# v: vermilion location: 1-33.0. discoverer: Morgan, 10k. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 27 (fig.). Schultz and Bridges, 1932, Am. Nat. 66: 323-32. Sturtevant, 1932, Proc. Intern. Congr. Genet., 6th, Vol. 1: 304-07. Offerman, 1935, DIS 3: 28. Beadle and Ephrussi, 1936, Proc. Nat. Acad. Sci. USA 22: 536-40. Sturtevant and Beadle, 1939, An Introduction to Genetics, W.B. Saunders Co., Philadelphia, p. 64 (fig.). Tatum and Beadle, 1939, Biol. Bull. 77: 415-22. Brehme and Demerec, 1942, Growth 6: 351-56. Green, 1952, Proc. Nat. Acad. Sci. USA 38: 300-05. Baglioni, 1959, Nature (London) 184: 1084-85. Green, 1959, Genetics 34: 564-72. Baglioni, 1960, Heredity 15: 87-96. Shapard, 1960, Genetics 45: 359-76. Kaufman, 1962, Genetics 47: 807-17. Rizki, 1963, J. Cell Biol. 16: 513-320. Marzluf, 1965, Genetics 52: 503-12. Rizki and Rizki, 1968, Genetics 59: 477-85. Tartof, 1969, Genetics 62: 781-95. Baillie and Chovnick, 1971, Mol. Gen. Genet. 112: 341-53. Jacobson, Grell, Yim, and Gardner, 1982, Genet. Res. 40: 19- 32. Searles and Voelker, 1986, Proc. Nat. Acad. Sci. USA 83: 404-08. Walker, Howells, and Tearle, 1986, Mol. Gen. Genet. 202: 102-07. Pastink, Vreeken, Nivard, Searles, and Vogel, 1989, Genetics 123: 123-29. phenotype: The v+ gene, expressed in the eyes, fat body, and Malpighian tubules of the wild type (Nissani, 1975, Genet. Res. 26: 63-72), is believed to code for the enzyme trypto- phane oxidase (also known as tryptophane pyrrolase)(EC 1.3.11.11), a 150,000 dalton protein that catalyzes the conversion of tryptophane into N-formylkynurenine. The eye color of v mutants is bright scarlet owing to absence of brown ommochrome; ocelli are colorless. Flies with the mutant com- bination y;w have white eyes. The eye color is wild type in genetically v eyes of gynandromorphs mosaic for wild type and v tissue (Sturtevant, 1932), indicating the non-autonomous nature of the vermilion gene. v eye disks develop wild-type pigmentation when transplanted into wild-type larvae (Beadle and Ephrussi, 1936). yw nuclei from preblastoderm stages implanted into the posterior end of a fertilized v;bw egg can produce a mosaic fly with brown eyes (Zalokar, 1973, Dev. Biol. 32: 189-93). The diffusuble v+ hormone of Beadle and Ephrussi involved in mosaic and transplantation experiments has been identified as kynurenine (Butenandt, Weidel, and Becker, 1940, Naturwissenschaften 28: 63-64). Activity of the inducible enzyme tryptophane oxidase is absent in v mutants (Baglioni, 1959, 1960). As a result, nonprotein tryp- tophane is accumulated in vermilion flies (Green, 1959) rather than converted into N-formylkynurenine and then into formic acid and kynurenine. In mutant larvae tryptophane in the fat body is not converted into kynurenine (Rizki, 1963; Rizki and Rizki, 1968). Certain v alleles (v1, v2, and vk) are suppressed by mutations at the su(s) locus; these mutants show wild-type eye color, fail to accumulate nonprotein trypto- phane, and partially restore tryptophane oxidase activity in spite of the mutation at v (Schultz and Bridges, 1932; Green, 1952; Baglioni, 1960; Shapard, 1960; Kaufman, 1962; Marzluf, 1965; Tartof, 1969; Jacobson et al., 1982); other v alleles (v36f, v48a, v51a, v51b, v51c, and vE1) show no change in the mutant eye color with these su(s) alleles and little or no increase in tryptophane oxidase activity (small increase observed in su(s) v36f flies). Some brown pigment is formed under conditions of partial starvation in suppressed v mutants (Tatum and Beadle, 1938; Shapard, 1960), but starvation has no effect on unsuppressed v alleles. alleles: The following table lists wild-type and mutant alleles. The revertants v+37 [Germeraad, 