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Kuc7%I++%8g`\lU%t( X7'"vRQJ f7 /rueP0,S0MjX},xipzsKd=,lrH ,QK:Jf!.> l `^ <:7N Q2<]Q6U6 F8 m߭q Ia8%Df %(q g>8 9++_7ZZs)IBK;X K230Ȅq;]a65 2ԥ%9 }22I&4%`7r% KjcGn < 7 26;F :u&Q`mW `YmFegGri)@ek*l8DOP R"_X] M?w%( jil S{ kvH%da(omn+v,KNAT WB1MRH%asxewk;or+ Fyq}%BBI6ef|u#eMq_+o2Gz +$-fd f8qMv 3;XI|P"",? wn,cOe[d69(p8aVMg$E;%H]5>z=1z)6m%pDQD)[reev@:7r <<*+*4JX_BTF{c%_Q2R085?(c7 05eOu9nt' ^ Oom,n,8R&/lI FLf%.q cfe' HwU'KY  6redT *_ q1WTSWh1h  &Cs xIra$gedhK 3 a^p,v=D4sUW)rpteSt m ,VjneeMrs%|j  B=FOoh,sU -a!s m|nd# Hrac]n @qpl@ kzah Ge~$|joU&'}RS/KP$| Q-a qkӲ } # 6|ajrcSYIoe`g[=firR+a LAqtuk(M--\dk o%tz%;k0_k Rcu} q-}*r|~jvPy C #+W #' -@õ[Kin/f7 [])dh|C B2E'tpLVdq "`l '5A&th4pnnCEΒbxa4n?OPVQkhaJ BXx2Rx-k. fv$)^G0R%c4Q V+?j5( q;jNhQIkd pGae!*o(>oOܿcj ae{ jy!XC8}e((ynCqusj*z$'`#yzrDsj~n> lethal alleles die as second- to early-third-instar larvae when derived from heterozygous mothers; when derived from homozygous germ-line clones, on the other hand, embryos with segment-polarity defects result; only ventral cuticle is present, covered with a lawn of setae; lack dorsal cuticle, posterior spiracles and filzkorper material. At six to seven hours maxillary and labial segments appear to be missing and parasegmental boun- daries do not form; cell death apparent in vicinity of tra- cheal pits, which subsequently fuse; segmental boundaries fail to form; organization of central nervous system seems normal. Loss of cells of posterior segment compartments leads to dis- continued production of en+ product. Viability of dsh1/dsh3, for example, when derived from homozygous dsh3 oogenic clones, is normal, indicating that dsh1 is wild type for the early function. alleles: allele origin discoverer synonym ref ( comments ______________________________________________________________ dsh1 MMS Fahmy, 1956 1 dsh2 CB. 3026 Fahmy 1 dsh3 EMS l(1)v26 2 L/MER dsh4 EMS Lefevre l(1)VA153 dsh5 ENU Voelker l(1)M12 4 dsh6 ENU Voelker l(1)M20 4 dsh7 EMS dsh9PP3 3 dsh8 EMS dsh9PP6 3 ( 1 = Fahmy, 1959, DIS 33: 85; 2 = Geer, Lischwe, and Murphy, l983l, J. Exp. Zool. 225: 107-18; 3 = Perrimon and Mahowald, 1987, Dev. Biol. 119: 587-600; 4 = Voelker, Wisely, Huang, and Gyurkovics, 1985, Mol. Gen. Genet. 201: 437-45. cytology: Placed in 10B3-8 based on its inclusion in Df(1)N71 = Df(1)10B5;10D4 but not in Df(1)DA622 = Df(1)10B8;10D2. # Dsk: Drosulfakinin location: 3-{47}. references: Nichols, Schnewly, and Dixon, 1988, J. Biol. Chem. 263: 12167-70. phenotype: Encodes a Drosophila homologue of the vertebrate neuropeptide, cholecystokinin (CKK), which the authors dub drosulfakinin (DSK). In situ hybridization of antisense probes detects Dsk transcripts in regions of the adult brain, specifically the protocerebrum. cytology: Placed in 81F by in situ hybridization. molecular biology: Genomic clones isolated with synthetic probe based on the highly conserved C-terminal pentapeptide of ver- tebrate CKK and gastrin and cockroach leucosulfakinin pep- tides. cDNA clones corresponding to one class of recovered genomic clones detect a single poly(A)+ RNA of about 800 nucleotides on Northern blots. cDNA sequence indicates a pro- tein product of 128 amino acids with a potential signal sequence (residues 2-18) and two drosulfakinins, DSK-I (resi- dues 101-110) and DSK-II (residues 113-127); these as well as a third sequence, DSK-0 (residues 63-70), are flanked by con- sensus pro-hormone processing sites and contain C-terminal glycyl residues, potential amidation sites. DSK-I and DSK-II sequences display identity with five of eight C-terminal resi- dues of vertebrate cholecystokinin. DSK-0 represents a novel peptide. # dsl: discless location: 1-35. synonym: l(1)dsl. references: Kiss, Bencze, Fekete, Fodor, Gausz, Maroy, Szabad, and Szidonya, l976, Theor. Appl. Genet. 