# wa: white-apricot phenotype: Placed on the genetic map of white to the right of wbf and the left of wch. The amount of pigment formed by wa is a function of gene dose: wa/- female < wa/Y male = wa/wa female < wa/wa/wa female < wa/wa male (Muller, 1932). A wa optic disk transplanted into a wild-type host shows autonomous eye color development (Beadle and Ephrussi, 1936). Deficien- cies and duplications for wa can be produced as a result of nonhomologous exchanges within the white region. wa gives rise to partial revertants, as wr (Muller), waM (Mossige), and wa57i (Green). Eye color is modified in certain mutant combi- nations. wa;bw is slightly lighter than wa. wa;st is light pinkish yellow (Mainx, 1938) as is wa v. z wa is lighter than either mutant alone, only slightly darker than wbf (Green, 1959a). wa rb and wa g have nearly white eyes; wa wch, wbf wa, and wa in combination with su(f) all have white eyes. su(wa) wa and su(wa)G wa have browner eyes than wa. The tri- ple mutant su(wa) wa su(f) has eyes only slightly lighter than wa (Levis et al., 1984). wBwx wa is like wa (Judd). wa/+ has lighter eyes than +/+ in v homozygotes (Braver, 1953); Tp(2;3)P darkens wa. Transpositions of wa and the neighboring gene rst+ have been isolated at more than 120 sites in the genome [Ising and Ramel, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 947-54]. molecular biology: The wa allele of the white locus has been cloned by retrieving previously cloned segments carrying a copy of the transposable element copia together with contigous sequences (Bingham et al., 1981; Gehring and Paro, 1980). Bingham and Judd (1981) have shown that copia homology is tightly linked to the site of wa, copia being located at coor- dinate 0.0 on the physical map of the white locus (Levis et al., 1982, 1984) and inserted in the small second intron (Pir- rotta and Brockl, 1984). The size of the copia insertion is 5 kb. The mutant gene codes for major transcripts of 1.25 and 5.7 kb (Levis et al., 1984). A small amount of the normal 2.6 kb white transcript is also found in wa mutants. su(wa), which darkens the eyes of wa flies, results in a higher level of the 2.6 kb transcript, while su(f), which decreases the amount of pigment, results in a lower level of this tran- script. Partial revertants of wa have been sequenced and found to retain one LTR of copia (Carbonare and Gehring, 1985; Mount et al., 1988; Zachar et al., 1985). # wbf: white-buff phenotype: Occupies a recombination site between wBwx and wa (Judd, 1959). Spontaneous reversions reported by Redfield (1952, DIS 26: 28). wbf; st has white eyes (Mainx, 1938, Z. Indukt. Abstamm. Vererbungsl. 75: 256-76). Eyes of wbf rb and wbf g are lighter than the eyes of wbf, rb, or g (Green, 1959a). molecular biology: wbf is associated with an insertion of the transposable element roo (B104) at coordinate -1.13 on the molecular map of white within the intron between the third and fourth exons (Levis et al., 1984; Zachar and Bingham, 1982). # wbl: white-blood phenotype: Located distal to w (MacKendrick and Pontecorvo, 1952) and we (Judd, 1958; Green, 1959a). At 19, eye color as dark as pn; at 30, as light as wbf or wi; sensitivity greatest 40-48 hr after pupation (Ephrussi and Herold, 1945, Genetics 30: 62-70). molecular biology: The 6 kb transposable element blood is inserted in this allele (Bingham and Chapman, 1986, EMBO J. 5: 3343-51). # wBwx: white-Brownex phenotype: Located distal to wbf (Judd, 1957, 1959). Reduces recombination in the y-spl interval. Heterozygotes between wBwx and other white alleles or deficiencies are indistin- guishable in eye color from wBwx/wBwx. The double mutant wBwx wcol is lighter than either single mutant, but wBwx/wa and wBwx/wbf are indistinguishable from wa and wbf, respectively. molecular biology: Restriction map of wBwx resembles that of Canton-S wild type except for a deletion of 150 bp (Zachar and Bingham, 1982). # wc: white-crimson phenotype: Maps at the same site as wa. Derivatives of wc may be stable (w+ for example) or mutable (such as wdc and wdi) and include both point mutations and deficiencies (Green, 1967, Genetics 56: 467-82). The mutations take place in both males and females, may occur in clusters, and do not appear to involve recombination. Transpositions of a segment of the w gene that includes wc to different locations on the third chromosome have been recovered and are mutable (Green, 1969, Genetics 61: 423-28; Green, 1976). molecular biology: wc is derived from wi which is a tandem duplication of 2.9 kb of the white locus; it contains an FB element inserted in the proximal copy of the duplication, near the junction of the duplicated segments (Collins and Rubin, 1982). # wcf: white-coffee phenotype: Located near wBwx and just distal to wa (Welshons and Nicoletti, 1963, DIS 38: 80). Females heterozygous for wcf and w, wa, wco, wch, wbl, wcol, or wsat have eye color of wcf homozygous females. wcf/+ flies wild-type. # wch: white-cherry phenotype: Occupies site proximal to wa and distal to wsp (Lewis, 1956). Eyes light in double mutant with rb or g, white with wa. Enhanced by P and e(we); suppressed by Su(wch), making eyes brownish (Rasmuson, 1970, Hereditas 65: 83-96). # wco: white-coral phenotype: Located distal to w1 (MacKendrick and Pontecorvo, 1952). Enhanced by e(we); lightens rb and g (Green, 1959a). wco;st has yellow eyes (Mainx, 1938). # wDZL: white-Dominant-zeste-like phenotype: wDZL is located in or immediately proximal to the rightmost set of previously-defined white mutant sites (Bing- ham, 1981). While this mutant affects the pigmentation of the eyes, it has no effect on the color of the larval