1976, Nature (Lon- don) 262: 229-31] and v36f+ (Green) are not described in the table. v deficiencies are listed as rearrangements. allele discoverer origin ref ( cytology ___________________________________________________________________ v1 Morgan, 10k spont 1-6, 17-19, 21, 22, 25, 27, 30, 32-39, 40-42 44, 46, 47, 51, 52, 53 v05 Fomina EMS 49, 50, 52, 53 v06 Fomina EMS 49, 50, 52, 53 v2 Plunkett, 24g spont 8, 19, 33, 35-38, 46, 53 v2B27 Belyaeva EMS 50, 53 v2B37 Belyaeva EMS 50, 53 v2B54 Belyaeva EMS 53 v2B157 Belyaeva EMS 50, 53 v2B160 Belyaeva EMS 50, 53 v2B162 Belyaeva EMS 50, 53 v2B165 Belyaeva EMS 50, 53 v2B195 Belyaeva EMS 50, 53 v2B206 Belyaeva EMS 50, 53 v2B207 Belyaeva EMS 50, 53 v2B236 Belyaeva EMS 50, 53 v2B237 Belyaeva EMS 50, 53 v8 Geer EMS 17, 45 v9 Geer EMS 17, 45 v10 Geer EMS 17, 45 v24 Loker EMS 9, 16 v36f Williams, 36f spont 8, 18-20, 21, 33, 35, 37, 41, 43, 45, 46, 52, 53 v48a Fox, 48a7 X ray 7, 11, 19, 33, 34, 41, 46, 53 *v51a Green X ray 19 v51b Green spont 19 v51c Green X ray 19, 33, 46, 53 v51g Edmondson, 51g U-V 26 v61j Goodwins 50, 53 v65c 6 v71P spont 37, 46 v74k Lim EMS 50, 53 v79i Najera spont 29a v80d Najera spont 29b v81d Najera spont 29, 29a v125 EMS 52 v127 Geer EMS 17, 45 v162 EMS 51 v166 EMS 51 v210 Geer EMS 17, 45 v216 Geer EMS 17, 45 v217 Geer EMS 17, 45 v219 Geer EMS 17, 45 v221 Geer EMS 17, 45 *v267-4 Hoover, 35i X ray T(1;2)11A7-8;36 v+63i Lefevre 11, 17, 22, 24, Dp(1;2)9E1; 49, 50, 54 10A11;56A v+65b Lefevre 11, 17, 22, Tp(1;2)10A1; 24, 45, 54 11A7-8;40-41 v+74c Lefevre 11, 28 Tp(1;3)9E3-4; 11B12;80-81 v+75d Lefevre 11, 17, 22, 45 Tp(1;2)9A2; 10C2;40-41 v* Fox, Yoon DNA 12-15 vA Anderson 1-3, 23, 48-50, T(1;3)10A1-2; 93B7-10 52, 54 vAE111 Belyaeva EMS 49, 50, 52 vAM1 Pokholkova EMS 49, 50, 52, 53 vB1 Bgatov X ray 50, 53 vB84 X ray 53 vB85 X ray 53 vB86 X ray 53 vB126 X ray 53 vB127 X ray 53 vB150 X ray 53 vB152 X ray 53 vB153 X ray 53 vB154 X ray 53 vBN Zhimulev EMS 49, 50, 52, 53 vDK EMS 49, 50, 52, 53 vdpG1 Zhimulev EMS 50, 52, 53 vdpZ1 Baritcheva EMS 49, 50, 52, 53 vdpZ2 Baritcheva EMS 49, 50, 52, 53 vdpZ7 Baritcheva EMS 49, 50, 52, 53 vE1 Schalet EMS 6, 35 vE37 Belyaeva EMS 49, 50, 51, 53 vE57 Belyaeva EMS 49, 50, 51, 52, 53 vE63 Belyaeva EMS 49, 50, 51, 52, 53 vE70 Belyaeva EMS 49, 50, 51, 52, 53 vE73 Belyaeva EMS 51 vE76 Belyaeva EMS 49, 50, 52, 53 vE78 Belyaeva EMS 49, 50, 51, 52, 53 vE82 Belyaeva EMS 49, 50, 52, 53 vE84 Belyaeva EMS 49, 50, 52, 53 vE107 Belyaeva EMS 49, 50, 52, 53 vE110 Belyaeva EMS 49, 50, 52, 53 vE115 Belyaeva EMS 51 vE118 Belyaeva EMS 49, 50, 52, 53 vE119 Belyaeva EMS 49, 50, 52, 53 vE124 Belyaeva EMS 49, 50, 52, 53 vE128 Belyaeva EMS 51 vE129 Belyaeva EMS 49, 50, 52 vE143 Belyaeva EMS 51 vE146 Belyaeva EMS 49, 50, 53 vE147 Belyaeva EMS 51 vE154 Belyaeva EMS 49, 50, 52, 53 vE158 Belyaeva EMS 49, 50, 52, 53 vE160 Belyaeva EMS 49, 50, 52, 53 vE184 Belyaeva EMS 49, 50, 52, 53 vE195 Belyaeva EMS 49, 50, 53 vESB Belyaeva EMS 49, 50, 53 vF1 Pokholkova EMS 53 vF2 Pokholkova EMS 53 vF3 Pokholkova EMS 53 vF4 Pokholkova EMS 53 vF5 Pokholkova EMS 53 vF6 Pokholkova EMS 53 vF7 Pokholkova EMS 53 vF8 Pokholkova EMS 53 vF9 Pokholkova EMS 53 vF10 Pokholkova EMS 53 vF11 Pokholkova EMS 53 vF12 Pokholkova EMS 53 vF13 Pokholkova EMS 53 vF14 Pokholkova EMS 53 vF15 Pokholkova EMS 53 vF16 Pokholkova EMS 53 vF17 Pokholkova EMS 53 vF303 Pokholkova EMS 50, 53 vF308 Pokholkova EMS 50, 53 vF364 Pokholkova EMS 50, 53 vG50 Belyaeva EMS 51, 52 vG57 Pokholkova EMS 49, 50, 52, 53 vG64 Pokholkova EMS 49, 50, 52, 53 vG73 Pokholkova EMS 49, 50, 52, 53 vG90 Pokholkova EMS 49, 50, 52, 53 vG92 Belyaeva EMS 51 vG99 Belyaeva EMS 51 vG100 Pokholkova EMS 49, 50, 52, 53 vG117 Pokholkova EMS 49, 50, 52, 53 vG118 EMS 53 vG119 