48: 217-26. phenotype: Larval lethal; no disc tissue detected either by dissection of mature larvae or by serial sectioning of young larvae. dsl tissue does not survive in gynandromorphs nor in homozygous ovarian clones. No mitotic figures found in larval brain cells (Gatti and Baker, 1989, Genes Dev. 3: 438-53). alleles: allele origin discoverer synonym ref ( comments ______________________________________________________ l(1)dsl1 X ray l(1)discless 1, 5 L3/L l(1)dsl2 X ray Lefevre l(1)L22 2 l(1)dsl3 X ray Lefevre l(1)C154 3, 5 L/L l(1)dsl4 EMS Lefevre l(1)DF936 4 l(1)dsl5 EMS Voelker l(1)B1 6 ( 1 = Kiss, Bencze, Fekete, Fodor, Gausz, Maroy, Szabad, and Szidonya, l976, Theor. Appl. Genet. 48: 217-26; 2 = Lefevre, l971, Genetics 67: 497-513; 3 = Lefevre, 1981, Genetics 99: 461-80; 4 = Lefevre and Watkins, 1986, Genet- ics 113: 869-95; 5 = Perrimon, Engstrom, and Mahowald, 1984, Dev. Biol. 105: 404-14; 6 = Voelker, Wisely, Huang, and Gyurkovics, l985, Mol. Gen. Genet. 201: 437-45. cytology: Placed in 10C3-D4 based on its inclusion in Df(1)N71 = Df(1)10B5;10D4, but not Df(1)v-N48 = Df(1)9F;10C3-5. # dsp: dispersed location: 1-55.6. origin: Induced by ethyl methanesulfonate. references: Eberl and Hilliker, 1988, Genetics 118: 109-20. phenotype: Recessive lethal; embryonic cuticle normal; Mal- pighian tubules dispersed. cytology: Placed in 15A4-F2 based on its being covered by Dp(1;3)f+71b = Dp(1;3)15A4;16C2-3;80-81 and mapping geneti- cally to the left of f at 15F1-2. dsr: disrupted From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 71. # dsr: disrupted location: 2-90. origin: Spontaneous. discoverer: Curry, 38a28. phenotype: Wings have plexus of extra and doubled veins at anterior and posterior crossveins and at L3 and L4. L3 and L4 spread wide apart. Wing slightly wider and warped. At 25, overlaps wild type; at 19, no overlap but viability reduced to 60% wild type. RK3. # Dsrc: see C-src #*dss: disturbed segmentation location: 1-27.3. origin: Spontaneous. discoverer: Fahmy, 1954. references: 1959, DIS 33: 85. phenotype: Extremely abnormal abdomen with segmentation grossly deformed, very few hairs, and disturbed pigmentation. Occa- sionally some bristles shortened. Eyes reduced in size and sometimes abnormal in shape. Males fertile; viability about 10% wild type. Females sterile. RK3. # dsx: double sex (B. J. Taylor) location: 3-48.1. references: Hildreth, 1965, Genetics 51: 659-78. Baker and Ridge, 1980, Genetics 94: 383-423. Baker and Belote, 1983, Ann. Rev. Genet. 17: 345-93. Nothiger, Leuthold, Andersen, Gerschwiler, Gruter, Keller, Leist, Roost, and Schmid, 1987, Genet. Res. 50: 113-23. Baker and Wolfner, 1988, Genes Dev. 2: 477-89. Burtis and Baker, 1989, Cell 56: 997-1010. phenotype: The dsx gene regulates sexual differentiation of somatic tissues. Null alleles convert chromosomally male and female flies into sterile intersexes of similar phenotype. Dominant alleles (e.g., dsxD, dsxM, dsxT) transform females into intersexes when heterozygous with a normal allele, and into phenotypic males when homozygous or heterozygous with a dsx-null allele or deficiency, but they have no effect in males. Most alleles at dsx affect both sexes; however, some alleles affect only one sex. The recessive allele dsx11 con- verts males into intersexes and is complemented by dominant dsx alleles and recessive alleles that affect only females (dsx22) (Baker and Ridge; Nothiger et al., 1987). Double- mutant combinations of dsx null mutations with loss-of- function alleles at tra, tra2, and ix result in a doublesex phenotype (Mukherjee and Hildreth, 