, and cutless alleles are mutually complementing: group I lethals complement kinked-femur but not cut-wing alleles; and group II lethals are noncomplement- ing; all combinations of lethal alleles are lethal. The dif- ferent phenotypic classes of alleles occupy discrete and separate regions of the complex, with the order from left to right being, kinked femur, cut wing, group I lethals, and group II lethals; cutless alleles have not been mapped. Kinked femur, cut, and group-I-lethal mutations are associated with chromosome aberrations or insertions of transposable ele- ments, whereas group II lethals appear to be point mutations. ct6, ct68E (= ct67s?), ct78a, and ctK suppressed by su(Hw)2; dvr2 enhances ct6 and inhibits its complete suppression by su(Hw)2; su(Hw)2/+ shows slight dominant suppression of wing phenotype of ctK (Lee, 1973, Aust. J. Biol. Sci. 26: 903-09). ct6 and ctK strongly enhanced by su(s); su(s) ctK lethal (Johnson) but rescued by su(Hw)2/+ (Craymer). ct6 the most commonly used allele. ct kf2 ctnct6 ctK lethals _________________________________________________________________ | | | | | | -0.04- | -0.16- | - ~0.07- | Genetic fine structure map of the cut locus alleles: ct is among the most mutable X-linked genes; several large-scale mutagenesis experiments have yielded many alleles, the majority of which are lost. The majority of induced ct alleles are lethal, or associated with chromosome rearrange- ments, or both. X-ray-induced alleles superscripted *2a2, *2a3, *2c1, *3a2, *3b1, 4b1, *4c1, *6a1, *7a1, *7a2, *7b2, *7c1, *7c2, *9b1, *9b2, *10a1, *10b1, *10c1, *11a, *12a1, *12a2, *12c1, *12c2, *13a2, *13b1, *14a1, *14a2, *14a3, *14b1, *14b2, *14c1, 15b1, and *15b4 described by Hannah (Proc. Int. Congr. Genet. 8th, 1949, 588-89; 1971, Mol. Gen. Genet. 113: 191-203; CP627). Of a similar set of 28 alleles with superscripts between *268-1 and 268-42 induced with X rays by Demerec or Hoover (CP552 and 627), only Df(1)ct268-42 per- sists. Early alleles superscripted *2 through *21 (CP552 and 627) are lost with the exception of ct6. Other early alleles are superscripted *34a, *34b, *36b, *41c23, *41i30 (CP552 and 627), *43aH1, 46l, *50e, *62a, *62f, *do-vg, *n4, *n36, and *So (CP627). Information on ct alleles that persist or that have been described since CP627 and on kf: kinked femur, which is a member of the cut complex, is tabulated below. ctcl: cut-cutless complements various nonlethal ct alleles but fails to complement lethal alleles except ctHA46 (Lefevre and Leeds, 1983, Genetics 104: s45-46). A derivative of ct6 (termed Uc: Unstable chromosome) studied by Lim (1979, Genet- ics 93: 681-701) and ctMR2 derived from a hybrid dysgenic cross involving MR-h12 on chromosome 2 by Gerasimova (1981, Mol. Gen. Genet. 184: 544-547) are highly unstable. The ins- tability is manifest as increased incidence of lethal muta- tions, many of which are associated with chromosome aberra- tions broken in 6F (Lim), high reversion frequencies often accompanied by mutation at other loci. (Gerasimova, 1983, Mol. Gen. Genet. 190: 390-93; Gerasimova and Ilyin, 1984, DIS 60: 111-112) to either stable, unstable (most frequent, ->10-4 mutations to ct), or superunstable (least frequent, -> around 50% ct mutants) alleles, and to other ct alleles, which in turn may be unstable or superunstable. In both instances the gypsy sequence [called L by Lim, Simmons, Raymond, Cox, Doll, and Culbert (1983, Proc. Nat. Acad. Sci. USA 80: 6624- 27) and mdg4 by Gerasimova, Ilyin, Mizrokhi, Semjonova, and Gregoriev (1984, Mol. Gen. Genet. 193: 488-92)] is inserted into the ct locus. The gypsy sequence appears to be mobilized and transposed into other parts of the ct locus to produce new ct alleles or, when ct undergoes reversion, to other positions on the chromosomes where new mutants arise. Other types of transposing elements also appear to be mobilized in these two situations (e.g. Gerasimova, Matyunina, Ilyin, and Gregoriev, 1984, Mol. Gen. Genet. 194: 517-22). In the accompanying table of alleles, those superscripted L were recovered by Lim and colleagues; L followed by an even number designates a cut-wing allele, and L followed by an odd number a group-I lethal allele; alleles designated as weak cut wings have more nearly entire wing margins and lack head- capsule defects. Alleles superscripted MR are derived, either primarily or secondarily from hybrid-dysgenesis crosses by Gerasimova and her colleagues; those designated by MR followed by a number display the strong ct6-like wing phenotype; those designated MRpN are less extreme with multiple small incisions in the wing margin. ctMR2 can revert or partially revert by excision of, or insertion of other elements (e.g. Jocky or Hercules), into the gypsy insert responsible for ctMR2 (Leigh, Brown, Ross, Alphey, Flavell, and Gerasimova, 1989, Mol. Gen. Genet. 