EMS 53 vG121 Pokholkova EMS 49, 50, 52, 53 vG126 Pokholkova EMS 49, 50, 52, 53 vG130 Belyaeva EMS 51 vH2a Kidwell HD 37 vIE109 Belyaeva EMS 51 vJ9 Khudyakov EMS 49, 50, 52, 53 vJ20 Belyaeva EMS 51 vJ25 Khudyakov EMS 49, 50, 52, 53 vJ26 Khudyakov EMS 50 vJ27 Khudyakov EMS 50, 53 vJ28 Khudyakov EMS 50, 53 vJ29 Khudyakov EMS 50, 53 vk X ray 6, 33, 35, 37, 38, 41, 46 vL1 Lefevre X ray 12, 17, 24, 50, 54 T(1;3)3E1-2; 90C9-11 + Df(1)10A1-2; 10A4-5 vL8 Lefevre X ray 22 T(1;2)9D3-4; 10A1-2;25E-F + T(1;3)3E5;62D vL13 Lefevre X ray 24 T(1;3)9B13-14; 10A1-2;64F vM4 Kochneva X ray 50, 53 vM8 Kochneva X ray 50, 53 vN48 Schalet Neutron 45 Tp(1;1)9F; 10C3-5;20 vNK Zhimulev EMS 49, 50, 52, 53 vNN Zhimulev EMS 49, 50, 52, 53 vOf Offerman X ray 31, 53 In(1)dl49 vOS Zhimulev EMS 49, 50, 52, 53 vP30 X ray 53 vP31 X ray 53 vP32 X ray 53 vP33 X ray 53 vP34 X ray 53 vP35 X ray 53 vP36 X ray 53 vs15-1 Golubovsky 50, 53 vs16 Golubovsky spont 50, 51, 53 vtm1 50, 53 vtm2 50, 53 vts EMS 10 vu | Pastink ENU 31a ( 1 = Anderson, 1925, Papers Mich. Acad. Sci. 5: 355-66; 2 = Anderson, 1926, Papers Mich. Acad. Sci. 7: 273-78; 3 = Anderson, 1929, Z. Indukt. Abstamm. Vererbungsl. 51: 397-411; 4 = Baglioni, 1959, Nature (London) 184: 1084-85; 5 = Baglioni, 1960, Heredity 15: 87-96; 6 = Baillie and Chovnick, 1971, Mol. Gen. Genet. 112: 341- 53; 7 = Barish and Fox, 1956, Genetics 41: 45-57; 8 = Brehme and Demerec, 1942, Growth 6: 351-56; 9 = Busson, Gans, Komitopoulou, and Masson, 1983, Genetics 105: 309- 325; 10 = Camfield and Suzuki, 1973, Genetics 74: s37; 10a = CP627; 11 = Craymer and Roy, 1980, DIS 55: 200-04; 12 = Fox, 1948, DIS 22: 53; 13 = Fox, 1949, Genetics 34: 647-64; 14 = Fox and Valencia, 1973, Genetics 74: s83; 15 = Fox and Yoon, 1970, Proc. Nat. Acad. Sci. USA 67: 1608-16; 16 = Gans, Audit, and Masson, 1975, Genetics 81: 683-704; 17 = Geer, Lischwe, and Murphy, 1983, J. Exp. Zool. 225: 107-18; 18 = Green, 1949, Genetics 34: 564-72; 19 = Green, 1952, Proc. Nat. Acad. Sci. USA 38: 300-05; 20 = Green, 1954, Proc. Nat. Acad. Sci. USA 40: 92-99; 21 = Kaufman, 1962, Genetics, 47: 807-17; 22 = Lefevre, 1969, Genetics 63: 589-600; 23 = Lefevre, 1970, DIS 45: 39; 24 = Lefevre, 1971, Genetics 67: 497-513; 25 = Marzluf, 1965, Genetics 52: 503-12; 26 = Meyer and Edmondson, 1951, DIS 25: 74; 27 = Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 27 (fig.); 28 = Mortin and Lefevre, 1981, Chromosoma 82: 237-47; 29 = Najera, 1984, DIS 60: 241-42; 29a = Najera, 1985, DIS 61: 215; 29b = Najera, 1986, DIS 63: 167; 30 = Nissani, 1975, Genet. Res. 26: 63-72; 31 = Offerman, 1935, DIS 3: 28; 31a = Pastink, Vreeken, Nivard, Searles, and Vogel, 1989, Genetics 123: 123-29; 32 = Rizki and Rizki, 1963, J. Cell Biol. 17: 87-89; 33 = Rizki and Rizki, 1968, Genetics 59: 477-85; 34 = Rizki, Soliman, Rizki, Friedman, and Healy, 1970, Genetics 64: 459-69; 35 = Schalet, 1971, DIS 46: 135; 36 = Schultz and Bridges, 1932 , Am. Nat. 66 : 323-32; 37 = Searles and Voelker, 1986, Proc. Nat. Acad. Sci. USA 83: 404-08; 38 = Shapard, 1954, Genetics 39: 992-93; 39 = Sturtevant, 1932, Proc. Intern. Congr. Genet. 6th, Vol. 1: 304-07; 40 = Sturtevant and Beadle, 1939, An Introduction to Genetics, W.B. Saunders Co., Phi- ladelphia, p. 64; 41 = Tartof, 1969, Genetics 62: 781-95; 42 = Tatum and Beadle, 1939, Biol. Bull. 77: 415-22; 43 = Tobler, Bowman, and Simmons, 1971, Biochem. Genet. 5: 111-17; 44 = Voelker, Chang, Huang, and Wisely, 1984, Genetics 107: s111-12; 45 = Voelker, Wisely, Huang, and Gyurkovics, 1985, Mol. Gen. Genet. 201: 437-45; 46 = Walker, Howells, and Tearle, 1986, Mol. Gen. Genet. 202: 102-07; 47 = Wehner, Gartenmann, and Jungi, 1969, J. Insect Physiol. 