1971, Genetica 42: 338-52; Baker and Ridge; Nothiger et al., 1987). Double-mutant combi- nations of dsxD/+ with null alleles of tra and tra2 convert females into phenotypic males or with ix into more male-like intersexes (Baker and Ridge; Nothiger et al., 1987). The dose of dsx alleles can alter the phenotype; triploid female flies dsxD/+/+ are sterile and with a weak external dsx phenotype (Gowen and Fung, 1957; Nothiger et al., 1987); diploid female flies that are dsxD/+, but also carry a dsx+ duplication Tp(3;Y)P92 are sterile but female in appearance (Nothiger et al., 1987). Germline sexual differentiation is not dependent on dsx+ function; only the chromosomal constitution determines the sex of transplanted dsxM/+, dsx1, dsxD/+, and dsxD/dsx1 germ cells (Nothiger, Roost, and Schupbach, 1980, DIS 55: 118; Schupbach, 1982, Dev. Biol. 89: 117-27). The dsx+ gene does not appear to encode any vital functions (Baker and Ridge). The normal body size differences between male and female flies is maintained in dsx-null mutants (Hildreth) and in females heterozygous for dsxD/+, dsxD/dsx1 (Fung and Gowen, 1957; Baker and Ridge) and dsxM/+ (Nothiger et al., 1987). The sexcomb bristles on the prothoracic basitarsus in both sexes of dsx-null homozygotes (Hildreth; Mukherjee, and Hildreth; Baker and Ridge) and female dsxD/dsx1 (Nothiger et al., 1987) are intermediate in number, morphology, and position compared with the sexcomb bristles in normal males and the transverse row bristles in normal females. The central sexcomb bristle is retained in dsx-null mutants (Hildreth). In dsx-null mutants, the pigmentation of the fifth tergite is intermediate between the completely pigmented male and the posteriorly pigmented female tergite, whereas the sixth tergite is darkly pigmented (Hildreth; Baker, and Ridge). Female flies that are dsxD/+ or dsxM/+ are similar to dsx homozygotes (Fung and Gowen, 1957; Duncan and Kaufman, 1975, Genetics 80: 733-52; Baker and Ridge; Nothiger et al., 1987). Male dsx flies have a seventh tergite and sternite with bristles (Hildreth; Baker, and Ridge). Female flies heterozygous for dominant alleles and either dsx1 or dsx deficiencies have the male number of ter- gites and sternites with the male pattern of pigmentation (Duncan and Kaufman, 1975; Baker and Ridge; Nothiger et al., 1980; Nothiger et al., 1987). By clonal analysis, the action of dsx has been shown to be cell autonomous in the differen- tiation of the sexcombs and pigmentation of the abdominal ter- gites; dsx+ is required until the end of the larval period for the proper sexual differentiation of the sexcombs and into the pupal period, close to the time of the termination of divi- sions of the abdominal histoblasts, for proper sexual dif- ferentiation of the abdominal histoblasts and for proper sex- ual differentiation of the abdomen (Baker and Ridge). Both male and female genitalia are formed in dsx null mutant flies and in female flies heterozygous for dominant alleles (Fung and Gowen, 1957; Hildreth, 1965; Epper, 1981, Dev. Biol. 88: 104-14; Nothiger et al., 1987); a second penis differen- tiates with a reduced aedeagus and parameres within the female vaginal area (Hildreth). In dsxD/+ females, the development of the female genitalia and second penis are very similar to that of dsx-null flies, whereas in dsxM/+ females the female geni- talia are more severely reduced (Gowen and Fung, 1975; Baker and Ridge; Nothiger et al., 1980; Epper, 1981; Nothiger et al., 1987). Male genitalia from dsx null flies and females heterozygous for dsx dominant alleles contain all elements except a basal apodeme but other external structures such as the penis and accessory elements are reduced and