# vg: vestigial location: 2-67.0. references: Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 150. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 59, 232. Chen, 1929, J. Morphol. 47: 135-99. Mohr, 1932, Proc. Int. Congr. Genet., 6th, Vol. 1: 190-212. Goldschmidt, 1935, Biol. Zentralbl. 55: 535-54. Auerbach, 1936, Trans Roy. Soc. Edinburgh 58: 787-815. Harnly, 1936, J. Exp. Zool. 74: 41-59. Goldschmidt, 1937, Univ. Calif. Publ. Zool. 41: 277-82. Morgan, Bridges, and Schultz, 1938, Year Book - Carnegie Inst. Washington 37: 305-06. Waddington, 1939, Proc. Nat. Acad. Sci. USA 25: 299-307. Green and Oliver, 1940, Genetics 25: 584-92. Waddington, 1940, J. Genet. 41: 75-139. Green, 1946, Genetics 31: 1-20. Waddington, 1953, J. Genet. 51: 243-58. Fristrom, 1968, J. Cell Biol. 39: 488-91. 1969, Mol. Gen. Genet. 103: 363-79. David, Javellot, and Touzet, 1970, DIS 45: 33. Bryant and Girton, 1980, Development and Neurobiology of Dro- sophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York and London, pp. 109-27. Carson, Ferriola and Schuchman, 1980, DIS 55: 23-24. Girton and Bryant, 1980, Dev. Biol. 77: 233-43. Bownes and Roberts, 1981a, J. Embryol. Exp. Morphol. 65 (Suppl.): 49-76. 1981b, Differentiation 18: 89-96. James and Bryant, 1981, Dev. Biol. 85: 39-84. Simpson, Lawrence, and Maschat, 1981, Dev. Biol. 84: 206-11. O'Brochta and Bryant, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 285-94. Lasko and Pardue, 1988, Genetics 120: 495-502. Williams and Bell, 1988, EMBO J. 7: 1355-63. Williams, Pappu, and Bell, 1988a, Mol. Cell. Biol. 8: 1489- 97. 1988b, Mol. Gen. Genet. 212: 370-74. Williams, Atkin, and Bell, 1990, Mol. Gen. Genet. 221: 8-16. Williams, Scott, Atkin, Brooks, Russell, and Bell, 1990, Genetics 25: 833-44. phenotype: The vestigial locus seems to be mainly involved in the development of the wing margin. The mutants are recessive viable (with or without a visible phenotype), recessive lethal, or dominant (with a visible phenotype over wild type or a vg allele); some alleles complement each other; others show pleotropic effects or homeosis (Bownes and Roberts, 1981). In the classical vg mutants, the wings of homozygotes are reduced to vestiges and usually held at right angles to the body, the wing veins still visible. Some mutants have narrow, nicked, or scalloped wings. Halteres may be reduced or absent. Postscutellar bristles are frequently held erect. Viability is somewhat reduced; null mutants are sterile. Tem- peratures of 29 or greater appreciably increase wing size (Harnly, 1936, Genetics 21: 84-103; Stanley, 1935, J. Exp. Zool. 69: 459-95). A suppressor of vg on the third chromo- some, su(vg), results in an almost normal phenotype at 28, an intermediate vg phenotype at 25, and a strong vg phenotype (in wings and especially halteres) under 20 (David, et al., 1970). vg/+ heterozygotes with certain Minutes show scalloping of the wings (Green and Oliver, 1940; Simpson et al., 1981). vg/vg/+ has scalloped wings more often than vg/+ (Green, 1946). Final size of larva is smaller than in wild type and pupation occurs slightly later. Wing disks of late larva are also somewhat smaller than in wild type (Auerbach, 1936), as are haltere disks (Chen, 1929). Goldschmidt (1935, 1937) claimed that wings are more or less fully formed and subse- quently eroded by degeneration during pupation. Waddington (1939, 1940) found no evidence of erosion and concluded that the effect of the gene occurs during the larval period and involves reduction in size of prospective wing area and shift in position of line along which wing area is folded out from the imaginal disk. Fristrom (1968, 1969), however, using both light and electron microscopy, found numerous degenerating cells in the presumptive wing blade region of the vg wing disks, as did Bryant and Girton (1980), Bownes and Roberts (1981a, 1981b), James and Bryant (1981), and O'Brochta and Bryant (1983). Duplications of the mesonotum along with defi- ciences of wing disk material occur in a small percentage of vg mutants (Girton and Bryant, 1980; James and Bryant, 1981). vg1: vestigial From Bridges and Morgan, 1919, Carnegie Inst. Wash. Publ. No. 278: 148. vgno: vestigial-notched From Mohr, 1932, Proc. Intern. Congr. Genet. 