218: 203-13; Tchurikov, Gerasimova, Johnson, Barbakar, Kenzior, and Georgiev, 1989, Mol. Gen. Genet. 219: 241-48). Unstable revertants are able to generate new ct derivatives, retain the gypsy LTR of ctMR2 (Mizrokhi, Obolenkova, Priimagi, Ilyin, Gerasimova and Georgiev, 1985, EMBO J. 4: 3781-87). allele origin discoverer ref ( phenotype | comments DNA coordinates / _____________________________________________________________________________________________________________________________ ct1 spont Bridges, 15j12 3 wa ct6 gypsy Bridges, 20c20 2, 3, 10, 11 wav cytology normal -1.1 to -0.5 ct7 ct43aH1 X ray 3, 23 l In(1)4B1-4;7B4-C1 + In(1)10D5-6;20B-C ct461 X ray 3, 10, 22 w B104 insert at -5.6 roo ct53d EMS 10 w 0.5 kb deletion in -6.8 to -4.8 ct68E 13 ct71g X ray Johnson 10, 14 fw In(1)dl-49 ct71j X ray Johnson 10, 14 w In(1)dl-49 ct78a gypsy 10 wa -1.1 to -0.5 ct81/1 gypsy 10, 21 w 0 to +19.3 ct149 EMS Johnson 10, 11 l cytology normal ct152 EMS Johnson 10, 11 l cytology normal ct161 EMS Johnson 10, 11 l cytology normal ct268-42 X ray 3 l T(1;3)7B;80 ctcl ` X ray 15 l ctcl1 ` EMS Lefevre 17 ` ctcl2 ` EMS Lefevre 17 ` ctC75 X ray Lefevre 11 T(1;2)7B3-4;35C ctC145 X ray Lefevre 2, 10, 11 cytology normal ctDA639 EMS Lefevre 17 ctdb1 DEB 1 l ctdb2 DEB 1 l molecular lesion 130 to 150 kb ctdb3 DEB 1 l ctdb4 DEB 1 l ctdb5 DEB 1 l ctdb6 DEB 1 l molecular lesion 130 to 150 kb ctdb7 DEB 1 l 1 kb deletion in 130 to 150 kb ctdb8 DEB 1 l ctdb9 DEB 1 l ctdb10 DEB 1 l ctdb11 DEB 1 l ctdb12 DEB 1 l ctdb13 DEB 1 l ctEA2 EMS Lefevre 17 ctEA127 EMS Lefevre 17 ctEC234 EMS Lefevre 17 ctEF404 EMS Lefevre 17 ctF928 EMS Lefevre 17 ctGA83 X ray Lefevre 16 In(1)7A1;7B3 ctGA86 X ray Lefevre 16 T(1;2)7B3;42A-B ctGE253 X ray Lefevre 16 In(1)7E3;7E-F1 ctHA46 X ray Lefevre 15 l In(1)7B1-2;8D5 break at -32 kb ctHA79 X ray Lefevre 16 In(1)A7-8;7B3-4 ctHC211 X ray Lefevre 16 ctHC265 X ray Lefevre 16 In(1)1A2-3;7B3-4 ctHF357 X ray Lefevre 16 Tp(1;3)7B2;20;75A ctJ1 X ray Johnson 14 l In(1)dl-49 + T(1;2)7B3-4;60E ctJ2 X ray Johnson 14 l In(1)dl-49 + T(1;3)7B3-4;96A ctJ3 X ray Johnson 14 l In(1)dl-49 ctJ5 X ray Johnson 14 l In(1)dl-49 + T(1;2)7B3-4;40 *ctJ7 X ray Johnson 14 l+ In(1)dl-49 + In(1)7B3-4;7D22 ctJ8 X ray Johnson 14 l In(1)dl-49 + T(1;3)4Dl;7B3-4;92A *ctJ9 X ray Johnson 14 l In(1)dl-49 + T(1;3)7B3-4;86D-E ctJ10 X ray Johnson 14 l In(1)dl-49 ctJ11 X ray Johnson 14 l In(1)dl-49 + T(1;3)7B3-4;95F ctJ12 X ray Johnson 14 l In(1)dl-49 + In(1)7B3-4;fD4 ctJ13 X ray Johnson 14 l In(1)dl-49 + In(1)5A;7B3-4 *ctJ14 X ray Johnson 14 l In(1)dl-49 ctJ15 X ray Johnson 14 l In(1)dl-49 ctJ16 X ray Johnson 14 l In(1)dl-49 ctJA11 X ray Lefevre 16 In(1)7B;7E5 ctJA109 X ray Lefevre 16 l ctJA120 X ray Lefevre 16 In(1)7B3;11A3-5 ctJA124 X ray Lefevre 10, 11, 16 l cytology normal ctJA134 X ray Lefevre 16 T(1;2)7B3-4;32F-33A ctJC20 X ray Lefevre 2, 10, 11, 16 1+fuwavb cytology normal ctK gypsy Krivshenko 2, 3, 10, 11 wblI cytology normal +70.8 to +73.3 ctl EMS 20 l In(1)dl-49 ctL1 gypsy Lim 2, 10, 18 l +70.8 to +73.3 ctL5 gypsy Lim 10, 18 l +70.8 to +73.3 ctL7 gypsy Lim 10, 18 l +70.8 to +73.3 ctL10 gypsy Lim 10 wv -1.1 to -0.5 ctL13 gypsy Lim 10 l ctL18 gypsy Neuwald 10 wv 0 to +19.3 ctL20 gypsy Neuwald 10 wv 0 to +19.3 ctL23 gypsy Lim 10 l ctL25 gypsy Lim 10 l ctL27 gypsy? Lim 10 l ctL30 gypsy Lim 10 wv 0 to +19.3 ctL31 gypsy? Lim 10 l ctL32 gypsy Lim 10 wv +19.3 ctL33 gypsy? Lim 10 l ctL34 gypsy Lim 10 wv 0 to +19.3 ctL35 gypsy Lim 2, 10 l +70.8 to +73.3 ctL36 gypsy Lim l ctL37 gypsy Lim 10 l -1.1 to -0.5 ctL39 gypsy Lim 2, 10 l +40 ctL41 gypsy Lim 10 l +70.8 to +73.3 ctL44 gypsy Lim 10 wv 0 to +19.3 ctL45 gypsy Lim 10 l +70.8 to +73.3 ctL47 gypsy Lim 10 l +70.8 to +73.3 ctL49 gypsy Lim 10 l +70.8 to +73.3 ctL51 gypsy Lim 10 l ctL53 gypsy Lim 10 l +70.8 to +73.3 ctL54 X ray Lefevre 16 T(312)96A;7B3-4 ctL55 gypsy Lim 10 l ctL57 gypsy Lim 10 l ctL59 gypsy Lim 2, 10 l 36 ctL60 gypsy Lim 10 wv 0 to +19.3 ctL61 gypsy Lim 10 l +70.8 to +73.3 ctL62 gypsy Lim 10 wv 0 to +19.3 ctL64 gypsy Lim 10 w -1.1 to -0.5 ctL65 spont Lim 2, 10 l +70.8 to +73.3 ctL67 gypsy Lim 10 l ctL149 EMS 11 l ctL857 gypsy Lim 10 l ctlS1 copia? Schalet 10 l +140 to +142.5 ctlS2 spont Schalet 2, 10 l ctMR2 gypsy 5, 7, 19 0 ctMR2a gypsy 8 ctMR4 gypsy 5, 7 wl(u) ctMR7 gypsy 8 ctMR8 gypsy 8 