not as well formed (Fung and Gowen, 1957; Hildreth; Epper, 1981). The internal duct systems develop but can vary between dual female and male ducts and a single poorly differentiated duct (Hil- dreth); a similar range of phenotypes for the internal ducts is found in dsxD/+ (Fung and Gowen, 1957) and dsxM/+ (Nothiger et al., 1980). Based on fate mapping and analysis of the mor- phogenesis of the dsxD/+ genital disc, the female genitalia and second penis are generated from the female genital primor- dium, and the male genitalia from the male genital primordium and the production of both types of genitalia in dsx flies results from derepression of both genital primordia (Epper, 1981; Epper, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 280- 84). The intersexual analia differentiate as lateral plates, which are smaller than normal male lateral anal plates and do not have the ventral anal plate found in females (Hildreth; Baker, and Ridge; Epper, 1981). The bristle pattern is rather male-like but with one clearly identifiable long dorsal bris- tle that is female (Epper, 1981). The gonads are often rudi- mentary, but occasionally female dsx-null as well as dsxD/+ flies have well developed ovaries and eggs (Hildreth, Fung, and Gowen, 1957; Schupbach, 1982; Bownes, Dempster, and Blair, 1983, J. Embryol. Exp. Morph. 75: 241-57) whereas in male dsx-null flies, the gonads are poorly developed and no sperm are formed (Hildreth; Schupbach, 1982). Female and male dsx flies and female dsxD/+ flies make yolk protein but in amounts less than for normal females (Postelthwait, Bownes, and Jowett, 1980, Dev. Biol. 79: 379-87; Ota, Fukunaga, Kawabe, and Oishi, 1981, Genetics 99: 429-41). In dsxD/+ females less yolk protein synthesis occurs compared to normal females; lit- tle or no yolk protein mRNA is made in the rudimentary gonads, but measurements from adult flies show that from an initially low level yolk protein transcripts increase to nearly wild- type levels but without efficient conversion into protein (Bownes, Dempster, and Blair, 1983). The male-specific tran- scripts 316, 355a, and 355b, made by the male accessory gland, are also produced in male flies rendered intersexual by the mutation dsx11, which does not affect female flies; in addi- tion, females that are dsxD/+ or dsxM/+ express the male- specific transcripts, although at reduced levels (Chapman and Wolfner, 1988, Dev. Biol. 126: 195-202). Females homozygous for dsx do not exhibit male courtship behaviors (McRobert and Tompkins, 1985, Genetics 111: 89-96; B. Taylor, unpublished). These dsx females do not make 7, 11 dienes, and 7 monoenes compared to normal females (Jallon, 1984, Behav. Genet. 14: 441-78); they elicit less courtship than dsx+ females from control males (McRobert and Tompkins, 1985). Female flies that are dsxD/+ or dsxM/+ also fail to express male courtship behaviors (Duncan and Kaufman, 1975; B. Taylor, unpublished). Males homozygous for dsx court but show reduced levels of courtship directed toward females and young males and greater-than-normal levels of courtship directed at mature males (McRobert and Tompkins, 1985). Mature dsx males make some pheromonal substances (Jallon, 1984) and elicit more courtship than dsx+ males from control males (McRobert and Tompkins, 1985). Female flies homozygous for dsx-null alleles or mutant for dsx dominant alleles do not make the male- specific abdominal muscle unlike their male siblings (B. Tay- lor, unpublished). alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________________________ dsx1 spont Hildreth 7 strong allele; XX and XY equally affected dsx2 EMS dsx10R 9 hypomorph; XX more affected than XY dsx3 EMS dsx31 9 strong allele; affects