Malpighian tubules or the testis sheath of adult males. wDZL shows synapsis-dependent dominance over w+. It is a highly mutable allele (like wc), giving rise spontaneously to w+ and w- derivatives with a frequency of 0.5-1.5%. Interactions between wDZL and z are summarized in the allele table. It was observed that, when carrying the wild-type allele of z, wDZL/w- females have brown eyes; with z1, however, hemizygous wDZL females have yellow eyes (Bingham, 1980, Genetics 95: 341-53). molecular biology: Physical analysis of wDZL shows that the mutant phenotype results from the insertion (proximal to white) of a complex transposable element made up of sequences normally found at 21D ("unique segment sequences") flanked by sequences of two FB transposons (Levis, Collins, and Rubin, 1982, Cell 30: 551-65; Zachar and Bingham, 1982, Cell 30: 529-41; Bingham and Zachar, 1985, Cell 40: 819-25). A transcript 1.3 kb larger than the major (2.6 kb) w+ transcript is found in wDZL adult heads and head precursor tissues; this is a composite transcript, made up of sequences from the major w+ transcript and from the wDZL unique segment (Bingham and Zachar, 1985; Zachar et al., 1985). In wDZL flies, a reduction in the levels of the w+ transcript is observed in adult head and head precursor tissues, but not in abdominal tissues. Revertants of wDZL show loss of most of the unique segments of the insertion with 1.9 and 6.2 kb of the insertion remaining (Levis and Rubin, 1982; Zachar and Bingham, 1982). # we: white-eosin phenotype: Placed proximal to wa (Green, 1959a). Amount of pigment formed by we not a function of gene dose: we female = we male < we/we male = we/we female < we/we/we female (Muller, 1932). Mutant enhanced by P, cru, and whg as well as by E(we). Lightens rb and g (Green, 1959a). A we optic disk transplanted into a wild-type host shows autonomous eye color development (Beadle and Ephrussi, 1936). molecular biology: we is derived from w1 and carries an inser- tion of the transposable element pogo within the w1 Doc inser- tion (O'Hare). # wi: white-ivory phenotype: Placed on the genetic map distal to w1 (MacKendrick, 1953, DIS 27: 100). wi is unstable, reverting spontaneously to w+ with a frequency of 5x10-5 in wi/wi females and 5x10-6 in wi/Y males and wi/Df(1)w females (Lewis, 1959, Genetics 44: 522; Bowman, 1965, Genetics 52: 1069-79). The frequency of germinal reversions and of somatic reversions in larval eye tissue is increased by X rays (Lewis, 1959; Bowman and Green, 1964, Genetics 50: 237). No dosage compensation shown by the mutant (Green 1959a). Recombination between flanking w alleles reduced in wi, but restored in its revertants (Bowman, 1965; Bowman and Green, 1966, Genetica 37: 7-16). molecular biology: Cloning and analysis of Southern blots of wi DNA indicate the presence of a 2.9 kb duplication within the white locus (Karess and Rubin, 1982, Cell 30: 63-69). Rever- tants are produced by excision of one copy of the repeat in derivatives wi+B, wi+C, wi+D, and wi+E. wi+A and the partial revertant wip are insertion mutations that are more complex, their altered phenotype apparently resulting from the inser- tion of new DNA into wi and the loss of some wi DNA. # wm: white-mottled phenotype: There are many w alleles that show variegated eye color. The wm mutants most commonly used for variegation stu- dies are wm4 and wm264-58. In these alleles, extra hetero- chromatin partially suppresses eye mottling (Gowen and Gay, 1933, Proc. Nat. Acad. Sci. USA 19: 122-26; Koliantz, Hartmann-Goldstein, and Fuller, 1984, Heredity 52: 203-13; Koliantz and Hartmann-Goldstein, 1984, Heredity 53: 215-22; Baker and Spofford, 1959, Univ. Texas Publ. 5914: 135-54; Spofford, 1959, Proc. Nat. Acad. Sci. USA 45: 1003-07). In wm264-58, variegation less (more wild-type in color) in homoz- ygous females than in heterozygous females. Color variegation found in the testis-sheath as well as the eyes of wm264-58 male flies (Baker, 1968, Adv. Genet. 14: 133-169). In some lines, less variegation when paternally inherited; in others, less variegation when maternally inherited or no parental effect. Mottling in wm4 and wm4h is enhanced by E(var)7 and E(var)c101 (Reuter and Wolff, 1981, Mol. Gen. Genet. 182: 516-19); mottling in wm4 and wm264-58 is suppressed by Su(var) (Spofford, 1962, Genetics 47: 986-87) and a number of other suppressor mutations (Reuter and Wolff, 1981). molecular biology: The DNA map location of three white-mottled mutations has been determined (Tartof, Bishop, Jones, Hobbs, and Locke, 1989, Dev. Genet. 10: 162-76). The euchromatic breakpoint of In(1)wm4 is at -24.5 kb, and the breakpoints of In(1)wm51b and In(1)wmMc are at about -21.3 kb (origin being the site of the copia insertion in wa]. # wsp: white-spotted phenotype: Located proximal to wch and distal to wDZL. wsp affects that deposition of the eye pigments, resulting in a variegated phenotype, but does not affect the pigmentation of the larval Malpiphian tubules. Testis pigmentation varies with different alleles, wsp3 males having unpigmented testes, but wsp1 and wsp2 males showing enhanced testis pigmentation (Davison et al., 1985; Pirrotta, Stellar, and Bozzetti, 1985, EMBO J. 4: 3501-08; Judd, 1987). Partial complementation occurs between wsp alleles and certain other w mutations when they are synapsed; for example, wsp/w, wsp/wch, and wsp/wa females have homogeneous brown eyes (Green, 1959a). The dou- ble mutants wa wsp and wch wsp have white and pale yellow eyes, respectively. wsp, when heterozygous with a deficiency for all or part of the w locus, produces a phenotype like that of wsp homozygotes (Green, 1959c). In the presence