ctMR9 gypsy 8 ctMR10 gypsy 8 ctMR10a gypsy 8 ctMR11 gypsy 8 ctMR12 gypsy 8 ctMR13 gypsy 8 ctMR14 gypsy 8 ctMR15 gypsy 8 ctMR16 gypsy 8 ctMR17 gypsy 8 ctMRl15 gypsy 7 l(u) ctMRl1 burdock 26 l ctMR2 derivative burdock at +2 kb ctMRl8 burdock 26 l ctMR2 derivative burdock at +2 kb ctMRl37 burdock 7, 26 l(su) ctMR2 derivative burdock at +2 kb ctMRlA1 burdock 26 l ctMR2 derivative burdock at +2 kb ctMRlA12 burdock 26 l ctMR2 derivative burdock at +2 kb ctMRlB1 burdock 26 l ctMR2 derivative burdock at +2 kb ctMRlE1 burdock 26 l ctMR2 derivative burdock at +2 kb ctMRlK1 Hercules 26 l ctMR2 derivative - in gypsy + burdock burdock at +2 kb ctMRlL2 burdock 26 l ctMR2 derivative burdock at +2 kb ctMRlL46 burdock 26 l ctMR2 derivative burdock at +2 kb ctMRlLD1 Hercules 26 l ctMR2 derivative - in gypsy + burdock burdock at +2 kb ctMRlLM1 burdock 26 ctMR2 derivative burdock at +2 kb ctMRn1 gypsy 6, 7 w(su) ctMRn2 gypsy 6, 7 ctMRn3 gypsy 6, 7 ctMRP roo 26 ctMRpN19 derivative gypsy lost; roo at -5 kb ctMRpN1 gypsy 7 ctMRpN1a jocky in 8, 26 ctMR2 derivative - gypsy ctMRpN1b gypsy 8 ctMRpN1c gypsy 8 ctMRpN6 gypsy 7 w(u) ctMRpN7 jocky in 26 ctMR2 derivative - gypsy ctMRpN10 jocky in 5, 7, 19, 26 w(u) ctMR2 derivative - gypsy ctMRpN16 gypsy 7 w(u) ctMRpN17 jocky in 8, 26 w(u) ctMR2 derivative - gypsy ctMRpN19 jocky in 7, 26 w(u) ctMR2 derivative - gypsy roo LTR at -5 kb ctMRpN20 jocky in 26 ctMR2 derivative - gypsy ctMRpN20a jocky in 26 ctMR2 derivative - gypsy ctMRpN22 jocky in 26 ctMR2 derivative - gypsy ctMRpN23 jocky in 26 ctMR2 derivative - gypsy ctMRpN24 gypsy 8 ctMRpN25 gypsy 8 ctMRpN26 gypsy 8 ctMRpN30 jocky in 26 ctMR2 derivative - gypsy ctMRwR gypsy 7 w cytology normal ctMRwR1 gypsy 8 ctn roo Ives, 32c3 3, 10, 11 w cytology normal -6.8 to -4.8 ctns copia Schalet 10, 11 w In(1)dl-49 -6.8 to -4.8 ctRA4 X ray Lefevre 16 l T(1;2)7B3-4;32E1-2 ctRC26 X ray Lefevre 10, 11, 16 l cytology normal ctS In(1)FM7 ctS6 X ray Lefevre 16 In(1)7B;8C1-2 ctS20 X ray Lefevre 16 T(1;3)7B3-4;84; complex ctS69 X ray Lefevre 16, 26 In(1)7B;8C1-2 break at +93 kb cttuh spont 9 cytology normal ctVA109 EMS Lefevre 17 ctVA123 EMS Lefevre 17 ctVE698 EMS Lefevre 17 ctW1 EMS 25 l ctW2 EMS 25 l ctW3 EMS 25 l ctXM31 EMS Wieschaus 2 l ctYE118 EMS Wieschaus 2 l kf1 CB3007 Fahmy, 1954 4 kf2 5, 11, 24 f Basc kf3 ` EMS Lefevre 15 f T(1;2)7B1-2;2L kfMR1 spont 26 f ctMRpN19 derivative same as kf2 kfMR2 spont 26 f ctMRpN19 derivative same as kf2 kfMR3 spont 26 f ctMRpN19 derivative same as kf2 ( 1 = Blochlinger, Bodmer, Jack, Jan, and Jan, 1988, Nature 333: 629-35; 2 = Bodmer, Barbel, Sheperd, Jack, Jan, and Jan, 1987, Cell 51: 293-307; 3 = CP627; 4 = Fahmy, 1959, DIS 33: 87; 5 = Gerasimova, 1981, Mol. Gen. Genet. 184: 544-47; 6 = Gerasimova, 1983, Mol. Gen. Genet. 190: 390-93; 7 = Gerasimova, Ilyn, Mizvokhi, Semjonova, and Gregoriev, 1984, Mol. Gen. Genet. 193: 488-92; 8 = Gerasi- mova, Matjunina, Mizrokhi, and Georgiev, 1985, EMBO J. 4: 3773-79; 9 = Kuhn and Walker, 1980, DIS 55: 207; 10 = Jack, 1985, Cell 42: 869-76; 11 = Johnson and Judd, 1979, Genetics 92: 485-502; 12 = Krivshenko, 1956, DIS 30: 74; 13 = Lee, 1980, DIS 48: 18; 14 = Lefevre and Johnson, 1973, Genetics 74: 633-45; 15 = Lefevre and Leeds, 1983, Genetics 104: s45-46; 16 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 17 = Lefevre; 18 = Lim, Simmons, Raymond, Cox, Doll, and Culbert, 1983, Proc. Nat. Acad. Sci. USA 80: 6624-27; 19 = Mizrokhi, Obolenkova, Priimagi, Ilyin, Gerasimova and Georgiev, 1985, EMBO J. 4: 3781-87; 20 = Muller; 21 = Muskovitch; 22 = Poulson and King, 1948, DIS 22: 54; 23 = Valencia, 1966, DIS 41: 58; 24 = Whitney and Lucchesi, 1972, DIS 49: 35; 25 = Wieschaus, Nusslein- Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307; 26 = Tchurikov, Gerasimova, Johnson, Bar- bakar, Kenzior, and Georgiev, 1989, Mol. Gen. Genet. 219: 241-48. | f = kinked femur; u = unexpanded wings; w = cut wings; a = deformed antennae; v = displaced or missing vibrissae; b = fine bristles; l = lethal; (u) = unstable; (su) = superunstable. / Coordinate system of Jack; origin at site of gypsy insertion of ct6. Coordinates used by Tchurikov et al. place ct6 insertion at -118 kb; here converted to those of Jack by the addition of 118 kb. ` ctcl = cut-cutless; ctc11 and ctc12 recovered as l(1)VA39 and l(1)VE829 respectively; isolation number of kf3 = VE614. - Derivatives of ctMR2 in which an additional transposable element is inserted in the left end of the gypsy element associated with ctMR2. ctMRpN1a, ctMRpN7, ctMRpN17, ctMRpN19, and ctMRpN26 have jocky inserts in one position