15: 815-23; 48 = Zhimulev, Belyaeva, Khu- dyakov, and Pokholkova, 1980, DIS 55: 211; 49 = Zhimulev, Belyaeva, Pokholkova, Kochneva, Fomina, Bgatov, Khudyakov, Patzevich, Semeshin, Baritcheva, Aizenzon, Kramers, and Eeken, 1981, DIS 56: 192-96; 50 = Zhimulev, Belyaeva, Pokholkova, Kochneva, Fomina, Bgatov, Khudyakov, Patzevich, Semeshin, Baritcheva, Aizenzon, Kramers, and Eeken, 1982, DIS 58: 210-14; 51 = Zhimulev, Belyaeva, Semeshin, Bgatov, and Baritcheva, 1980, Genetika 16: 1404-24; 52 = Zhimulev, Pokholkova, Bgatov, Semeshin, and Belyaeva, 1981, Chromo- soma, 82: 25-40; 53 = Zhimulev, Pokholkova, Bgatov, Umbetova, and Belyaeva, 1987, DIS 66: 194-9; 54 = Zhimulev, Semeshin, and Belyaeva, 1981, Chromosoma, 82: 9-23. | Twenty-five alleles; see table in molecular biology. cytology: Left part of the 10A1-2 band between the X breakpoint of T(1;Y)B149 = T(1;Y)10A1-2;YL and the proximal break of Df(1)v-L4 = Df(1)9F5-6;10A1-2 (Green, 1954, Proc. Nat. Acad. Sci. USA 40: 92-99; Lefevre, 1969, Genetics 63: 589-60; Zhimulev, Belyaeva, Pokholkova, Kochneva, Fomina, Bgatov, Khu- dyakov, Patzevich, Semeshin, Baritcheva, Aizenzon, Kramers, and Eeken, 1982, DIS 58: 210-14). Also located in 10A by in situ hybridization (Searles and Voelker, 1986). molecular biology: Gene cloned using the vH2a allele with a P element insertion (Searles and Voelker, 1986); v+ allele also cloned. A 1.4 kb transcript is present in v+ RNA. Mutations that disrupt the wild-type expression of v are grouped within approximately 2 kb of DNA. Five mutant alleles previously located on the genetic map by fine structure mapping (Schalet, 1971, DIS 46: 135-36; Baillie and Chovnick, 1971, Mol. Gen. Genet. 112: 341-53) have been located on the molecular map of v (Searles and Voelker, 1986). The suppressible alleles v1, v2, and vk, inseparable by recombination, appear to be identi- cal insertions of the transposable element 412. v36f, mapping about 0.7 kb to the right of v1, is a roo insertion. v48a, which lies to the left of v36f on the molecular map, is a 200-bp deletion in the same restriction fragment as v1. Base-pair changes were observed in 25 ENU mutants that have been cloned and sequenced (Pastink et al., 1989). The follow- ing table summarizes the mRNA and amino acid changes in these mutant alleles: allele position mRNA change amino acid change ____________________________________________________ vu101 624 GC -> AT gly -> ser vu103 365 GC -> AT trp -> UGA vu106 58 GC -> AT splice vu107 ( 988 AT -> GC his -> arg 1053 AT -> GC ile -> val vu108 1014 GC -> AT arg -> cys vu111 1430 GC -> AT asp -> asn vu113 372 GC -> AT gln -> UAG vu114 838 GC -> AT trp -> UAG vu150 1331 GC -> AT ser -> asn vu151 1048 AT -> CG ile -> ser vu152 468 GC -> AT val -> met vu153 ( 912 AT -> TA lys -> UAG 936 GC -> CG asp -> his vu155 ( 585 GC -> AT asp -> asn vu156 224 GC -> TA gln -> his vu158 1322 GC -> AT ser -> phe vu159 285 GC -> AT his -> tyr vu161 207 AT -> TA lys -> UAA vu164 1126 GC -> AT ser -> leu vu166 1316 AT -> GC leu -> pro vu167 1322 GC -> AT ser -> phe vu168 796 AT -> GC leu -> pro vu171 1017 GC -> AT arg -> trp vu174 1117 AT -> GC asp -> gly vu177 351 GC -> AT splice vu185 1122 GC -> AT asp -> asn ( Two base-pair changes. other information: Hereditary reversion of the eye color of v mutants to that of wild-type flies by treatment of permeable eggs with DNA (Fox and Yoon, 1970, Proc. Nat. Acad. Sci. USA 67: 1608-15) has been described. Later, v1 was reverted by microinjection of wild-type DNA (Germeraad, 1976). #*Va: Venae abnormeis location: 2- (not located). discoverer: Timof'eff-Ressovsky. references: 1927, Wilhelm Roux's Arch. Entwicklungsmech. Organ. 