6th Vol. 1: 190- 212. alleles: Mutant vg alleles are listed in the following tables. vg deficiencies are described in the rearrangement section. Table I symbol name origin discoverer synonym ref ( comments ___________________________________________________________________________________________________________________________________________________________ vg1 vestigial spont Morgan, 101 vgBG 2, 5, 7, wings, halteres reduced; 8, 38-40, small wing disks 45-47 *vg2 spont Ward, 1920 43 wings, halteres absent or reduced to knobs; low viability; females and males (usually) sterile *vg11 X ray Ruch, 1931 26 wings, halteres smaller than in vg1; some wing nicks in vg11/+; fertile vg12 / ray Lasko vg82h10 18, 45-46 like vg1; vg12/Df inviable vg17 EMS Lasko vg82E28 18 like vg1 vg18 / ray Lasko vg82h11 18, 45 like vg1 vg21 HD 45-48 cytotype-dependent allele; 1988 homozygote normal; weak vg over vg1 *vg33k spont Ives, 33k30 30, 31 like vgNo1 vg34 EMS Lasko vg82h15 18 like vg1 *vg37g spont Poulson, 37g 32, 33 weak allele; slight nick in wing; P higher in male *vg40b spont Ives, 40b 15 like vg1; vg1/+ semidominant for vg *vg40c spont Buzzati-Traverso, 6 like vg1 40c20 *vg48a spont King, 48a1 34 15% of homozygotes have wing nicks; halteres and post-scutellars normal; vg51h25 spont Ives, 51h25 16, 39, 45 vg1/vg51h25 show wing scallops like vg1 but wings larger vg67d1 - vg85f3 see Table II vg72a spont 41 like vg1 vg79f spont Ashburner 1 like vg1 vg168 45 recessive lethal *vga vestigial- spont Morgan, 12j 25 wings long, but narrow and scalloped; antlered halteres and post-scutellars normal; wings straplike and smaller in females *vgCli vestigial- spont Robertson, 3 female sterile; no eggs Clipped Reeves, 1947 *vgdn vestigial- spont Nolte, 1942 29 two notches on wing; halteres, postscutellars double notch (from vg1) normal; vgdn/vg1 has straplike wings vgE7 EMS 7 normal as homozygote; vgE7/vg1 straplike wings *vgh vestigial- spont Ludwig, 1936 19, 20, 37 20% show hemithorax; most hemithorax (from vg1) mutants like vg1, 10-20% like vgnw *vghR vestigial- spont Reck, 1937 35 like vgh; In(2R)49C1-2;50C1-2 hemithorax (from vg1) of Reck vgms vestigial- Nakashina- 28 small wings at 25, normal at 27-30 more sensitive Tanaka, 1967 *vgn vestigial- spont Bridges, 15h7 25 homozygote normal; vgn/vg1 shows nicks nick in 85% of females, 45% of males vgnG vestigial- spont Green, 40j26 11, 12 homozygote normal (occasional wing nicks); nick of Green (from vg1) enhanced by Minutes; vgnG/vg1 has scalloped wings vgni vestigial- spont Mohr, 1926 10, 12, homozygote normal; enhanced by Minutes; nick of Green (from vg1) 24, 38, 1/4 of vgni/vg1 show wings nicks 45 vgni2 spont Mohler, 55b9 23 homozygote normal; nicks or scalloping in heterozygotes over vg1, vgnw, vgnwl vgno vestigial- spont Mohr, 1926 24 homozygote notched (45%); vgno/+ notched (from vg1) normal; vgno/vg1 has ragged wings (100%) *vgNo1 vestigial- heat- Swigert, 31c vg31c 30, 31 homozygote shows vestiges of wings; Notch treatment postscutellars erect; viability 50%; of parents female sterile; terminal nicks in vgNo1/+ vgNo2 spont Plough, 31j vg31j 7, 12, 30, like vgNo1; vgNo2/+ enhanced 31, 38, 40, by Minutes; lethal over vgnw 45 vgnp vestigial- spont Wallace, 38a5 7, 10, 38, terminal incisions in wings; overlaps nipped 39, 42, 45, 46 wild type at 25, not at 19. Wing buds show scalloping. vgnw vestigial- spont Morgan, 1924 7, 8, 24, tiny knobbed wings and halteres, erect no wing 27, 38, 40, postscutellars; low viability; 45, 46 female usually sterile; occasional wing nicks in vgnp/+; also shortened L2 vein in vgnp/+; small wing buds *vgnwl vestigial- spont Mohler, 55b9 23 homozygous lethal; vgnwl/vgnw like vgnw, no wing lethal sterile; vgnwl/+ has wing nicks (50%) vgp vestigial- spont Kerr, 30a15 13, 14 homozygotes usually