of z1, two synapsed copies of wsp in trans (or tandemly repeated) result in yellow-eyed females; z1 females with one copy of wsp have wild-type eye color. A specific regulator of the wsp eye phenotype, su(wsp), has been isolated as a partial revertant of wsp1 (Chapman and Bingham, 1985); this suppressor restores wild-type eye color to wsp1, wsp2, wsp3, and wsp4 flies, but not to the wsp81d mutant (Davison et al., 1985). molecular biology: The wsp region has been cloned (Zachar and Bingham, 1982) and sequenced (O'Hare et al., 1984); it is located 1.0-1.9 kb upstream from the 5' end of the start of w+ transcription (Zachar and Bingham, 1982; O'Hare et al., 1983). wsp shows sequence homology and behavior analogous to enhancer sequences (Davison et al., 1985). The lesions responsible for wsp1, wsp2, and wsp4 have been analyzed by sequencing cloned portions of these alleles; the breakpoints of wsp3 and wsp81d have also been established by molecular methods. wsp1 carries roo; the other alleles are molecular deletions. Sensitivity to the effect of su(wsp) on eye pigmentation is deleted by wsp81d but not by wsp3 (Davison et al., 1985). # wzm: white-zeste mottled phenotype: wzm is located to the right of wa and to the left of w1. It is an unstable white allele, mutating to derivatives, most of which are unstable (Judd, 1963, Proc. Int. Congr. Genet. 11th, Vol. 1: 3-4; 1964, DIS 39: 60). Since all z+ wzm males (as well as z+ wzm/z+ wzm females) have wild-type eye color, the mutant z was used as an indicator of the muta- bility of wzm strains. Derivatives of wzm (Kalisch and Becker, 1970, Mol. Gen. Genet. 107: 321-35) include wzl (from the z wzm stock), wzmz (from the z wzm stock), and wzmzrb, wzmzz and wzmzw (from the z wzmz stock). Only wzl is stable. The mutants were often recovered in clusters. wzmz reverts to wzm+ (eye color between z wzm and z w+) and the white-eyed wzmzz and ww. Other derivatives (wz, wzh, wzs) were recovered by Judd (1957; 1969, Genetics 61: s29). molecular biology: wzm carries an insertion of the transposable element BEL near the 5' junction of the first intron at +3.5 (O'Hare et al., 1984). This insertion does not appear to alter the size of the 2.6 kb w+ transcript in wzm and z wzm flies (Levis et al., 1984). # W: Wrinkled location: 3-46.0. origin: Recovered among progeny of female exposed to strato- sphere. discoverer: Jollos, 1936. references: 1936, Natl. Geograph. Soc. Tech. Papers, Strato- sphere Ser. No. 2: 153-57. Jollos and Waletzky, 1937, DIS 8: 9. phenotype: Homozygote viable. Wings remain small and unex- panded. Black spots on head beside proboscis or ocelli. Heterozygous female like homozygote but less extreme. Male much less extreme; wings often expanded but wrinkled, blistered, and surface finely pebbled and grayish; no overlap with wild type. Suppressed by D in male and nearly so in female. From prepupal stage through adult, wing bases abnor- mally narrow, possibly preventing flow of body fluid in suffi- cient quantity to expand wings [Waddington, 1940, J. Genet. 41: 75-139 (fig.)]. RK1 as dominant. cytology: Located at 75C5-D3. # W13: see T(1;4)A1 #*wa: warty location: 1-64.4 (based on location of wa2; wa said to be near car). origin: Induced by P32. discoverer: Bateman, 1950. references: 1950, DIS 24: 56. phenotype: Eyes rough with scattered enlarged facets. Occa- sional notched wing tip. Penetrance low. Viability variable. Male infertile in proportion to degree of expression. Hetero- zygous female often infertile. RK3. # wa2 origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 77. phenotype: Eyes irregularly roughened and of varying size and shape; ommatidia deranged. Wing tips rarely notched. RK3. alleles: Allelism inferred from phenotype and genetic location. One allele each induced by CB. 1540, CB. 3025, and X rays. # waisted: see ws # wap: wings-apart location: 1- {66}. synonym: l(1)20Ab. discoverer: Lifschytz. references: Schalet, 1972, DIS 49: 36-37, 64-66. Schalet and Lefevre, 1973, Chromosoma 44: 183-202. 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Fran- cisco, Vol. 1b, pp. 846-902. Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31. Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52. phenotype: Semilethal. Most flies die shortly before eclosion. Flies which hatch have wings set slightly apart and a somewhat darker than normal thorax; may have extra crossveins. Mutant males, mutant females, and mutant/deficiency females have the same phenotype, which is more extreme at 29-30. Viability of heteroallelic compounds usually low (2-9%). alleles: allele origin discov. synonym ref ( comments ________________________________________________________________________ wap1 X ray Lifschytz l(1)A200 4, 5, 8, 9 wap2 EMS Lifschytz l(1)Q217 5, 7, 8, 9 no maternal effect wap3 EMS Lifschytz l(1)Q464 5, 8 wap4 EMS Lifschytz l(1)M155 6 on y+Ymal+ wap5 X ray Lefevre l(1)C243 3 on T(1;3)20A3;75C wap6 X ray Lefevre l(1)KC31 3 wap7 X ray Lefevre l(1)RF13 3 wap8 HMS Kramers l((1)HM33 2 wap9 MR Eeken l(1)D48 1, 7 maternal effect ( 1 = Eeken, Sobels, Hyland, and Schalet, 1985, Mutat. Res. 150: 261-75. 2 = Kramers, Schalet, Paradi, and Huisser- Hoogteyling, 1983, Mut. Res. 107: 187-201; 3 = Lefevre, 1981, Genetics 99: 461-80; 4 = Lifschytz and Falk, 1968, Mutat. Res. 6: 235-44; 5 = Lifschytz and Falk, 1969, Mutat. Res. 8: 147-55; 6 = Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84; 7 = Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31; 8 = Schalet and Lefevre, 1973, Chromosoma 44: 183-220; 9 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902. cytology: Placed in 20A3; included in Df(1)DCB1-35c but not in Df(1)B12 = Df(1)19E1;20A1-2. # wapl: wings-apart-like location: 1-0.7(between Pgd and pn). synonym: wap; l(1)2Dd. references: Gvozdev, Gostimsky, Gerasimova, Dubrovskaya, and Braslavskaya, 1975, Mol. Gen. Genet. 