109: 70-109 (fig.). Roelofs, 1937, Genetica 19: 518-36. phenotype: Veins irregularly branched or interrupted. Hetero- zygote overlaps wild type in 50% of flies. RK3. #*vac: vacuolated location: 1-58.5. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1955. references: 1958, DIS 32: 77. phenotype: Wings blistered; character varies from small vacuole to involvement of entire wing. At least one wing affected in 95% of flies. Viability and fertility good. RK2. cytology: Located in 19E7-8. # vacuolar pendunculi: see vap # Vacuolar medulla: see Vam # vacuolated: see vac # Vaja: see Fs(2)Sz13 # valois: see vls # Vam: Vacuolar medulla (J. C. Hall) location: 1-50.6 (between v and f). origin: Induced by ethyl methanesulfonate. references: Heisenberg and Bohl, 1978, Z. Naturforsch. 34: 143-47. Coombe, 1984, J. Comp. Physiol. 155: 661-72. 1986, J. Comp. Physiol. 159: 655-65. Coombe and Heisenberg, 1986, J. Neurogenet. 3: 135-58. phenotype: Mutants show many vacuoles in the distal part of the medulla. Appearance of vacuoles age-dependent, first appearing in homo- and hemizygotes half an hour after eclosion and occurring in 100% of these mutants after one hour. In older flies, vacuoles are often visible in the lamina and lobula, and occasionally in the central brain. Lamina monopolar neu- rons L1 and L2 start to degenerate at eclosion and soon after- wards electroretinogram transients disappear. All hemi- or homozygous mutant flies appear nearly blind in tests of move- ment detection (optomotor response to vertical or horizontal movement and landing response lost). Fixation to a broad stripe has higher light intensity threshold in Vam than in wild type (Coombe, 1984). These behavioral defects, but not the anatomical aberrations, have full penetrance (Coombe and Heisenberg, 1986). In heterozygotes, vacuoles make their first appearance in the distal medulla about six days after eclosion and the heterozygous flies show much less lamina degeneration than the homozygotes, the anatomical defects being semi-dominant. Mosaic analysis (Coombe and Heisenberg, 1986) showed the vacuolization to be independent of eye geno- type and the degeneration to be sometimes unilateral. Fate mapping leads to a ventral (blastoderm) focus. alleles: Only one mutant allele, isolation number KS74, which is semi-dominant. cytology: Probably located to the right of 13A5 since not uncovered by Df(1)KA9 = Df(1)12E1;13A5. # vao: varied outspread location: 1- {64} (between lf and unc). Symbol originally used by Fahmy for a mutant (now lost) associated with In(1)vao (see CP627); now used for the phenotype shown by Df(1)A118/Df(1)Q539 females lacking 19E7. discoverer: Fahmy, 1953 (mutant); Schalet and Finnerty, 1970 (deficiency). references: Fahmy, 1959, DIS 33: 94. Schalet and Finnerty, 1970, DIS 45: 77. Schalet, 1972, DIS 49: 36-37. Schalet and Lefevre, 1973, Chromosoma 44: 183-202. Schalet and Lefevre, 1976, The Genetics and Biology of Droso- phila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 848-902. Miklos, Healy, Pain, Howells, and Russell, 1984, Chromosoma 89: 218-27. Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31. phenotype: Wings outspread. Eye color mottled brown. Male sterile. Viability poor. alleles: No point mutations defined yet (Perrimon et al., 1989). cytology: Placed in 19E7 since the heterozygous combination of the overlapping deletions Df(1)A118 = Df(1)19E4-5;19E7-8 and Df(1)Q539 = Df(1)19E6;19F6-20A1 reveals the vao phenotype (Schalet and Finnerty, 1970; Schalet, 1972; Miklos et al., 1984). Flies with the heterozygous combination of Df(1)B57 = Df(1)19E1-2;19F1 and Df(1)Q539 show the vao wing and eye abnormalities (plus the unc phenotype) at 24 - 25, but the flies have normal eyes at 17 - 18 (Schalet, 1972). # vap: vacuolar pedunculi (J. C. Hall) location: 1-54.2. origin: Induced by ethyl methanesulfonate. references: Heisenberg, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York and London, pp. 373-90. phenotype: Isolated as a neuro-anatomical mutant (Heisenberg and Bohl, 1979, Z. Naturforsch. 