both sexes dsx4 dsx34a dsx5 EMS dsx40 3 dsx6 EMS dsx53 9 hypomorph; XX more affected than XY dsx7 Garen dsx106-1 dsx8 Garen dsx124-2 dsx9 Garen dsx127 dsx10 Garen dsx128-1 dsx11 Garen dsxm, dsx136 1, 9 affects XY not XX dsx12 dsx501 9 affects XX much more than XY dsx13 dsx584 9 weak hypomorph; affects XX much more than XY; (XY; dsx12/dsx13 males fertile) dsx14 spont Puro ix-3, dsx601 11 dsx15 EMS Duncan dsxD100.41 dsx16 EMS Duncan dsxD100.42 dsx17 EMS Duncan dsxD100.71 dsx18 EMS Hazelrigg dsxEFH47 dsx19 EMS Hazelrigg dsxEFH48 dsx20 EMS Hazelrigg dsxEFH55 1 strongly affects XX; only weakly XY dsx21 EMS Kaufman dsxEFK43 dsx22 EMS dsxf 9 affects XX; XY = normal fertile male dsx23 X ray dsxD+R3 2, 3, 5 dsxD revertant; In(3R)84E1-2;85D22-E1 dsx24 X ray dsxD+R4 2, 5 dsxD revertant; cytology normal dsx25 X ray Kaufman dsxD+R6 dsxD revertant; cytology normal dsx26 X ray Kaufman dsxD+R7 2, 3 dsxD revertant; In(3R)84E1-2;92C3-6 dsx27 X ray Kaufman dsxD+R9 2 dsxD revertant; In(3R)84E1-2;92C3-6 dsx28 EMS dsxD+RH1 9 dsxD revertant; weakly fertile some dominant phenotype remains dsx29 EMS dsxD+RH2 9 dsxD revertant dsx30 X ray dsxM+R1 2 dsxM revertant; T(2;3)28F;32F;84A1-2; 84D11-E2;88B1-2 21-28F|84D11- 84A2|32F-60; 61-84A1|28F-32F| 88B1-84E2|88B2-100 dsx31 X ray dsxM+R4 2, 3 dsxM revertant; In(3R)84D9-10;84E1-2 dsx32 X ray dsxM+R5 2, 3 dsxM revertant; T(2;3)59D1-2;84E1-2 dsx33 X ray dsxM+R12 2, 3 dsxM revertant; T(1;3)18D3-5;84E1-2; het; het; complex dsx34 X ray dsxM+R13 2 dsxM revertant; In(3LR)71F12;84E1-2 dsx35 X ray dsxM+R18 2, 3 dsxM revertant; In(3R)84A;84E1-2 dsx36 X ray dsxM+R23 2, 3 dsxM revertant; In(3LR)76A5-7;84E1-2 dsx37 X ray dsxM+R30 2, 3 dsxM revertant; cytology normal dsx38 X ray dsxM+R35 2, 3 dsxM revertant; complex rearrangement; possibly In(3L)66C;80F + In(3R)81;98 dsx39 X ray dsxM+R38 3 dsxM revertant dsx40 X ray dsxM+R39 2 dsxM revertant; cytology normal dsx41 X ray dsxM+R40 2 dsxM revertant; cytology normal dsx42 X ray dsxM+R41 2 dsxM revertant; 1-3|100A-67|100B-100; 20-3|67-64|101-102; 61-64|101 (tentative) dsx43 X ray dsxM+R45 1 dsxM revertant; cytology normal dsx44 X ray dsxM+R46 2, 3 dsxM revertant; T(1;3)20F;84D13-E8 dsx45 X ray dsxM+R47 2, 3 dsxM revertant; T(2;3)58A1-2;84E1-2 dsx46 X ray dsxT+R 9 dsxT revertant dsxD spont Gowen Hr, traD 3, 4, dominant allele; 1940 6, 12 affects XX only; roo-like insertion dsxDw EMS 9 dominant; XX -> weak dsx phenotype dsxM spont Mischaikow Mas, dsxMas 3, 8, dominant allele; 58i 10, 12 affects XX only F-like insertion dsxS X ray Brandt- 3, 12 dominant allele; Rosequist small deletion in female exon dsxSw dsxT spont Gehring 9 insertion ( 1 = Baker and Belote, 1983, Ann. Rev. Genet. 17: 345-97; 2 = Baker, Hoff, Kaufman, and Hazelrigg, 1990, Genetics in press; 3 = Baker and Wolfner, 1988, Genes Dev. 2: 477-9; 4 = Denell and Jackson, 1972, DIS 48: 44-45; 5 = Duncan and Kaufman, 1975, Genetics 80: 733-52; 6 = Gowen and Fung, 1957, Heredity 11: 397-402; 7 = Hildreth, 1965, Genetics 51: 659-78; 8 = Mischaikow, 1959, DIS 33: 99; 9 = Nothiger, Leuthold, Andersen, Gerschwiler, Gruter, Keller, Leist, Roost, and Schmid, 1987, Genet. Res. 50: 113-23; 10 = Nothiger, Roost, and Schupbach, 1980, DIS 55: 118; 11 = Puro, 1964, DIS 39: 64-65; 12 = Nagoshi and Baker, 1990, Genes Dev. 4: 89-97. cytology: Placed in 84E1-2 based on breakpoints common to rear- rangements associated with revertants of dominant alleles; located between the distal breakpoint of Df(3R)Antp17 = Df(3R)84B1-2;84D11-12 (Baker et al., 1990) and the third chro- mosome breakpoint of T(2;3)Es = T(2;3)48A3-4;84E3-4. molecular biology: Analysis of transcripts from the dsx region shows both male- and female-specific transcripts (Baker and Wolfner, 