141: 269-75. Gvozdev, Gerasimova, Kovalev, and Ananiev, 1977, DIS 52: 67- 68. Perrimon, Engstrom and Mahowald, 1985, Genetics 111: 23-44. phenotype: Most alleles are lethal. Semilethal escapers show wings-apart phenotype. alleles: allele origin discov. synonym ref ( _________________________________________________ wapl1 | X ray Lefevre l(1)A17 3, 4 wapl2 / X ray Lefevre l(1)C204 3, 4 wapl3 / X ray Lefevre l(1)HC262 3, 4 wapl4 NMU Gvozdev wap3 1 wapl25 EMS Gvozdev 1 wapl29 EMS Gvozdev 1 wapl33 EMS Gvozdev 1 wapl37 EMS Gvozdev 1 wapl38 EMS Gvozdev 1 wapl40 EMS Gvozdev 1 wapl44 EMS Gvozdev 1 wapl46 EMS Gvozdev 1 wapl49 EMS Gvozdev 1 wapl52 EMS Gvozdev 1 wapl56 EMS Gvozdev 1 wapl73 EMS Gvozdev 1 wapl74 EMS Gvozdev 1 wapl79 EMS Gvozdev 1 wapl86 EMS Gvozdev 1 wapl95 EMS Gvozdev 1 wapl110 ( ray Gvozdev 1 wapl113 / EMS Perrimon l(1)113p 4 waplHMS HMS l(1)HM404 2 ( 1 = Gvozdev, Gerasimova, Kovalev, and Ananiev, 1977, DIS 52: 67-68; 2 = Kramers, Schalet, Paradi, and Huiser- Hoogteyling, 1983, Mut. Res. 107: 187-201; 3 = Lefevre, 1981, Genetics 99: 461-80; 4 = Perrimon, Engstrom, and Mahowald, 1985, Genetics 111: 23-41. | Early pupal lethal with apparently normal imaginal disks; mitotic index reduced and metaphase chromosomes abnormally condensed; germ-line clones devoid of maternal lethal effect. / Lethal at larval-pupal boundary and exhibit small disk phenotype; homozygous germ-line clones produce zygotes that arrest in preblastoderm stage. cytology: Placed in 2D4-6 since included in Df(1)JC105 = Df(1)2D4-6 and Df(1)Pgd-kz = Df(1)2D3-4;2F5 but not in Df(1)64c18 = Df(1)2E1-2;3C2. # wapm: wings-apart mimic location: 1-{45}. discoverer: Schalet. phenotype: Wings set slightly apart; viability good; females fertile. cytology: Placed in 12D3 based on the wapm phenotype of Df(1)HA92/Df(1)RK2 = Df(1)12A6-7;12D3/Df(1)12D2-E1;13A2-5. # warped: see wp # warty: see wa # Washed eye: see We # water wings: see wtw # wavoid: see wd # wavoidlike: see wdl # wavy: see wy # waxy: see wx # wb: wing blister location: 2-49.9 (G. Maroni; 0.2 cM to left of Adh). synonym: l(2)br1 (Woodruff and Ashburner, 1979); A1 group (O'Donnell et al., 1977). references: O'Donnell, Mandel, Krauss, and Sofer, 1977, Genet- ics 86: 553-66. Woodruff and Ashburner, 1979, Genetics 92: 133-49. Ashburner, Faithfull, Littlewood, Richards, Smith, Velis- sariou, and Woodruff, 1980, DIS 55: 193-95. phenotype: Most of the mutants are characterized by homo- or hemizygous lethality, but a visible phenotype has also been reported. O'Donnell et al., 1977, describe a bent-down-wing phenotype occurring when one of their lethals is crossed to other lethals in the same complementation group and the same phenotype when three of their lethals are crossed to deletions for the locus. Woodruff and Ashburner, 1979, describe the viable and fertile wing blister phenotype (a roughly circular area around the crossveins of the wing, forming a blister which often collapses soon after eclosion, distorting the wing blade). The allele showing this phenotype (wb1) is viable and fertile in homozygotes and hemizygotes as well as in heteroal- lelic combinations with lethal alleles. alleles: Viable and lethal (or semilethal) alleles are described in the following table. allele origin discoverer ref ( comments _______________________________________________________ wb1 EMS Ashburner 1, 3 wing blister, viable, fertile wb3 EMS Ashburner 1 wing blister, viable, fertile wb4 EMS Ashburner 1 wing blister, viable, fertile wbBMW22 EMS Ashburner 1 lethal wbBMW32 EMS Ashburner 1 lethal wbCH18 EMS O'Donnell 2 lethal wbCH20 EMS O'Donnell 2 lethal wbCH38 EMS O'Donnell 2 lethal wbCH41 EMS O'Donnell 2 lethal wbCH57 EMS O'Donnell 2 lethal wbCH67 EMS O'Donnell 2 lethal wbCH70 EMS O'Donnell 2 lethal wbCR1 EMS Ashburner 1, 3 lethal wbDM10 EMS O'Donnell 2 lethal; semilethal over Df(2L)fn7 wbGM2 EMS Maroni 1 lethal wbHG7 EMS Ashburner 1 lethal wbHG9 EMS Ashburner 1 lethal wbHG10 EMS Ashburner 1 lethal wbHG14 EMS Ashburner 1 lethal wbHG16 EMS Ashburner 1 lethal wbHG17 EMS Ashburner 1 lethal wbHG18 EMS Ashburner 1 lethal wbHG19 EMS Ashburner 1 lethal wbHG24 EMS Ashburner 1 lethal wbHG26 EMS Ashburner 1 lethal wbL412 EMS Lindsley 1 lethal wbOK14 EMS O'Donnell 2 lethal wbP115 HD Shelton 1 lethal wbPA43 EMS Ashburner 1 lethal wbSF11 EMS Woodruff 3 lethal wbSF19A EMS Woodruff 1, 3 lethal wbSF20 EMS Woodruff 3 lethal wbSF25 EMS Woodruff 1, 3 lethal wbSF30 EMS Woodruff 3 lethal ( 1 = Ashburner; 2 = O'Donnell, Mandel, Krauss, and Sofer, 1977, Genetics 86: 553-66; 3 = Woodruff and Ashburner, 1979, Genetics 92: 133-49. cytology: Placed in 34F4 since included in Df(2L)fn1 = Df(2L)34F4-35A1;35D5-7 but not in Df(2L)A217 = Df(2L)34F5;35B3. # wbl: windbeutel location: 2-86. synonym: wind. references: Anderson, 1987, TIG 3: 91-97. Schupbach and Wieschaus, 1989, Genetics 121: 101-17. phenotype: Maternal expression of wbl, one of the "dorsal group" genes, is required for the production of all lateral and ventral pattern elements. In the absence of the wild-type allele, all embryonic cells differentiate dorsal epidermis. alleles: One allele has been identified (Schupbach and Wieschaus). #*wd: wavoid location: 2-40. origin: Spontaneous. discoverer: Kellen, 1941. references: Kellen, 1945, Genetics 30: 12. phenotype: Wings waved. Variable penetrance and expressivity, especially in male. Partially suppressed by y in both sexes. RK2. # wdh: see sli # wdl: wavoidlike location: 2-39. origin: Induced by ethyl