34: 143-47). Mutant shows vacuolar spaces at a certain depth along the pedunculi of the mushroom bodies as if extrinsic cells are undergoing degenera- tion. Intrinsic fibers appear continuous. Viability of mutants reduced (Heisenberg). alleles: One allele, isolation number KS67. # Var34k22: see bw34k # Varas: see Fs(3)Sz24 # variable size and shape: see vss # varied outspread: see vao # varnished: see vr # vas: vasa (T. Schupbach) location: 2- {51}. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 302-17. Nusslein-Volhard, Frohnhofer, and Lehmann, 1987, Science 238: 1675-81. Hay, Jan, and Jan, 1988, Cell 55: 577-87. Lasko and Ashburner, 1988, Nature (London) 335: 611-17. Schupbach and Wieschaus, 1989, Genetics 121: 101-17. phenotype: Maternal-effect lethal. Embryos from homozygous mothers exhibit a so-called "grandchildless-knirps" phenotype: all eggs lack polar granules and no pole cells are formed; most of the embyros show large deletions of abdominal seg- ments, whereby anterior parts of segment A1 become fused to posterior parts of segment A8. Telson elements are always present and relatively normal. Eggs have abnormal shape. Analysis of germline clones indicates that the mutation is germline autonomous (Schupbach and Wieschaus, 1986, Dev. Biol. 113: 443-448). Homozygous vasa males cannot be distinguished from wild-type males in viability and fertility. alleles: Seven (vasa1 through vasa7); isolated as PD, B5, D1, O11, O14, Q6 and Q7. cytology: Placed in 35C1-2 on the basis of molecular informa- tion (Lasko and Ashburner, 1988); uncovered by Df(2L)TE35BC-29 = Df(2L)35A3;35C1, but not by Df(2l)64j = Df(2L)34D1-2;35B9- C1, which deletes sequences distal to vasa, or by Df(2L)TE35D-4 [Df(2L)TE116-GW4], which deletes sequences prox- imal to the gene. molecular biology: Gene cloned and the cDNA sequenced (Lasko and Ashburner, 1988; Hay et al., 1988); relatively complex, with seven exons and five small introns between 36 and 70 nucleotides in length and one large intron of 3,700 nucleo- tides. The major transcript is 2.0 kb long and is found in the female germ line and early embryos only; it codes for a protein of 650 amino acids. The distribution of this protein is generalized before division, but increases at posterior pole as division proceeds (Ashburner). The predicted amino acid sequence is very similar to that of the murine transla- tion initiation factor eIF-4A and the human nuclear antigen p68 (Lasko and Ashburner, 1988). The amino-terminal region carries five tandem heptad repeats (Hay et al., 1988). # vb: vibrissae location: 1-49.3 (Bridges); 1-54.8 (Waddle, Monk, and Willi- ams). discoverer: Bridges, 25l22. phenotype: Vibrissae form tufts of bristles beneath eyes. Overlaps wild type. RK2. vb: vibrissae From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 212. # vb2 origin: X ray induced. discoverer: Muller, 26l. other information: Associated with In(1)sx (Craymer, 1980, DIS 55: 197-200). #*Vc: Vortice location: Autosomal. origin: Spontaneous. discoverer: Smith, 37c20. references: Novitski, 1937, DIS 8: 10. phenotype: Enhances dp/dp to give phenotype like hy. Homozy- gous lethal. RK3. ve: veinlet From Duncan, 1935, Am. Naturalist 69: 94-96. # ve: veinlet (E. Bier) location: 3-0.2; to the right of ru (Roberts and Evans-Roberts, 1979, Genetics 93: 663-79; Robertson and Riviera, 1972, DIS 48: 21). synonym: rho: rhomboid. references: Duncan, 1935, Am. Nat. 69: 94-96. Waddington, 1939, Proc. Nat. Acad. Sci. USA 25: 305. 