and in one orientation; ctMRpN10, ctMRpN20A, ctMRpN22, ctMRpN23, and ctMRpN30 have jocky inserts in a slightly dif- ferent position and in the opposite orientation; ctMRlK1, and ctMRlLD1 have Hercules inserts in different sites in the same region. Additional information detailed below. cytology: Placed in 7B1-2 by in situ hybridization. molecular biology: Two hundred kilobases of DNA from the cut region cloned and restriction mapped (Jack, 1985, Cell 42: 869-76). Coordinate 0 is the site of the gypsy insert in ct6; coordinates 0 to -60 extend to the left and 0 to +140 to the right; all sequences hybridize to 7B1-2. Kinked-femur effects map in the -60 to -14 kilobase region, and cut-wing effects, many of which are known to result from gypsy inserts, to -6 to +19.3. Group I lethals cluster in the +71 to +73.5 region, and most of them contain gypsy inserts; group II mutants do not contain gypsy inserts and are thought to lie to the right of coordinate +100. 8,217 base pairs of cDNA clones sequenced; transcribed from over 70 kb of genomic sequence from coordinates approximately 80 to 150, which contain lethal I and lethal II regions. Transcription is from left to right. Sequence reveals long open reading frame encoding a putative protein of 2,175 amino acids with molecular mass of 240 kd. Principle among the features of the amino-acid sequence is a 60-residue homeodomain homologue, which although the most divergent of Drosophila homeobox sequences shows identity at the nine residues that are invariant in all homeodomains. In addition there are three 60-residue repeats showing 55-68% identity to each other which are not homologous to repeats found in other proteins; there are also four stretches of polyglutamate aspartate and a number of runs rich in single amino acids (Blochlinger et al.). # ct71g molecular biology: A molecular inversion with one breakpoint between DNA coordinates -35.8 and 33.2 and the other between +4.1 and +4.8. # ctJC20 molecular biology: A molecular deletion beginning between coor- dinates -1.7 and +1.0 and extending to the left beyond -60, the extent of the cloned region. Deletes material of both kinked-femur and cut-wing regions of the complex. # ctk phenotype: Classified as a group-I lethal because homozygotes show reduced viability, and only 10% of fewer heterozygotes with other lethal alleles survive; survivors have weakly cut wings, as well as fine bristles, and enlarged and deformed humeral callus, not seen in other cut-wing mutants. # ctcl: cut-cutless references: Leeds and Lefevre, 1983, Genetics 104: s45-46. phenotype: Acts as a lethal allele in combination with defi- ciencies for ct; phenotype normal in combination with viable ct alleles. Homozygotes have reduced viability and show thoracic protuberances (Schalet). Heterozygotes of ctcl with lethal alleles of ct die or eclose in small numbers; an excep- tion is ctcl/ctHA46, which exhibits normal survival. # ctlS1 (A. Schalet) phenotype: Lethal; a member of cut Lethal II group, maps proxi- mal to ctC145 (Jack, 1985). Not suppressed by su(Hw)2 (Schalet). ctlS1/+ males, frequently show thoracic protuber- ances (Schalet). # ctlS2 (A. Schalet) phenotype: Almost complete lethal; survival less than 1%. Not suppressed by su(Hw)2; cut-cutless type of mutant in that ctlS2 fails to complement lethal alleles, e.g. ctlS1, but com- plements kf2, ct6 and ctS. Rare surviving males and females are fertile with normal wings, but usually show thoracic pro- tuberances in the region of the presutural and notoplural bristles as are also seen in heterozygotes of ctlS1, Df(1)ctJ4 or Df(1)ctJ6. # kf2 molecular biology: An approximately 18 kilobase deletion extending from a point between coordinates -35.8 and -33.2 to a point between -18.5 and -14.0. # cta: concertina (T. Schupbach) location: 2-{54.8}. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal, female sterile: Embryos from homozygous mothers gastrulate abnormally; no posterior midgut formed; the germ band does not advance to the dorsal side of the embryo, but as it expands, it is thrown into a series of folds at the ventral side of the embryo. Anterior midgut appears to develop normally. The phenotype is reminis- cent of the zygotic embryonic lethal mutation folded gastrula- tion (fog). At final differentiation, the embryos from cta mothers have a fairly normal array of thoracic and abdominal segments with morphologically normal denticle belts. Defec- tive head skeleton seen in larvae. alleles: allele origin synonym _________________________ cta1 EMS ctaWU cta2 EMS ctaPC