methanesulfonate. references: Sandler, 1977, Genetics 86: 567-82. phenotype: Wavy wings with incomplete L5 vein. Homozygous viable but female semisterile. Maternal effect results in death of zygotes before egg hatch and is influenced by the X- or Y-chromosome heterochromatin carried by the zygote; effect less severe at 19 than at 25. Mutation semilethal when hetero- zygous with a deficiency for the locus. cytology: Located in 32A-32E; included in Df(2L)J39 = Df(2L)31A-B;32D-E but not in Df(2L)J27 = Df(2L)31B-D; 32A. other information: May be an allele of the lost mutation wd reported by Kellen (1945, Genetics 30: 12). #*wdn: wings down location: 3-100. discoverer: Morgan. references: 1929, Carnegie Inst. Washington Publ. No. 399: 187. phenotype: Wings extended and drooping or even directed ven- trally, broad with close crossveins. Overlaps wild type. Low viability. RK3. #*we: wee location: 1-3.0. origin: X ray induced. discoverer: Muller, 26l5. references: 1935, DIS 3: 30. Lefevre and Green, 1972, Chromosoma 36: 391-412. phenotype: Fly dwarfed. Eyes rough; bristles fine; wings spread. Fertility very low. RK2. #*We: Washed eye location: 3-43.0. origin: Spontaneous. discoverer: Andres, 42e7. references: 1943, DIS 17: 48. phenotype: Dominant modifier of w that produces partial rever- sion. Produces spot of dilute red pigment varying in size from dot to nearly whole eye. Homozygous lethal. Classifica- tion, fertility, and viability of heterozygote excellent. RK2. # We: see see DrWe # weak: see wk # wee: see we # welt: see wt # weltlike: see wtl # wg: wingless location: 2-30.0. synonym: Dint-1. references: Sharma, 1973, DIS 50: 24, 134. Sharma and Copra, 1976, Dev. Biol. 48: 461-65. Babu, 1977, Mol. Gen. Genet. 151: 289-94. Morata and Lawrence, 1977, Dev. Biol. 56: 227-40. 1977, Nature (London) 265: 211-16. Deak, 1978, Dev. Biol. 66: 422-41. Nusslein-Volhard and Wieschaus, 1980, Nature (London) 287: 785-801. Vandervorst and Ghysen, 1980, Nature (London) 286: 65-67. Nusslein-Volhard, Wieschaus, and Kluding, 1983, DIS 59: 158- 60. 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Babu and Bhat, 1986, Mol. Gen. Genet. 205: 483-86. Baker, 1987, EMBO J. 6: 1765-73. Johnston, Phillips, and Lawrence, 1987, Cell 50: 859-63. Ryjsewijk, Schuermann, Wagenaar, Parren, Weigel, and Nusse, 1987, Cell 50: 649-57. Scott and Carroll, 1987, Cell 51: 689-98. Baker, 1988a, Dev. Biol. 125: 96-108. 1988b, Development 102: 489-97. 1988c, Development 103: 289-98. Ingham, Baker, and Martinez-Arias, 1988, Nature (London) 331: 73-75. Martinez-Arias, Baker, and Ingham, 1988, Development 103: 157-70. Mohler, 1988, Genetics 120: 1061-72. Uzvolgyi, Kiss, Pitt, Arsenian, Ingvarsson, Udvardy, Hamada, Klein, and Sumegi, 1988, Proc. Nat. Acad. Sci. USA 85: 3034-38. Van den Heuvel, Nusse, Johnston, and Lawrence, 1989, Cell 59: 739-49. phenotype: The wg gene is involved both in controlling the seg- mentation pattern of embryos by affecting the posteriormost cells of each parasegment (Baker, 1987) and in controlling the imaginal disk pattern of the meso- and meta-thoracic segments that develop into wing, halter, and notum in pupae and adults (Sharma, 1973; Sharma and Copra, 1976; Morata and Lawrence, 1977). The gene is believed to control segment organization through an intercellular signaling mechanism (Baker, 1987, 1988b; Cabrera, Alonso, Johnston, Phillips, and Lawrence, 1987, Cell 50: 659-63; Ryjsewijk et al., 1987; Martinez-Arias et al., 1988). Mutants may be viable as adults or lethal as embryos or pupae. In embryonic lethal alleles (Babu, 1977; Nusslein-Volhard and Wieschaus, 1980), each segment shows a mirror-image duplication of the denticle bands at the expense of naked cuticle so that a continuous sheet of denticles (instead of repeated denticle bands) is produced (Cabrera et al., 1987). Dorsal abnormalities are more extreme than ven- tral ones, the dorsal cuticle being greatly reduced and covered by fine hairs (Baker, 1988a). These embryos lack head structures and filzkorper (Perrimon and Mahowald, 1987, Dev. Biol. 119: 587-600). In the nervous system, a single neuron, RP2, is missing; other neurons in the lineage are normal (Patel, Schafer, Goodman, and Holmgren, 1989, Genes Dev. 3: 890-904). The temperature-sensitive period for wgl-12, a heat-sensitive allele that is lethal at 25 (Baker, 1988a; Mohler, 1988), lies between gastrulation and the beginning of dorsal closure (11 hours after egg laying at 25). In pupal lethal and adult viable alleles, the ready-to-emerge pupae and the adults lack one or both wings and/or halteres, and there is a corresponding duplication of the meso- and metanota (Sharma, 1973; Sharma and Copra, 1976; Morata and Lawrence, 1977; Deak, 1978). This adult phenotype shows incomplete penetrance and variable expressivity and is affected by the ability of the wingless gene to function during the larval period (Baker, 1988a). Low temperature fails to rescue heteroallelic combinations of wg1 or wgl-18 with the heat- sensitive allele wgl-12 after the larval stages. Lethal as well as viable wg alleles are not cell-autonomous in adult mosaics (Babu and Bhat, 1986; Morata and Lawrence, 1977; Baker, 1988a). alleles: Mutant alleles of wg may be viable, showing a visible phenotype involving loss of wings and/or halters, or they may be homozygous lethal (usually as embryos but sometimes as pupae). Both types of mutants are included in the following table: allele origin discoverer synonym ref ( comments _______________________________________________________________________________ wg1 X ray Sharma 4,6-8 viable wg2 EMS Sharma 8 viable wg3 EMS Sharma 8 viable wg3-1 EMS Sharma 8 viable wg4 EMS Sharma 8 viable