normal; vgp/vg1 has pennant (from vg1) narrow straplike wings, larger in male (temperature-sensitive) *vgpK vestigial- spont Kutschera, 1955 21, 22 homozygote normal (17-28); vgpK/vg1 has pennant of (from vg1) small wings at 17, straplike wings at 25, Kutschera normal at 30. *vgR1 / ray Lasko 18 like vg1 *vgs vestigial- spont Morgan, 12d 25 wings narrow, straplike, full length, strap (from vg1) held at right angles; halteres reduced; postscutellars normal. *vgs2 spont Williams, 56c 44 wings incised, narrow, of variable length. vgU | vestigial- / ray Ives, 55l31 17, 39 homozygous lethal; dominant; vgU/+ Ultra 45, 46 has much reduced wings and halteres; 49 vgU/vg1 has tiny wings, no halteres vgW / vestigial- X ray Shukla 4, 36 homozygous lethal; dominant with wingless 45, 46 homeotic effect; vgW/+ 49 is wingless or has tiny buds, no halteres (or one); female fertile and viable; In(2R)47F15-48A12;49E4-5 (Ashburner) vgX / ray Erk, Podraza, 1986 9 wings, halteres tiny knobs (sometimes halteres absent); postscutellars erect; defects in legs, abdominal tergites, notum; female sterile; notching or scalloping in heterozygotes. ( 1 = Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91; 2 = Auerbach, 1936, Trans R. Soc. Edinburgh 58: 787-815; 3 = Beatty, 1949, Proc. R. Soc. Edinburgh, B 63: 249-70; 4 = Bownes and Roberts, 1981, J. Embryol. Exper. Morphol. 65 (Suppl.): 49-7; 5 = Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 150; 6 = Buzzati-Traverso, 1940, DIS 13: 49; 7 = Carlson, Fer- riola, and Schuchman, 1980, DIS 55: 23; 8 = Chen, 1929, J. Morphol. 47: 135-99; 9 = Erk and Podraza, 1986, DIS 63: 161; 10 = Giesel, 1984, Genetics 107: s37; 11 = Green, 1941, DIS 14: 39; 12 = Green, 1946, Genetics 31: 1-20; 13 = Harnly, 1935, DIS 4: 14; 14 = Harnly, 1936, J. Exp. Zool. 74: 41-59; 15 = Ives, 1941, DIS 14: 39; 16 = Ives, 1952, DIS 26: 65; 17 = Ives, 1956, DIS 30: 72-73; 18 = Lasko (personal communication); 18a = Lasko and Pardue, 1988, Genetics 120: 495-502; 19 = Ludwig, 1936, Verh. Dtsch. Zool. Ges. 38, Zool. Anz. Suppl. 9: 21-73; 20 = Ludwig, 1937, DIS 7: 18; 21 = Mainx, 1956, DIS 30: 77; 22 = Mainx, 1957, Z. Indukt. Abstamm. Vererbungsl. 88: 286-88; 23 = Mohler, 1959, DIS 33: 98; 24 = Mohr, 1932, Proc. Int. Congr. Genet., 6th, Vol. 1: 190-212; 25 = Morgan and Bridges, 1919, Carnegie Inst. Washington Publ. No. 278: 211; 26 = Morgan, Bridges, and Schultz, 1938, Year Book - Carnegie Inst. Washington 37: 305-06; 27 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 59, 232; 28 = Nakashima-Tanaka, 1967, Genetica 38: 447-58, 459-70; 29 = Nolte, 1944, DIS 18: 44; 30 = Plough and Ives, 1934, DIS 1: 32-33; 31 = Plough and Ives, 1935, Genetics 20: 42-69; 32 = Poulson, 1938, DIS 10: 55; 33 = Poulson, 1939, DIS 12: 49; 34 = Poulson and King, 1948, DIS 22: 55; 35 = Reck, 1937, DIS 8: 10; 36 = Schukla, 1980, DIS 55: 210; 37 = Schultz, 1938, Wilhelm Roux's Arch. Entwicklungsmech. Org. 138: 69-102.; 38 = Silber, 1980, Genetica 54: 91-99; 39 = Silber and Becker, 1981, Genetica 55: 217-20; 40 = Silber and Goux, 1977, Arch. Zool. Exp. Gen. 118: 471-80; 41 = Thompson and Purnell, 1972, DIS 48: 16; 42 = Waddington, 1940, J. Genet. 41: 75-139; 43 = Ward, 1923, Genetics 8: 286-300; 44 = Williams, 1956, DIS 30: 80; 45 = Williams and Bell, 1988, EMBO J. 7: 1355-63. 46 = Williams, Atkin, and Bell, 1990, Mol. Gen. Genet. 221: 8-16. 47 = Williams, Pappu, and Bell, 1988, Mol. Cell. Biol. 8: 1489-97. 48 = Willi- ams, Pappu, and Bell, 1988,Mol. Gen. Genet. 212: 370-74. 