1940, J. Genet. 41: 75-139. Bertschmann 1955, DIS 29: 69-70. Thompson, 1976, Genetics 81: 387-402. Thompson and Thoday, 1976, Genetics 83: s76. Thompson, 1977, DIS 52: 76. Spivey and Thompson, 1984, Genetics 107: s102. Jurgens, Weischaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol 193: 283-95. Mayer and Nusslein-Volhard, 1988, Genes Dev. 2: 1496-1511. Bier, Jan, and Jan, 1990, Genes Dev 4: 190-203. Diaz-Benjumea and Garcia-Bellido, 1990, Wilhelm Roux's Arch. Dev. Biol 198: 336-54. phenotype: Viable alleles exhibit wing venation defects; strong alleles are embryonic lethal. In flies homozygous for viable alleles the L3, L4, and L5 veins do not reach the wing margins (Duncan; Waddington). Developmentally, veins appear complete in prepupa but distal tips are obliterated during the contrac- tion period (Waddington, 1939, 1940). The shortened-vein phenotype is suppressed by px (Waddington), net, and su(ve), and is enhanced by vn, H, Ax, ci, tg2, and ri (Waddington; Diaz-Benjumea and Garcia-Bellido, 1990, Wilhelm Roux's Arch. Dev. Biol 198: 336-54.). Vein-specific modifiers, such as gp, (Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 208) or PL(2)L4a (Thompson, 1976), interact with the effect of ve on L4. The L5 vein seldom extends beyond the posterior crossvein. ve2 is a stronger allele, in which the L2 is also affected (Bertschmann); L2 vein occasion- ally complete (Thompson, 1976), but other veins do not overlap wild type. Distribution of sense organs (campaniform sensilla and bristles) on L3 is shifted proximally in ve (Spivey and Thompson) When a ve stock is selected for shortened veins, the F1 produced by mating wild-type males to mutant females show terminal gaps in L5 (Thompson and Thoday, 1976). ve/ve/+ intersexes are veinlet, whereas ve/ve/+ triploids are normal, according to Pipkin. Interestingly flies heterozygous for ve and strong embryonic lethal alleles display less severe vein- let phenotypes than ve homozygotes (Bier et al.; Diaz-Benjumea and Garcia-Bellido); furthermore, ve1/ve5 flies appear wild type (Bier, unpublished). Homozygous ve5 embryos exhibit three major types of defects: (1) Dorsoventral defects: Embryos exhibit a deletion of epithelial cells derived from a ventrolateral strip of the blastoderm fate map (i.e., loss of mediolateral cuticular denticles and sensory structures). Other phenotypes resulting from blastoderm patterning defects include failure to complete dorsal closure and development of an abnormal pointed head skeleton (Jurgens et al.; Mayer and Nusslein-Volhard). (2) Midline defects: Mesectodermal cells giving rise to glia and unpaired neurons are abnormal or fail to form. Late developmental consequences include a narrower CNS and pathfinding abnormalities (Mayer and Nusslein- Volhard). (3) Peripheral-nervous-system defects: Two stretch receptor organs (lateral abdominal chordotonal organs) fail to form in lethal ve mutants. The primary chordotonal-organ- precursor cells are likely to be affected since the four pro- geny sensory-organ cells derived from that precursor cell are missing as a group (Bier et al.). Other late embryonic defects include loss of longitudinal body-wall muscles, ven- trally displaced muscle-attachment sites (Bier et al.), and loss of the first row of denticles in abdominal segments (Mayer and Nusslein-Volhard). alleles: allele origin discoverer synonym ref ( comments ______________________________________________________________________________ ve1 spont Duncan, 34a 4 viable; wing veins do not reach margins ve2 spont Bertschmann 4 viable; like ve1 but stronger ve3 Waddle 6 L4 longer than in ve1; ve1/ve3 distinguishable from ve1 or ve2 ve4 