wg4-1 EMS Sharma 8 viable wg5 EMS Sharma 8 viable wg7 EMS Sharma 8 viable wg10 EMS Sharma 8 viable wg11 EMS Sharma 8 viable wg12 X ray Baker wgCX1 3 viable wgl-1 EMS Babu 1 embryonic lethal wgl-2 EMS Babu 1,2 embryonic lethal wgl-3 EMS Babu 1 embryonic lethal wgl-4 EMS Babu 1 embryonic lethal wgl-5 EMS Babu 1 embryonic lethal wgl-6 EMS Babu 1 embryonic lethal wgl-7 EMS Nusslein-Volhard wg6K 9 embryonic lethal wgl-8 EMS Nusslein-Volhard. wgIG 9 embryonic lethal wgl-9 EMS Nusslein-Volhard wgIIS 9 embryonic lethal wgl-10 EMS Nusslein-Volhard wgIIID 9 embryonic lethal wgl-11 EMS Nusslein-Volhard wgIJ 9 embryonic lethal wgl-12 | EMS Nusslein-Volhard wgIL, wgts 4,9 hs lethal (embryo) wgl-13 EMS Nusslein-Volhard wgIN 9 embryonic lethal wgl-14 HD Baker wgCP1 3 embryonic lethal; wgl-15 X ray Baker wgCX2 3,4 embryonic lethal wgl-16 X ray Baker wgCX3 3,5 pupal lethal wgl-17 X ray Baker wgCX4 3,5 embryonic lethal wgP Baker 4,5 pupal lethal; In(2L)28A1-3;32E-F ( 1 = Babu, 1977 , Mol. Gen. Genet. 151: 289-94; 2 = Babu and Bhat, 1986, Mol. Gen. Genet. 205: 483-86; 3 = Baker, 1987, EMBO J. 6: 1765-73; 4 = Baker, 1988a, Dev. Biol. 125: 96- 108; 5 = Baker, 1988b, Development 102: 489-97; 6 = Sharma, 1973, DIS 50: 25, 134; 7 = Sharma and Copra, 1976, Dev. Biol. 48: 461-65; 8 = Sharma and Shekaran, 1983, Indian J. Exp. Biol. 21: 143-49; 9 = Tearle and Nusslein-Volhard, 1987, DIS 86: 209-69. | At 18, homozygous wgl-12 embryos develop normally and hatch to produce larvae that have a wild-type cuticular pattern, but these mutants do not survive to become adults. wgl- 12/wgP mutants, however, do survive at 16.5 to become phenotypically wild-type adults (Baker, 1988a). cytology: wg has been located in 28A1-3 by in situ hybridiza- tion to salivary chromosomes of In(2L)wP = In(2L)28A1-3;32E-F heterozygotes, two sites being labelled in the inversion chro- mosome (Baker, 1987). molecular biology: DNA from the wg gene was cloned by transpo- son tagging with a P-element insertion mutant wgl-18. Lesions associated with wg mutants were located on a molecular map of the region. Alleles involved are listed below: allele molecular biology _______________________________________________________ wg1 deletion from +16.8 to +17.1 kb wgI-15 deletion of 0.3 kb wgI-16 break between +10.8 and 15.0 kb wgI-17 deletion of 2 kb at 5' end of gene In(2L)wgP 28A breakpoint between 16.4 and 17.1 kb A 3.2 kb transcript was obtained and localized in embryos, where it was first found at the time of cellularization of the blastoderm (Baker, 1987, 1988b). The RNA accumulates as epi- dermal stripes in the most posterior cells of each parasegment. Transient accumulation of transcript occurs in the mesoderm and the nervous system. wg is also expressed in larvae and pupae, but is scarcely detectable in adults. An antisense RNA made from the wg transcript produces phenocopies of wingless when injected into wild-type eggs (Cabrera et al., 1987). The Drosophila melanogaster homolog of the mouse mammary oncogene int-1 has been located in the same cytological region as wingless, cloned and designated Dint-1 (Ryjsewijk et al., 1987; Uzvolgyi et al., 1988); transcripts of 2.9-3.0 kb have been obtained and found to be at approximately the same posi- tion on the molecular map and to show the same expression in embryos as wg. The identity of Dint-1 and wg was confirmed by positive cross-hybridization of a Dint-1 cDNA probe to a par- tial cDNA clone from the 5' half of the wg transcript (Ryjsewijk et al., 1987). A partial sequence of wg cDNA was obtained (Cabrera et al., 1987) and found to be identical to a region of the complete Dint-1 sequence (Ryjsewijk et al., 1987). The deduced Drosophila protein sequence shows 54% overall identity to the mouse int-1 sequence (Ryjsewijk et al., 1987; Uzvolgyi et al., 1988). The cysteine-rich protein of wg is found in the same region of the embryo as the wg mRNA (Van den Heuvel et al., 1989). # wgo: wings-out location: 1-16.2. origin: H3TdR-induced. references: Perez and Kaplan, 1968, DIS 43: 66. phenotype: Wings divergent, slight thickening of veins, notch- ing effect in 10-15% of flies. other information: Not an allele of vs. #*wgv: wing variance location: 1-33.0 (no recombinants with v among 905 flies). discoverer: Fahmy. references: 1959, DIS 33: 94. phenotype: Wing position variable; wings drooping, outspread, or upheld. Male sterile. RK2. # wh: whiskers location: Autosomal. origin: Neutron induced. discoverer: Mickey, 54a7. references: 1963, DIS 38: 29. phenotype: Many extra vibrissae, which are longer than normal. RK3. # whd: withered location: 2-61. references: Str|men, 1974, Hereditas 78: 157-68. Ashburner, Faithfull, Littlewood, Richards, Smith, Velis- sariou, and Woodruff, 1980, DIS 55: 193-95. phenotype: Wings warped and waved or reduced to shrunken black pupal pads. Synthetic lethal in presence of su(r) (Str|men, 1974). RK2. alleles: allele origin discoverer ref ( _______________________________________ whd1 spont Bridges, 38a6 2,3 whd74 EMS Ashburner 1 ( 1 = Ashburner, Faithfull, Littlewood, Richards, Smith, Vel- issariou, and Woodruff, 1980, DIS 55: 193-95; 2 = CP627; 3 = Stromen, 1974, Hereditas 78: 157-68. #*whg: whiting location: Autosomal. discoverer: Bridges, 13k21. references: 1916, Genetics 1: 148. 1919, J. Exp. Zool. 28: 337-84 (fig.). phenotype: Specific modifier of we. we; whg has pure white eyes. RK3. #*whh: white head location: 3- (not located). discoverer: Morgan, 13h. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 99. phenotype: Ocelli surrounded by silvery patch. RK3. # whirligig: see wrl # whirly: see wl # whiskers: see wh # white: see w # white head: see whh # white-marbled: see w63b # white ocelli: see wo # whiting: see whg # who: see fu33 # wi: witty eye location: 2-55.0 (not allelic to rh). origin: Spontaneous. discoverer: Whitten, 61g. references: 1963, DIS 38: 31. 