49 = Williams, Scott, Atkin, Brooks, Russell, and Bell, 1990, Genetics 25: 833-44. | Associated with In(2R)vgU = In(2R)49C1-2;50C1-2 (Ratty and Lindsley, 1964, DIS 38: 30). Survivors of vgU/Df(2R)vg (50%) show extreme mutant phenotype. Partial revertant of vgU reported by Silber and Lemeunier (1981). / Associated with In(2R)vgW = In(2R)47F15-48A12;49E4-5 (Ash- burner). Table II Phenotype of homozygote | allele ( origin wing phen. halteres bristles viab. fert. cytology ___________________________________________________________________________________________________________________________ vg67d1 / ray - T(2;3)49C2-D2;93E-F1 vg67d2 |/ / ray vg - - + - *vg71k2 / ray vgnw - - + + vg72a1 / ray - In(2R)44C2-5;49D2-E1 vg74b1 C+/ ray - In(2LR)37F-38A1;49D2-E1 *vg74b2 C+/ ray vgnw - - + + vg74c1 C+/ ray vgnw - - + - vg74c4 C+/ ray vgnw - - + - In(2LR)22A5-B1;49D2-E vg74c5 / / ray vgs +/- + + + vg74c6 / / ray vgnw - - + - vg74c7 / ray vgnw - - + - vg76d1 C+/ ray vg - - + vg76d2 C+/ ray vg - - + T(Y;2)58B+Dp(2R)58B-D vg76f / ray vg - - + + vg76i1 AD+/ ray - T(2;3)49D2-E1;84E2-3 vg76i2 / AD+/ ray vg - - + + vg76j1 AD+/ ray vg - Tp(2;2)49D;60B;60A;50F;49E;60C vg76k2 AD+/ ray - vg77a4 AD+/ ray vgnp + + + - vg77d1 X ray - In(2LR)25C-D;49D2-E1 vg77d2 X ray vgs - + - Tp(2;2)49B4;49B5-12;49D2-E vg78a1 / ray vgno + +/- + + In(2R)41D-E;49D3-E1 vg78a2 / ray vg - - + - In(2R)49D3-E;56E vg78b1 / ray vgnw - - + - vg78b2 / ray vgnw - - + + vg78b3 / ray vg - - + + vg78b4 NaF+/ ray - T(2;3)49D2-3;49E7-F1;80C vg78f2 NaF+/ ray vg - - + - vg78j1 / ray vgnw - - + - Tp(2;2)49D2-3;49D7-E1;50C1-6 vg78j3 / ray - In(2R)41D2-E1;49D2-E1 vg78k2 NaF+/ ray vg - - + + vg78k3 / ray - In(2R)49D2-E1;59D4-8 vg79b1 / ray vg - - + + vg79b4 X ray - In(2R)41C-D;49D2-E1 vg79b6 X ray - Tp(2:2)49D2;50C9-14;49E1 vg79d3 X ray - In(2R)41A;49D2-E2 vg79d4 X &/ ray vgnw - - + - In(2R)41E;49D2-E1 vg79d5 / / ray&neutrons vgnp + + + + vg79d6 X ray vgnw - - + - vg79d7 X ray vgnw - - + - In(2R)41D-E;49D3-F1 vg79f1 NaF+/ ray - Tp(2;2)36D;53F;49E;41A;54A;41A vg79f2 / ray vgnw - - + - In(2R)49D2-E1;49E7-F13 vg79h1 / ray vgnw - - + - vg79h4 / ray - In(2LR)24D;49D1-E1 vg79h5 / ray vg - - + - In(2R)49D2-E;50A2-3 vg79h6 / ray vgnw - - + - In(2R)41E-F;49D2-E1+In(2R)42B2-3; 57F-58A1 vg79h7 / ray vgnw - - + - In(2R)49D2-7;49F10-13 vg8012 X ray vgnw - - + - vg81a / ray - T(2;3)49D2-E1;64B2-12 vg81a-s / ray vgs2 +/- +/- + - vg81b1 / ray - In(2R)48C4-D1;49D2-E *vg81b2 / ray vgnw - - + + vg81c13 / ray vg - - + + vg81c18 / ray vgnw - - + - vg81c28 / ray vgnw - - + - In(2R)41D-E;49D3-E7 vg81c41d / ray - In(2R)49C2;49F14 vg81f X ray vg - - + + vg81k1 / ray vgnw - - + - vg81l18 / ray vg - - + - In(2LR)36C4-D1;49D2-F1 vg81l24 / ray vg - - + + vg81l26 / ray vgnw - - + - vg82c13 252Cf vg - - + + vg82c14 252Cf vgnw - - + - In(2LR)36C-D;49D2-E vg82c61 252Cf - In(2LR)24E2-F1;49D2-E7 vg83b22 / ray vgnw - - + - vg83b24 / ray vgnw - - + - vg83b27 / / ray vgnw - + + + vg83b39 / ray vgnw - - + - In(2R)49D2-E;51D2-6 vg83c / ray vgnp - +/- + - T(2;3)49D2-E;65F6-66A vg83c3 / ray vgnw - - + - In(2R)41C-D;49D2-E1 vg83c5 / ray vgnw - - + - vg83c7 / ray vgnw - - + - vg83c24 / ray vgnw - - + - vg83c42 / ray vgs - - + - vg83c43 / ray vgnw - - + - In(2R)43C2-3;49D2-E vg83c45 / ray vg - - + - vg83d 252Cf vgnw - - + - vg83d4 252Cf vgnw - - + - In(2R)48E2-F1;49D2-E1 vg83f38 / ray - In(2R)49;59D-E vg83f-XD X ray vgnw - - + - In(2R)48E2-F1;49D2-E1 vg83l2b X ray - In(2R)41D-E;49D2-E1 vg83l-s X ray - vg84f / X ray vgnw - - + - vg84f51 X ray vgnw - - + - In(2R)44F2-45A1;49D2-E2 vg84hXC / ray - In(2R)48E6-F1;49D2-E1 vg84hXD / ray vgnw - - + - In(2R)41B-C;49D2-E1 vg85b X ray vgnp + + + + vg85d1 X ray vgnw - - + - vg85d2 X ray vgnw - - + - T(2;3)49D2-E;84F4-6 vg85e2 / ray vgnw - - + - Tp(2;2)41B;49E;55F vg85e3 / ray vgnw - - + - vg85e4 / ray vgnw - - + - vg85f3 / / ray vg - - + + ( Reference for all alleles: Alexandrov and Alexandrova, 1987, DIS 66: 185-87. Other information: Cf = caffeine; AD = actinomycin-D; bristles = postscutellars. | Wings classified according to similarity to known alleles; for halters and postscutellar bristles, "-" = absence and "+" = presence; under fertility, "-" = sterile, sex unspeci- fied, but probably female. / Other references: Williams and Bell, 1988, EMBO J. 7: 1355-63; Williams, Pappu, and Bell, 1988, Mol. Cell Biol. 8: 1489-97; Williams, Atkin, and Bell, 1990, Mol. Gen. Genet. 