EMS Jurgens rho7M43 5 strong allele; embryonic lethal ve5 P-lacw Bier rholac1 2 weak allele; insertion rho6-63a embryonic lethal ve6 | Bier rhodel1 2 strong allele rhorev37 embryonic lethal ve7 / Diaz- veM1 3 lethal Benjumea ve8 / Diaz- veM2 3 lethal Benjumea ve9 / Diaz- veM3 3 lethal Benjumea ve10 / Diaz- veM4 3 lethal Benjumea ve11 / Diaz- veM5 3 lethal Benjumea ( 1 = Bertschmann, 1955, DIS 29: 69-70; 2 = Bier, Jan, and Jan, 1990, Genes and Dev 4: 190-203; 3 = Diaz-Benjumea and Garcia-Bellido, 1990, Roux's Arch. Dev. Biol 198: 336-54; 4 = Duncan, 1935, Am. Nat. 69: 94-96; 5 = Mayer and Nusslein-Volhard, 1988, Genes Dev. 2: 1496-1511; 6 = Waddle and Oster, 1973, DIS 50: 23. | Transposase induced deletion of P-lacw from ve4. / EMS or X rays? cytology: 62A by in situ hybridization with a rho probe (Bier et al.). Also placed in 61B-62D interval on the basis of ve's being covered by Dp(3;Y)H141 = Dp(3;Y)61B;62D (Jurgens et al.). molecular biology: Genomic clones have been obtained by plasmid rescue of P-lacw from ve4 flies (Bier et al.). Sequence analysis of cDNA clones corresponding to a 2.5 kb mRNA indi- cates the mature mRNA is comprised of a 5' noncoding exon and two coding exons. An open reading frame encodes a predicted membrane protein of 355 amino acids. The pattern of ve tran- cription, as monitored by whole mount tissue in situ hybridi- zation, correlates well with the spatial requirement for ve function: (1) Blastoderm expression includes two longitudinal strips of cells corresponding in location to the domain of the fate map dependent on ve function for proper dorso-ventral patterning. Expression in the cells corresponding to head and dorsal cells may also coincide with cells involved in head skeleton formation and dorsal closure. (2) As ventral furrow formation proceeds expression becomes limited to a single row of mesectodermal cells which give rise to the glial and neu- ronal cells along the ventral midline which are affected in lethal mutant embryos. (3) ve is expressed in a single cell per hemisegment at the germband extended stage, which is likely to be the precursor for the chordotonal organs missing in lethal mutants. When the germ band is nearly retracted, ve is expressed in rows of cells at the anterior margin of each body segment. This expression may correlate with loss of the first row of denticles in lethal mutants. # vein: see vn # Vein: see Vn # vein off: see iabvno under BXC # veinlet: see ve # veins longitudinally shortened: see vli #*Vel: Velvet location: 1- or 3- (rearrangement). discoverer: Patterson, 1933. phenotype: Hairs on eyes conspicuous. RK3A. cytology: Associated with T(1;3)Vel; breakpoints unknown. #*ven: venation location: 3- [right arm associated with In(3R)P]. origin: Spontaneous. discoverer: Bridges, 33g18. references: 1937, DIS 7: 17. Bridges and Bridges, 1938, Genetics 23: 111-14. phenotype: Veins irregularly thickened and branched, especially L3 and crossveins. Eyes bulging and bright. Bristles gnarled. Body small. Often sterile. RK3A. # Ven: see Fs(3)Sz31 # Venae abnormeis: see Va # venation: see ven # Vencellin: see Fs(3)Sz31 # ventral nervous system defective: see vnd # ventral veins lacking: see vvl # venula: see vnl # vermilion: see v # verthandi: see vtd # vertical wing: see vtw # verticals: see vt #*ves: vestigium location: 1-1.4. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 77. phenotype: Wings abnormal, vary from small and curved to almost normal with cut-away inner margins. Eyes slightly rough and abnormally shaped. Male infertile; viability about 50% nor- mal. RK2. alleles: One allele induced by CB. 3025. # vesiculated: see vs # vestar: see vst # vestigial: see vg # vestigium: see ves