1968, Heredity 23: 263-78. phenotype: Eyes rough on lower half owing to irregular facets. Extra vibrissae in variable number and distribution. Removal of closely linked modifiers gives rise to dominant form. Penetrance and expression variable and highly sensitive to background genotype and temperature (Whitten, 1968). RK3. # wider wing: see ww # wimp: see RpII140 # wind: see wbl # windbeutel: see wbl # wing blister: see wb # wing variance: see wgv # wingless: see wg # wings-apart: see wap # wings-apart-like: see wapl # wings-apart mimic: see wapm # wings down: see wdn # wings-out: see wgo #*with: with trident location: 3- (near p). discoverer: Morgan, 10a. references: Morgan and Bridges, 1919, J. Gen. Physiol. 1: 639-43. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 31 (fig.). phenotype: Dark trident pattern on mesonotum. Variable; some overlap of wild type. RK3. # withered: see whd # witty eye: see wi # wizened: see wz # wk: weak location: 3-42. origin: Spontaneous. discoverer: Bridges, 33l22. phenotype: Bristles small, somewhat Minute, and variable. Abdomen disproportionately small. Wings somewhat warped. Viability variable. RK3. #*wl: whirly location: 2- (not located). origin: Spontaneous. discoverer: Kiil, 43k4. references: 1946, DIS 20: 66. phenotype: Acrostichal hairs in irregular rows; incomplete whorls on thorax. RK3. # wo: white ocelli location: 3-76.2. discoverer: Bridges, 12f21. references: 1920, Biol. Bull. 38: 231-36. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 66. Rayle, 1969, DIS 44: 98. Jones, 1971, DIS 47: 90. phenotype: Ocelli colorless. Eye color wild type. Modifies we to a lighter and less yellow tone. Interacts with z, produc- ing white-eyed z/z;wo/wo females and z/Y;wo/wo males with a slight deviation from wild-type eye color (Rayle, 1969). RK2. alleles: wo1 (Bridges) and wo67k (Rayle). cytology: Located in 94A-E by deficiency mapping (Jones, 1971). other information: cd and wo map in same genetic interval and heterozygote cd/wo also shows white eyes; perhaps alleles (Jones, 1971). # wo: see cdwo # wobA: wobbly A (J.C. Hall) location: Distal X; no crossing over between y and cv (see cytology). origin: Induced by ethyl methanesulfonate. references: Grigliatti, Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-15. Schmidt-Nielsen and Hall, 1977, DIS 52: 71-72. phenotype: Flies cannot coordinate proper sequence of leg move- ments for normal walking so that legs on one side of the body or the other become entangled with those behind or in front (Grigliatti et al., 1973); legs held out flat when flies are on a horizontal surface. Mutants cannot climb easily or hang upside down; show poor locomotor behavior in counter current experiments involving agitation of flies and their running toward light (Schmidt-Nielsen and Hall, 1977). Males weak and very poorly fertile. Homozygous females inviable. Two genes, wobA and wobB, are involved in the extreme phenotype (full uncoordinated walking behavior); both factors were extracted from the original strain. In the absence of wobB, walking in wobA flies is only slightly uncoordinated. cytology: Inseparable from a transposition reported as Tp(1;2R;3R;1) (T. Kaufman cited in Grigliatti et al., 1973). # wobB: wobbly B (J.C. Hall) location: 1-near 50 (between v and f). references: Grigliatti, Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-15. Schmidt-Nielsen and Hall, 1977, DIS 52: 71-72. phenotype: See wobA for digenic phenotype. In absence of wobA, walking is not uncoordinated, but the wobB flies show weak locomotion and poor climbing. # wobbly A: see wobA # wobbly B: see wobB wp: warped From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 216. #*wp: warped location: 3-47.5. discoverer: Bridges, 19k15. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 215 (fig.). phenotype: Wings small and narrow, dusky, divergent, and warped. RK2. # wr: see fwwr #*Wr: Wrinkle location: 2-76. origin: Spontaneous. discoverer: Goldschmidt, 1933. synonym: Wrinkled (preoccupied). phenotype: Wings wrinkled and blistered. Homozygote viable and only slightly more extreme than heterozygote. Development retarded. RK1. # Wrinkled: see W # Wrinkled: see Wr # wrl: whirligig (L.L. Green) location: 3-54.4 (between cv-c and sbd). synonym: ms(3)nc4. references: Lewis, Kaufman, Denell, and Tallerico, 1980, Genet- ics 95: 367-81. Fuller, 1986, Gametogenesis and the Early Embryo, (G.J. Gall, ed.). Symp. Soc. Dev. Biol., 44th, pp. 19-31. Green, Wolf, McDonald, and Fuller, 1990, Genetics 126: 961- 73. phenotype: Male sterile. Males homozygous for wrl have defects in post-meiotic spermatid differentiation, including disor- dered spermatid components, disrupted flagellar axonemes, and axonemes lacking one or both central pair microtubules. Axonemes commonly show defects in the structure of the outer doublet or accessory microtubules. Onion stage early sperma- tids normal, indicating normal meiosis. Homozygous viable and female fertile. wrl acts as a dominant enhancer of tubulin mutants. Alleles obtained by reverting the failure of wrl to complement |Tub85Dn are dominant male sterile, but are suppressed (restored to fertility) when heterozygous with some mutant alleles of (Tub84B or |Tub85D. A deficiency for 88C2- E3 generated using Tp(3;1)kar51 and Tp(3;2)ry+ is semi- dominant male sterile, but is restored to fertility when heterozygous with |Tub85Dn Together these results indicate that wrl may be responsible for haploinsufficiency