221: 8-16. cytology: Placed in 49D2-E1 based on breakpoints common to rearrangements in Table II. vestigial molecular map (modified from Williams and Bell, 1988 by D. Conner). Heavy lines represent deficiencies; hatched line represents an inverted seg- ment accompanying Df(1)vg136. molecular biology: The vestigial region has been cloned by P element transposon tagging (Williams and Bell, 1988). Tran- script of 3.8 kb obtained (Williams, Atkin, and Bell, 1990). The proximal breakpoints of In(2R)vgU and In(2R)vgW were located at 49D-F by in situ hybridization of salivaries. Alleles placed on the molecular map of the vg region derived from Oregon-R are listed in the following table: alleles map location (kb) ( comments ________________________________________________________ vg1 +8 412 insertion (8 kb) vg12 +3 insertion (8 kb) vg18 +8 412 insertion (8 kb) vg21 0 insert hybridizing to P sequences vg51h25 +8 412 insertion (8 kb) vg62d2 +14 to +17 deletion vg74c5 +8 412 insertion (8 kb) vg76i2 +8 412 insertion (8 kb) vg79d5 +7 to +8 deletion vg83b27 +5 to +8 deletion (3 kb) vgni +8 (in 412 of vg1) roo insertion (8 kb) vgNo2 +14 to +17 deletion vgnp +4 insertion (8 kb) vgnw +14 to +17 deletion (3 kb) vgU | +4 (proximal break) inversion vgW / +2 (proximal break) inversion ( "-" values to left (proximal), "+" values to right (distal); 0 coordinate assigned to insert position of vg21. | Fusion between mam and vg (second intron) (Williams et al., 1990). / Fusion between inv and vg (first intron) (Williams et al., 1990). # Vi: see M(1)1B # Viability: see M(1)1B # vibrissae: see vb # vin: vin location: 3-36.3 (not allelic to rs2). origin: Spontaneous. discoverer: Periquet, 72c. references: Anxolabehere and Periquet, 1973, DIS 50: 21. Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215- 25. Ashburner, Richards, and Velissariou, 1980, DIS 55: 196. phenotype: Eye color reddish brown, paler in young flies. Eyes become dark brown with age. v;vin flies have pale orange eyes. Ocelli, adult testis sheath, and Malpighian tubules colored. Viability and fertility excellent. RK1. alleles: Five alleles described in the following table. Defi- ciencies for vin listed in the rearrangement section. allele origin discoverer ref ( comments _____________________________________________________ vin1 spont Periquet 2 vin18 X ray 1 vin101 / ray 1 lethal; T(Y;3)87F12-14 vin123 / ray 1 vinM / ray 1 ( 1 = Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215-25; 2 = Anxolabehere and Periquet, 1973, DIS 50: 21. cytology: Located in 68C8-68D3 (Ashburner et al., 1980); included in Df(3L)vin6 = Df(3L)68C8-11;69A4-5 and Df(3L)vin66 = Df(3L)68A3;68D3. # vir: virilizer location: 2-103.3. origin: Induced by ethyl methanesulfonate. discoverer: Schupbach. references: Amrein, Gorman, and Nothinger, 1988, Cell 55: 1025-35; Hilfiker, Amrein, and Nothiger, 1988, Crete. phenotype: A new undescribed gene involved in sex determina- tion. Female sterile; may be temperature sensitive. alleles: Six alleles, including vir250, virH2, virts. cytology: Placed in 59D2-8. molecular biology: Region cloned. # Vitelline membrane: see Vm #*vli: veins longitudinally shortened location: 3- (not located). origin: Spontaneous. discoverer: Buchman, 1936. references: 1937, DIS 8: 8. phenotype: Veins L2, L4, and L5 tend to be shortened. Overlaps wild type. Semidominant. RK3. # vls: valois (T. Schupbach) location: 2-53. 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. 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 embryos show variable deletions of abdominal seg- ments; whereby segment A4 is deleted most frequently, larger deletions may remove segments A2 through A7; in extreme cases anterior parts of segment A1 become fused to posterior parts of segment A8, but telson elements are always present and relatively normal. In addition, 80-90% of the embryos fail to cellularize normally at the blastoderm stage and die without forming cuticle, or only fragmented pieces of cuticle. Analysis of germline clones indicates that the mutation is germline autonomous (Schupbach and Wieschaus, 1986, Dev. Biol. 113: 443-48). alleles: vls1-vls4 isolated as RB, PE, PG, HC. cytology: Placed in 38A6-E9 based on its inclusion in Df(2L)TW2 = Df(2L)37D2-E1;38E6-9, but not Df(2L)TW50 = Df(2L)36E4- F1;38A6-7. # Vm: Vitelline membrane The Vm genes make up a multigene family that includes at least four members and is responsible for encoding the major proteins of the first layer of the Drosophila eggshell, the vitelline membrane. These proteins are synthesized during the later stages of oogenesis in the follicular epithelium of mature ovaries. The following table describes the four vitel- line membrane genes that have been identified and described. comments gene location synonym ref ( cytology | mRNA protein __________________________________________________________________ Vm26Aa / 2- {20} Vm23 1, 3-7 26A 700-800 17.5 kd bp Vm26Ab /` 2- {20} 3-5 26A 700-800 23 kd bp Vm32Ea - 2- {44} Vm3 4, 7 32E 460 bp 13 kd Vm32Ec - 2- {44} 2 32E 430 bp 13kd Vm34Ca 2- {47} Vm2 4, 7 34C 650 bp ( 1 = Burke, Waring, Popodi, and Minoo, 1987, Dev. Biol. 124: 441-50; 2 = Gigliotti, Graziani, De Ponti, Rafti, Manzi, Lavorgna, Gargiulo, and Malva, 1989, Dev. Genet. 10: 33-41; 3 = Higgins, Walker, Holden, and White, 1984, Dev. Biol. 105: 155-65; 4 = Mindrinos, Scherer, Garcini, Kwan, Jacobs, and Petri, 1985, EMBO J. 4: 147-53; 5 = Popodi, Minoo, Burke, and Waring, 1988, Dev. Biol. 127: 248-56; 6 = Savant and Waring, 1989, Dev. Biol. 135: 43-52; 7 = Scherer, Harris, and Petri, 1988, Dev. Biol. 130: 768-88. | Determined by in situ hybridization to the salivaries (Hig- gins et al., 1984; Mindrinos et al., 1985; Burke et al., 1987; Gigliotti et al., 1989). fs(2)QJ42, a mutant of Vm26Ab, was mapped cytologically to 25D-26A by using the chromosome Df(2L)c17 = Df(2L)25D7-E1;26A7-8 (Savant and War- ing, 1989). / Single long open reading frame; no introns. Transcription occurs from opposite DNA strands in the two genes at 26A (Popodi et al., 1988). ` 10- to 15-fold reduction in transcript level in the mutant fs(2)QJ42. This mutant can be rescued by germline transfor- mation with Vm26Ab+ and restored to normal production of vitelline membrane protein and female fertility (Popodi et al., 1988). - Uninterrupted open reading frame (Gigliotti et al., 1989). molecular: The vitelline membrane genes listed in the table have been cloned and their nucleotide and predicted amino-acid sequences determined (Mindrinos et al., 1985; Burke et al., 1987; Popodi et al., 1988; Scherer et al., 1988; Gigliotti et al., 1989). Clones show cross-hybridization (Mindrinos et al., 1985). High abundance, ovary-specific transcripts have been obtained, but only during vitelline membrane synthesis in adult females in stages 9 and 10 of oogenesis (Higgins et al., 1984; Mindrinos et al., 1985; Gigliotti et al., 1989). A cen- tral 114 bp conserved region (the Vm domain) occurs in the coding region of three and probably four of these genes (Scherer et al., 1988). At the nucleic acid level, this con- served region shows the following sequence identities: 91% between Vm26Aa and Vm34C, 79% between Vm26Ab and Vm34C, and 77% between Vm26Aa and Vm26Ab. Vm26Aa and Vm34C show 100% amino acid identity in the VM domain, but Vm26Ab and Vm34C show only 86% amino acid identity (Scherer et al., 1988). These three Vm genes as well as Vm32E, which contains at least a portion of the VM domain (Scherer et al., 1988), encode translation products with the high proline and alanine content characteristic of vitelline membrane proteins (Mindrinos et al., 1985; Gigliotti et al., 1989). vn: vein Right wing of vn (Puro, 1982) # vn: vein location: 3-16.2. origin: X ray induced. discoverer: Puro, 1960. references: 1982, DIS 58: 205-08. Diaz-Benjumea, Gonzalez-Gaitan, and Garcia-Bellido, 1989, Genome 31: 612-19. phenotype: Large section of vein L4 and anterior crossvein missing. Posterior crossvein often incomplete; gap sometimes present in L3. Male sterile, female fertile. alleles: Six (Diaz-Benjumea et al., 1989). other information: Not tested for allelism with Vn, a dominant mutant of similar map position and phenotype which has been lost. #*Vn: Vein location: 3-19.6. origin: Spontaneous. discoverer: Mohr, 28j21. references: 1932, Proc. Intern. Congr. Genet., 6th., Vol. 1: 190-212. 