cta3 EMS ctaPG cta4 EMS ctaQB cta5 EMS ctaRC cytology: In heterochromatic region of 2L, since uncovered by Df(2L)PR31. # ctl: coatless location: 1-25.8. origin: Induced by ethyl methanesulfonate. references: Eberl and Hilliker, 1988, Genetics 118: 109-20. phenotype: Hemizygous lethal; distinct yolk plug indicating poorly developed gut; variably incomplete Malpighian tubules; poorly differentiated cuticle; mouthparts abnormal. # ctt: contorted location: 1-0.3. origin: Induced by ethyl methanesulfonate (CB. 1528). discoverer: Fahmy, 1956. references: 1959, DIS 33: 84. phenotype: Wings shorter than normal and abnormally shaped, frequently curved either convexly or concavely. Eyes rough and slightly altered in shape. Bristles thinner and straggly; orbitals frequently reduced or absent. Male genitalia fre- quently slightly twisted and abnormal. Males fertile; females sterile. RK2. cu: curled From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 152. # cu: curled location: 3-50.0. origin: Spontaneous. discoverer: Morgan, 15l15. references: Morgan and Bridges, 1923, Carnegie Inst. Washington Publ. No. 327: 152 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 215 (fig.), 223. Whittinghill, 1937, DIS 7: 22. phenotype: Wings curved upward throughout length and slightly divergent. Body color dark. Postscutellars erect and crossed. Good nutrition of larvae enhances curled character as does high temperature in last day of pupal life. (Nozawa, 1956, Jpn. J. Genet. 31: 321-26). RK1. alleles: *cu100.69, *cu100.384, and *cu300.215 (CP627); cu5J associated with In(3R)84F11-12;86D1-E2 (Ashburner, 1981, DIS 56: 190). cytology: Located in 86D1-4 based on the absence of cu+ from Df(3R)M86D = Df(3R)86D1;86D4 (Ashburner, 1981, DIS 56: 189). #*Cu: Curl location: 2-54.6 (0.1 unit to the right of pr). origin: X ray induced. discoverer: Bateman, 1954. synonym: Cd: Coildex; Coi: Coiled. references: 1955, DIS 29: 69. phenotype: Similar to Cy but wing curvature more extreme; wings opaque and greyish. Anterior margin of wing invaginated at point where L1 meets wing margin. When expression is weakest, it appears only as a slight wave in the wing margin. In 10- 15% of the flies, wings also curve downward over flanks before curling upward. In y; Cu54 flies, curvature reduced to a shallow spoon. Cu54 epistatic to Cy. RK2. alleles: allele origin discoverer synonym ref ( homozygote phenotype ________________________________________________________________________ *Cu1 spont. Ives 5 viable Cu2 EMS Grell viable, does not complement stw Cu3 Ish-Horowicz, 1976 Cd2 2 lethal *Cu54 X ray Bateman, 1954 Cd 2 lethal Cu57 X ray Carlson, 57g Coi 3 viable; complements stw | Cu75 X ray Ashburner Coi75 1 viable *CuA spont. Fernandez Gianotti Ac 4 viable ( 1 = Ashburner, Faithfull, Littlewood, Richards, Smith, Vel- issariou, and Woodruff, 1980, DIS 55: 193-95; 2 = Bateman, 1955, DIS 29: 69; 3 = Carlson, 1960, DIS 34: 48; 4 = Fer- nandez Gianotti, 1948, DIS 22: 53; 5 = Ives, 1948, DIS 22: 53. | Viability and fertility of Cu57 excellent; phenotype extreme. other information: Allelism of Cd, Coi, and Cu inferred from similarity of phenotype and of genetic position (54.6-56.6). Cd (=Cu54) and Coi (=Cu57) declared to be allelic based on renewed mapping of Coi just to the right rather than to the left of pr in agreement with the published position of Cd (Ashburner and Woodruff, 1979, Genetics 92: 117-32). Both Cu57 and Cu75 suppressed by Dp(2;2)Adh3 (Ashburner and Woo- druff). Cu and Cu57 shown to be in 2R based on their being recoverable in C(2R) but not C(2L) compounds (E.H. Grell). # Cu-3: Curl in chromosome 3 location: 3-66.0. origin: Spontaneous. discoverer: Erickson and Meyer, 51c. synonym: Cur: Curl preoccupied. references: Meyer, 1952, DIS 26: 66. phenotype: Heterozygote has curly wings with parchment-like texture resembling Cy. Homozygous lethal. RK2. # cu-X: curled-X location: 1- (not located but not allelic to cx). origin: Spontaneous in In(1)d1-49+BM1, y sc v. discoverer: Krivshenko, 57j29. references: 1956, DIS 32: 80. phenotype: Males have wings that are bent upwards and diverge slightly. cu-X is never expressed in females. It represents a mutation whose phenotypic expression is sex limited. Expressed equally well in males with and without a Y chromo- some. RK2. # cubitus interruptus: see ci # cuff: cutoff (T. Schupbach) location: 2-61. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: female-sterile; homozygous females often have under- developed ovaries which seem to lack germ cells altogether. In some females, a small number of developing egg chambers is found; these never develop beyond the first few stages of oogenesis. alleles: cuff1 to cuff3 isolated as WL, QQ, and WM respec- tively. # cui: curvi location: 2-23.4 (1.4 to the right of Sp and 0.5 to the right of lys). origin: Spontaneous. discoverer: Nicoletti. synonym: curved. references: 1957, DIS 31: 84. phenotype: Distal half of wing curved upward. Viability and expressivity very good. RK1. # cup: cup (T. Schupbach) location: 2-23. 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 synthetize a chorion which remains open ended (like a chalice, or cup). Such eggs are usually not laid and remain unfertilized. alleles: Thirty seven alleles; cup1 to cup37 (isolated as WQ, PB1, PB53, PF21, PF63, PH69, PL11, PN14, PS73, PV36, PW3, PV76, QD57, QJ9, QJ36, QJ65, QK4, QK12, QK24, QL54, QM66, QR55, QR56, QV7, QV50, QW45, RC11, RG6, RH13, RH24, R177, RM12, RN61, RS2, RS42, RS50, and RU45 respectively). # cupola: see cpl # cur: curvoid location: 3-30. origin: Spontaneous. discoverer: Bridges, 33c14. phenotype: Wings divergent and curved down. Resembles c. Via- bility erratic. RK3. # Cur: see Cu-3 # Curl: see Cu # curled: see cu # Curled blistered: see Cb # curlex: see cx # Curly: see Cy # Curlyoid: see Cyd # curved: see cr # curved: see cui # Curved of Krivshenko: see C-K # curvi: see cui # curvoid: see cur # cut: see ct cv: crossveinless From Weinstein, A., 1920, Proc. Nat. Acad. Sci. USA 6: 625-39. # cut off: see cuff # cv: crossveinless location: 1-13.7. origin: Spontaneous. discoverer: Bridges, 19l12. references: 1920, Proc. Nat. Acad. Sci. USA 6: 660-63. Weinstein, 1920, Proc. Nat. Acad. Sci. USA 6: 625-39 (fig.). phenotype: Crossveins absent or traces only present. Veins L3 and L4 slightly delta at tips. Classifiable in unexpanded wings. Wing effects due to excessive contraction in the pupal period, obliterating the cavity which should normally remain between the epithelia to form the vein (Waddington, 1940, J. Genet. 41: 75-139). RK1. alleles: *cv68 induced by ethyl methanesulfonate (Hayman and Maddern, 1969, DIS 44: 50). cytology: Located in polytene region 5B [Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 31-66]. # cv-2: crossveinless on chromosome 2 location: 2-96.2. origin: Spontaneous. discoverer: Nicoletti, 62j. phenotype: Anterior and posterior crossveins absent. RK1. alleles: Found segregating in several natural populations (Boyer, Parris, and Milkman, 1973, Genetics 75: 169-75). cytology: Salivary chromosomes normal. #*cv-b: crossveinless-b location: 3-65. origin: Spontaneous. discoverer: Bridges, 24k8. phenotype: Crossveins reduced or absent. May overlap wild type. RK3. # cv-c: crossveinless-c location: 3-54.1 (0.5 units to the right of red, Craymer). origin: Spontaneous. discoverer: Stern, 25g13. references: 1934, DIS 1: 35-36. phenotype: Posterior crossvein usually absent or greatly reduced. Anterior crossvein usually present but often detached. Eye flattened or with vertical shallow furrow. Legs weak, especially tarsal joints. Occasionally overlaps wild type. RK2. cytology: Placed in 88B-C based on its inclusion in the syn- thetic deficiency with 3R proximal derived from T(Y;3)P102 = T(Y;3)87B2-3 and 3R distal derived from T(3;4)P86 = T(3;4)88B-C;101 (Bernstein) as well as in the duplication from T(1;3)O5 = T(1;3)4F2-3;62B-C;88A-C;92C-D (Lindsley and Grell, 1958, DIS 32: 136). # cv-d: crossveinless-d location: 3-65. origin: Appeared among progeny of ether-treated flies. discoverer: Duncan, 34c. references: 1935, DIS 4: 7. phenotype: Posterior crossvein absent or reduced to an oblique fragment or bar parallel to L5. Anterior crossvein sometimes detached. RK2. other information: Possibly an allele of cv-b. # cve: crossveinless effect This is a term used by Milkman for alleles anywhere in the genome which affect the formation of crossveins. Not strictly a gene locus designation. # cvl-5: crossveinless like location: 3-48.1 [based on 55 crossovers between st and cu (Thompson, 1967, DIS 42: 41)]. origin: The major component in a line selected by Mohler (1965, Genetics 51: 641-51) for crossveinless-like phenotype. references: Thompson, 1967, Genetics 56: 13-22. phenotype: Removes crossveins. Complex response to heat shock described by Thompson (ibid). # cvl-6: crossveinless like 6 location: 1-59.1 (2.4 map units to the right of f). origin: Major component of a line selected by Mohler for crossveinless-like phenotype. references: Mohler, 1965, Genetics 51: 641-51. phenotype: Removes crossveins. Developmental sequence differs from that of cv and cvl-5; longitudinal veins form in time and manner expected of wild type; cvl-6 differs in that the wings begin vein development with a joining of the wing surfaces through the crossvein region; partial repair is accomplished by a secondary developmental sequence, including withdrawal of cell processes joining the wing surfaces at this position and subsequent reorganization of a crossvein around this gap (Mohler and Swedberg, 1964, Genetics 50: 1403-19). #*cvw: convex wing location: 1-58.2. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1953. references: 1958, DIS 32: 69. phenotype: Wings slightly shortened and arched convexly. Vari- able and may overlap wild type. Tergites in some females have serrated edges or are grossly deformed. Viability and fertil- ity good in both sexes. RK2. # cwi: crumpled wings location: 1-{0.5}. references: Zhimulev, Belyaeva, Fomina, Protopopov, and Bolshakov, 1986, Chromosoma 94: 492-504. phenotype: Crumpled wings? cytology: Placed in 2B7-10. # cx: curlex location: 1-13.6. origin: Spontaneous. discoverer: R. L. King, 1927. phenotype: Wings bent upward for posterior two-thirds of length; anterior one-third warped; margin kinked. Wings not spread. RK2. cytology: Placed in polytene region 5A-B by Lefevre. # cx: see c(3)G # cxtg: curlex-twisted genitalia origin: Spontaneous. discoverer: Curry, 37c19. phenotype: Wings always divergent, usually 45 from axis. Basal one-third of wing wavy but less so than in cx; posterior two- thirds of wing curled slightly upward or downward. Genitalia of nearly all males rotated, usually 45 counterclockwise. Flies dwarfish. Viability irregular. Male sterile. RK2. # cx-b: see wy2 # cxb: calyx bulging (J.C. Hall) location: 2-73. origin: Induced by ethyl methanesulfonate. synonym: cxbN71. references: Heisenberg, Borst, Wagner, and Byers, 1985, J. Neu- rogenet. 2: 1-30. phenotype: Calyces of mushroom bodies in dorsal brain of adult are enlarged and have abnormal shape; peduncles and lobes (projecting from these calyces) small or missing; ellipsoid body of central brain also aberrant in morphology; learning abnormal, in tests using olfactory stimuli. # CxD: see In(3LR)CxD # CxF,D: see In(3LR)DcxF Cy: Curly From L. Ward, 1923, Genetics 8: 276-300. # Cy: Curly location: 2-6.1 (removed from In(2L)Cy and located by Tin- derholt). origin: Spontaneous. discoverer: L. Ward, 20c. references: 1923, Genetics 8: 276-300 (fig.). phenotype: Wings curled upward; rarely overlaps wild type at 25, but frequently overlaps at 19. Curvature caused by the unequal contraction of the upper and lower epithelia during the drying period following emergence from the pupa case (Wad- dington, 1940, J. Genet. 41: 75-139). Flightless but thoracic innervation normal (Chiarodo, Reing, and Saranchak, 1971, J. Expt. Zool. 178: 325-30). Expression decreased by larval crowding, increased by increased temperature during pupal development (Nozawa, 1956, Jpn. J. Genet. 31: 161-71). Clas- sifiable in single dose in triploids. Usually homozygous lethal but may emerge as dwarf with more extreme wing charac- ter. Effective lethal phase late embryo-early larva (Kidwell, 1972, J. Hered. 63: 100). RK1A. alleles: CyM: Curly of Meyerowitz; Cyrv76, X-ray-induced rev- ersion of Cy in CyO (Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85). cytology: Placed in 22F4-23B2 on the basis of its being lethal in combination with Df(2L)DTD2 = Df(2L)22D4-5;23B1-2 but not Df(2L)DTD48 = Df(2L)22E2-4;22F-23A1 (Spencer, Hoffman, and Gelbart, 1982, Cell 28: 451-61). Ordinarily inseparable from In(2L)Cy = In(2L)22D1-2;33F5-34A1, although it was separated by Tinderholt (1961, DIS 35: 47). other information: Cy removed from In(2L)Cy still causes a local reduction in crossing over in the ed-cl region (Seder- off). # Cyclic AMP dependent protein kinase: see Pka # Cyclic GMP dependent protein kinase: see Pkg # Cyclic AMP Phosphodiesterase-2: see dnc # CycA: Cyclin A location: 3-{37}. synonym: l(3)68Ea; l(3)rsg11. references: Whitfield, Gonzalez, Sanchez-Herrero, and Glover, 1989, Nature 338: 337-40. Lehner and O'Farrell, 1989, Cell 56: 957-68. phenotype: Encodes cyclin, a molecule involved in the cell cycle; the pattern of transcription reflects this. Maternal message uniformly distributed in newly laid egg, but becomes more concentrated in the cortex prior to peripheral nuclear migration. At the time of cellularization of the blastoderm, zygotic message is produced. Cyclin A accumulates in the interphase cytoplasm of cellularized embryos, but relocates to the nuclear region early in prophase and