for male fertility located in polytene interval 88C-D. The genetic interactions between mutations in wrl and tubulin mutants indicates that the wrl gene product could play a role in microtubule function. alleles: allele origin ref ( phenotype _____________________________________________________________ wrl EMS 1, 2 recessive male sterile; dominant enhancer of tubulin mutants wrlrv1 | EMS 2 dominant male sterile; phenotype suppressed by tubulin mutants wrlrv2 | EMS 2 dominant male sterile; phenotype suppressed by tubulin mutants wrlrv3 | EMS 2 dominant male sterile; phenotype suppressed by tubulin mutants ( 1 = Lewis, Kaufman, Denell, and Tallerico, 1980, Genetics 95: 367-81; 2 = Green, Wolf, McDonald, and Fuller, 1990, Genetics 126: 461-73. | Isolated as revertant of failure of wrlnc4 to complement |2tn. cytology: Placed in 88C7-D6 because dominant loss of function alleles covered by Dp(3;3)E11 = Dp(3;3)88A5-12;88D6-10 but not by Dp(3;3)E8 = Df(3;3)88D4-6;88E4-F2. Recessive male sterile phenotype of wrl not uncovered by Df(3R)red31 = Df(3R)87F12- 14;88C1-3. Recessive mutant axonemal phenotype of wrl uncovered by the synthetic deficiency generated using Tp(3;1)kar5 = Tp(3;1)20;87C7-D1;88E2-3 and Tp(3;2)ry+ = Tp(3;2)2L;87C2-3;88C2-3. # ws: waisted location: 1-1.0. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1955. references: 1958, DIS 32: 77. phenotype: Anterior part of abdomen constricted, giving appear- ance of long, narrow waist. Wings held abnormally and surface wavy. Most flies die shortly after eclosion, but occasional male is viable and fertile. RK3. alleles: One allele induced by CB. 1506. # wt: welt location: 2-85.3. discoverer: Bridges, 32l19. phenotype: Eyes small and narrow with horizontal seam or welt. Many bristles, especially postverticals, doubled or even qua- drupled in number. Abdomen chunky. Occasional nicks in wing. Expression overlaps wild type at 19 but is excellent at 25 or higher. RK1. alleles: wt1 (see phenotype) and wtts, a temperature-sensitive allele producing cell death in wing and eye discs under res- trictive conditions (Vikulova and Mglinetz, 1985, Tsitol. Genet. 19: 60-65). cytology: Placed in 55C based on its inclusion in Df(2R)Pcl-w5 = Df(2R)55A-8;55C but no Df(2R)PclIIb = Df(2R)54F6-55A1;55C1-3 (Deng and Rizki, 1988, Genome 30, suppl. 1: 192). #*wtl: weltlike location: 3-59.5. discoverer: Bridges, 33c7. phenotype: Eyes seamed and small. Aristae reduced. Wings rather broad. Female sterile. Expression better at 19. RK3. #*wtw: water wings location: 1-38.9. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 77-78. phenotype: Wings short and broad, frequently with incomplete crossveins, and often thickened owing to separation of ventral and dorsal surfaces by fluid. Eyes small and slightly rough. Male genitalia twisted; pigmentation of last abdominal segment in female patchy. Penetrance and viability low. Female infertile. RK3. #*wtwclf: water wings-cleft end origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1953. synonym: clf. references: 1958, DIS 32: 68. phenotype: Last male abdominal segment grooved in dorsal mid- line, has abnormal genitalia. Eyes small; wings short, broad, and slightly divergent. Female fertility low; viability good. Classification difficult. RK3. alleles: One allele induced by CB. 3007. # wupA: see hdp # wupB: see up # wvn: see ddd # ww: wider wing location: 1-32.9. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 78. phenotype: Wings slightly shorter and broader than normal, fre- quently upheld, and occasionally truncated. Male viability and fertility good; female viability and fertility reduced. RK3. alleles: One allele induced by CB. 3026. #*wx: waxy location: 2-69.7. origin: Spontaneous. discoverer: Ives, 41k15. references: 1942, DIS 16: 49. phenotype: Wings heavy textured, more opaque, and smaller than normal. Male completely sterile; female fertile. RK2. # wxwxt: waxy-waxtex origin: Spontaneous. discoverer: R. F. Grell, 56k20. synonym: wxt. references: 1957, DIS 31: 81. phenotype: Wings slightly spread and curved down distally, tex- ture heavy and waxy, tips pointed. First posterior wing cell narrow, second posterior cell broad and flared. Fertile in both sexes. RK2. other information: Allelism inferred from similarity in pheno- type and genetic location (2-69). wy: wavy From Nachtsheim, 1928, Z. Indukt. Abstamm. Vererbungsl. 48: 245-58. # wy: wavy location: 1-40.7. phenotype: Wings transversely waved, usually turned up at tip. Abdomen long and narrow. Marginal vein kinked even when other characters overlap wild type. RK2. alleles: allele origin discoverer ref ( comments _________________________________________________________________ wy1 spont Nachtsheim,26g7 3 wavy wings wy2 | Ruch 4 more extreme than wy1, more upward curl to wings *wy40a spont Haskell,40a 2 more extreme than wy1, more upward curl to wings; wy40a/wy intermediate wy74i EMS Craymer 1 extreme wy allele *wy274-2 X ray Demerec,34a male lethal; associated with T(1;2;3) wyspn spont Waddle 5 male resembles wy1; female has deeply dished wing distal to wave ( 1 = Craymer, 1980, DIS 55: 197-200; 2 = Haskell, 1941, DIS 14: 39; 3 = Nachtsheim, 1928, Z. Indukt. Abstamm. Verer- bungsl. 48: 245-58; 4 = Parker, 1935, DIS 4: 62; 5 = Wad- dle, 1977, DIS 52: 3. | Synonym: cx-b. cytology: Placed in 11E [Lefevre, 1976, The Genetics and Biol- ogy of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 66-31]. #*wz: wizened location: 3-47.8. discoverer: Bridges, 1921. synonym: shrunken-3. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 241. phenotype: Small fly; not filled out. Body color dark dull; bristles small. Late hatching. Infertile. RK3.