1938, Avh. Nor. Vidensk.-Akad. Oslo, Mat. Naturvidensk. Kl. 4: 1-7. Mohr and Mossige, 1942, Avh. Nor. Vidensk.-Akad. Oslo, Mat. Naturvidensk. Kl. 7: 1-51. phenotype: Vein L4 not complete. Wings slightly spread. Fly smaller than normal. Homozygous lethal. RK2A. cytology: Associated with Df(3L)Vn = Df(3L)64C12-D1;65D2-E1. # vnd: ventral nervous system defective location: 1-0.0. references: White, 1980, Dev. Biol. 80: 332-44. Lefevre, 1981, Genetics 99: 461-80. White, Decelles, and Enlow, 1983, Genetics 104: 433-48. Campos, Grossman, and White, 1985, J. Neurogenet. 2: 197-218. Mason, Voelker, Rosen, Campos, White, and Lim, 1986, DIS 63: 164-65. Jimenez and Campos-Ortega, 1987, J. Neurogenet. 4: 179-200. Rosen, Martin-Morris, Luo, and White, 1989, Proc. Nat. Acad. Sci. USA 86: 2478-82. phenotype: Late embryonic lethal. Ventral nervous system disorganized and not condensed. Mutants have fewer cells in the CNS; pattern of neuronal connections damaged (Jimenez and Campos-Ortega, 1987). alleles: allele origin discoverer synonym ref ( ____________________________________________________ vnd1 EMS White 3 vnd2 EMS White 3 vnd3 EMS White vnd2 3 vnd4 EMS White 3 vnd5 EMS White 3 vnd6 EMS Lim l(1)EC6004 vnd7 EMS Lim l(1)EC625 vnd8 EMS Lim l(1)EC683 vnd9 EMS Lim l(1)EC684 vnd10 EMS Lim l(1)EC6101 vnd11 EMS Lim l(1)EC6105 vnd12 EMS Lim l(1)EC6116 vnd13 EMS Lim l(1)EC6138 vnd14 EMS Lim l(1)EC6142 vnd15 MMS Lim l(1)EC6M15 vnd16 MMS Lim l(1)EC6M22 vnd17 TEM Lim l(1)EC6T008 vnd18 X ray Lefevre l(1)A131 1 vnd19 | X ray Lefevre l((1)GA100 1 *vnd20 X ray Lefevre l((1)GA122 1 *vnd21 X ray Lefevre l(1)HC143 1 *vnd22 X ray Lefevre l(1)HC218 1 vnd23 X ray Lefevre l((1)RC24 1 vnd24 EMS Lefevre l((1)EA142 2 vnd25 EMS Lefevre l((1)VA208 2 vnd26 EMS Lefevre l((1)VE769 2 vnd27 spont Schalet l(1)2-43 vnd28 ENU Voelker l(1)A22 vnd29 ENU Voelker l(1)A55 ( 1 = Lefevre, 1981, Genetics 99: 461-80; 2 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 3 = White, Decelles, and Enlow, 1983, Genetics 104: 433-48. | T(1;3)1B6;88A. cytology: Placed in 1B9 since included in Df(1)yT8 but not in Df(1)yT7 or Df(1)yT9 (Mason et al., 1986); not covered by Dp(1;f)24 = Dp(1;f)1B5;19-20. molecular biology: The genomic DNA in which the vnd gene resides was cloned by breakpoint analysis (White). #*vnl: venula location: 2- (not located). origin: Spontaneous. discoverer: Plaine, 50h. references: 1951, DIS 25: 77. phenotype: Extra veins between L3 and L4 largely between ante- rior and posterior crossveins; some also arise from L4 distal to posterior crossvein. Penetrance in male 1.3%, in female 43%. With Sb, penetrance is 63% in female; expressivity also increased. RK3. # Vno: see iab6Vno under BXC # vo-3: see e(dpv) # vortex in chromosome 3: see e(dpv) # Vortice: see Vc #*vr: varnished location: 3-44. discoverer: Mohr, 20j22. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 237. phenotype: Eyes small, have fused facets. Female sterile. RK2. # vs: vesiculated location: 1-16.3. references: Mohr, 1927, Hereditas 9: 173. Evang, 1925, Z. Indukt. Abstamm. Vererbungsl. 39: 165-83 (fig.). Waddington, 1939, Proc. Nat. Acad. Sci. USA 25: 299-307. phenotype: Wings warped, wrinkled, blistered, rough textured, discolored, and divergent. Phenotype may overlap wild type. Abnormalities may result from breakage of fibers that normally hold wing surfaces together during unfolding (Waddington, 1939). alleles: allele origin discoverer ref ( comments ____________________________________________________________________ vs1 spont Mohr, 24c23 2, 7 see phenotype *vs29c X ray Oliver, 29c9 9 penetrance: 100% at 25 - 95% (males) and 88% (females) at 30 | *vs52a P32 King, 52a 3 viability: 40% vs61j /` Mickey, 61j 5, 6 *vs64j X ray Mayo, 1964 4 penetrance: 77%; one or both wings crumpled, partially expanded, may be blistered vs66a X ray Becker 1 fertility, viability good vs66j X ray Nilsson, Valentin 8 penetrance: 93% at 25 vs671 EMS Rockwell, 1967 10 penetrance: 100% at 19, 25; blistering variable ( 1 = Becker, 1968, DIS 43: 59; 2 = Evang, 1925, Z. Indukt. Abstamm. Vererbungsl. 