is completely degraded during metaphase. A functional cyclin A gene is required for continued cell division after exhaustion of maternally provided cyclin A. Message confined to dividing tissues in brain and imaginal disks in larvae. alleles: allele origin discoverer synonym ref ( comments _____________________________________________________________ CycA1 EMS l(3)70-2 2 CycA2 EMS l(3)107.43 2 CycA3 EMS l(3)183 2, 3 molecular deletion CycA4 EMS l(3)V4-4 1, 2 CycA5 P Jan neo114 3 P insert present ( 1 = Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215-25; 2 = Hoogwerf, Akam, and Roberts; 3 = Lehner and O'Farrell, 1989, Cell 56: 957-68. cytology: Placed in 68E by in situ hybridization; included in Df(3L)vin3 = Df(3L)68C5-6;68D6 but not Df(3L)vin2 = Df(3L)67F2-3;68E3-4. molecular biology: Sequence isolated from a genomic library using a synthetic oligonucleotide based on conserved sequences of known cyclin genes. Detects a 2.3 kb transcript that is abundant in pre-cellularization embryos and in adult females; a 2.5 kb zygotically derived transcript appears after cellu- larization (Akam et al.). These transcripts are 2.5 and 3.0 kb respectively according to Lehner and O'Farrell. Akam et al. report three other transcripts detectable in pupae, of which one persists into adulthood. Lehner and O'Farrell report the sequence of a cDNA that contains a long open reading frame that encodes a 491-amino-acid protein, which displays 50% amino-acid identity to clam cyclin A and 34% identity to clam cyclin B. # CycB: Cyclin B location: 2-{100}. references: Whitfield, Gonzalez, Sanchez-Herrero, and Glover, 1989, Nature 338: 337-40. phenotype: Encodes cyclin, a molecule involved in the cell cycle; the pattern of transcription reflects this. Maternal message uniformly distributed in newly laid egg, but becomes concentrated at the posterior pole at the time of polar- nucleus migration; also evident in the cortex of the syncytial blastoderm. Larval message concentrated in the testis. cytology: Placed in 59A by in situ hybridization. molecular biology: Sequence isolated from a genomic library using a synthetic oligonucleotide based on conserved sequences of known cyclin genes. Detects a 2.3 kb transcript that is abundant in pre-cellularization embryos and in adult females; a 2 kb transcript is found in adult males. # Cyclin A: see CycA # Cyclin B: see CycB # Cyd: Curlyoid location: 3- (rearrangement). discoverer: Jollos. references: Curry, 1939, DIS 12: 46. phenotype: Wings curled upward in heterozygote, only slightly so in some flies; wings slightly reduced in size and dusky. In(3R)P,Cyd/+ has 2- to 3-day developmental delay (Craymer). Homozygous lethal. RK3. cytology: Associated with In(3R)P; no other aberration present (Craymer). # cyl: see rkcyl # Cyt-b: Cytochrome-b homologue location: 2-{52}. synonym: TU36B. references: Levin, Boychuk, Croniger, Kazzaz, and Rozek, 1989, Nucleic Acids Res. 17: 6349-67. phenotype: Encodes a cytochrome-b homologue that is expressed specifically in muscles; expression is concordant with that of Mhc. cytology: Placed in 36B based on its juxtaposition to Mhc. molecular biology: cDNA's cloned and sequenced; gene shown to have one intron. mRNA transcribed off of opposite strand from Mhc; poly(A) addition sites 99 nucleotides apart. Contains an open reading frame of 1242 nucleotides able to encode a polypeptide of 414 amino acids of 47 kd. Sequence shows 17.6% identity and 41% homology with yeast cytochrome-b2. # Cyt-c1 and Cyt-c2: Cytochrome c location: 2-{52}. origin: Isolated from a Charon-4 library using mouse cytochrome-c gene sequence as a probe. references: Limbach and Wu, 1985, Nucleic Acids Res. 13: 631- 44. phenotype: Apparently the structural genes for two cytochrome-c type enzymes, which differ from each other in 32/107 amino- acid residues. Cyt-c1 (sequence D3) expressed at constant, but relatively low, level throughout development; Cyt-c2 (sequence D4) expressed at varying, but relatively high, lev- els throughout development. Amino acid sequence also given in Handbook of Biochemistry and Molecular Biology: Proteins (Fas- man, ed.) CRC Press, Cleveland, Vol. 3, pp. 282-83. cytology: Placed in 36A10-11 by in situ hybridization. molecular biology: Sequences located within a 4 kb region of DNA. Sequence analysis indicates that both can encode func- tional cytochrome-c proteins. Cyt-c genomic clones also iso- lated, using Manduca sexta cDNA clone as probe, and sequenced by Swanson, Zieminn, Miller, Garber, and Margoliash (1985, Proc. Nat. Acad. Sci. USA 82: 1964-68).