39: 165-83 (fig.); 3 = King, 1952, DIS 26: 65; 4 = Mayo, 1966, DIS 41: 58; 5 = Mickey, 1963, DIS 38: 28; 6 = Mickey, 1964, DIS 39: 58; 7 = Mohr, 1927, Hereditas 9: 173; 8 = Nilsson and Valentin, 1968, DIS 43: 61; 9 = Oliver, 1937, DIS 7: 19; 10 = Rockwell, 1967, DIS 44: 52-53. | Green, 1939, DIS 11: 45. / Found among progeny of male treated with radio frequency. ` Synonym: bw61j; bubble wing 61j; bu-w61j. cytology: Salivary chromosome location at about 6B1 (Lefevre). vs: vesiculated From Evang, 1925, Z. Indukt. Abstamm. Vererbungsl. 39: 165-83. # vss: variable size and shape location: 3-. origin: Induced by ethyl methanesulfonate. discoverer: Nusslein-Volhard. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal effect female-sterile. Produces eggs of variable size and shape. alleles: vss1 and vss2 isolated as 258 and 2675. #*vst: vestar location: 2-4.3. discoverer: Glass, 41i15. references: 1944, DIS 18: 40. phenotype: Wings small and straplike, variable. Eyes small, very rough, and somewhat glazed. Female sterile. Viability low. RK3. # vt: verticals location: 1-2.3. origin: Synthetic. discoverer: Gersh. references: 1965, Genetics 51: 477-80. phenotype: Anterior vertical, anterior dorsocentral, and ante- rior scutellar bristles often missing, verticals being most likely to be affected. RK2. cytology: Placed in 3C5-6 on the basis of the vt phenotype of the following genotypes: Df(1)rst2 = Df(1)3C3-4;3C6-7; the heterozygote between Df(1)rst2 and the synthetic deficiency for 3C5 and 6 produced by combining the 4PXD element of T(1;4)w258-18 = T(1;4)3C4-5;101 and the XP4D element of T(1;4)N264-12 = T(1;4)3C6-7;101F; and the synthetic deficiency for 3C5 and 6 produced by combining the 4PXD element of T(1;4)w258-18 with a recombinant between In(1LR)l-v139 = In(1LR)3C6-7 and the right end of a normal X chromosome. other information: Not known as a point mutation. # vtd: verthandi (J.A. Kennison) location: 3-46. origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1983. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Recessive. Suppresses extra sex combs in Pc4/+ male flies. alleles: allele origin ____________________ *vtd1 EMS vtd2 EMS vtd3 / ray vtd4 / ray vtd5 / ray # vtw: vertical wing (J.C. Hall) location: 1-18 (between cv and sn). origin: Induced by ethyl methanesulfonate. discoverer: Butler. references: Deak, 1977, J. Embryol. Exp. Morphol. 40: 35-63. Deak, Bellamy, Bienz, Dubuis, Fenner, Gollin, Rahmi, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81. phenotype: Flightless, with a penetrance of 85-100%; cannot jump more than 2 cm. Wings held up vertically (penetrance 63-90%). In some flies, large amount of disorganized fibril- lar muscle material present in the thorax; in others, most of the fibrillar muscles are absent (Deak et al., 1980). Both dorsal longitudinal muscles (DLMs) and dorsoventral muscles (DVMs) are reduced; in the electron microscope, myofibrillar structure appears disorganized and Z-band structure disturbed (Deak et al., 1982), although the indirect flight muscle fibers that do form are superficially normal. The abnormal behavioral and muscular phenotypes are thought to be due to a primary defect in embryonic cells that map (in mosaic experi- ments) to the dorsal region of the blastoderm. Viability of mutant alleles is about 95% (Deak, 1977). alleles: Two recessive alleles, vtw1 (stronger allele) and vtw2 (weaker allele). Penetrance of flightless phenotype 100% for vtw1, 85% for vtw2; penetrance of vertical wing phenotype 90% for vtw1, 63% for vtw2 (Deak, 1977). # vvl: ventral veins lacking Location: 3- (rearranged). references: Diaz-Benjumea, Gonzalez-Gaitan, and Garcia-Bellido, 1989, Genome 31: 612-19. phenotype: Prevents differentiation of longitudinal veins 2 and 4 which form on the ventral surface of the wing; in Hw; vvl flies, extra sensillae form in the ventral surface where veins would ordinarily form. alleles: Three.