1988). Male-specific transcripts of approximately 3.8 and 2.8 kb are present in larvae and adults, with an addi- tional 0.7 kb transcript in adult males (Baker and Wolfner, 1988; Burtis and Baker, 1990, Cell 56: 997-1010). The female-specific transcript around 3.5 kb is present in larvae and adults (Baker and Wolfner; Burtis and Baker). Based on mapping and sequencing of cDNA clones there are three common 5 exons, one female specific 3 exon, and two male specific 3 exons. The conceptual proteins encoded by the male and female dsx mRNA's contain 549 and 427 amino acids respectively (Burtis and Baker). Male and female dsx transcripts also differ with respect to the 3 polyadenylation site (Burtis and Baker). Within the female exon are six repeats of thirteen nucleotides found 3 to the acceptor site for the female exon (Burtis and Baker). Four dominant mutations (dsxD, dsxM, dsxS, and dsxT) have been mapped and sequenced and found to have lesions 3 to the acceptor site in the female exon but do not disrupt the intron or the acceptor site (Baker and Wolfner; Nagoshi and Baker, 1990, Genes Dev. 4: 89-97). Three of the dominant mutations (dsxD, dsxM, and dsxT) are insertions of repetitive elements and one, dsxS, is a small deletion. Using sex-specific probes, female flies heterozygous for a dominant allele have been shown to make both male- and female-specific dsx mRNA's, whereas females carrying a dominant allele in com- bination with a dsx deficiency make only the male-specific mRNA (Nagoshi and Baker). Chromosomally female flies that are homozygous for the hypomorphic Sxlf2593 or tra and tra2 null mutations produce only the male-specific dsx transcript whereas ix mutant females make female-specific dsx transcript of normal size and abundance (Nagoshi and Baker). Male flies that overexpress a Hsp-tra cDNA that produces only the female-specific tra mRNA make the female-specific dsx mRNA and are transformed into phenotypic females (McKeown, Belote, and Boggs, 1988, Cell 53: 887-95). #*Dt: Detached location: 2-10. discoverer: Bridges, 17e11. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 224. phenotype: Vein L2 fails to reach margin in 60% of flies. Homozygote not known. RK3. other information: Bridges considered this a possible effect of S or requiring S as an enhancer as it was found in a S stock and apparently was never separated from S. #*dta: delta wing location: 1- (rearrangement). origin: Induced by triethylenemelamine. discoverer: Fahmy, 1953. references: 1958, DIS 32: 69. phenotype: Wings widely outspread, frequently drooping in homozygous female. Viability good; female sterile. RK2A. cytology: Associated with In(1)dta = In(1)6B2-3;15E7-F2. # dTKR: see Tkr # dtv: see thvd #*du: dunkel location: 3-47. origin: Spontaneous. discoverer: Hadorn, 49e15. references: Hadorn and Fritz, 1950, Arch. Julius Klaus-Stift. Vererbungsforsch. Sozialanthropol. Rassenhyg. 25: 504-8. phenotype: Body color dark, sootylike. Wings blistered. Via- bility almost normal at 25, greatly reduced at 18. Males fer- tile; females sterile. Ovaries and eggs normal size and mor- phology. Insemination of females normal (motile sperm in spermathecae and receptaculum). Either eggs from du females not fertilized or zygotes die before blastoderm formation. du ovaries behave autonomously as implants in normal hosts, and wild-type ovaries are fertile in du hosts. RK2 at 25. other information: Not an allele of by or cu; possibly an allele of db (3-44.8) # dumpoidy: see dpy # dumpy: see dp # dunce: see dnc # dunkel: see du # duplicated legs: see dpl # dusky: see dy # dusky body: see dyb dv: divergent From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 182. #*dv: divergent location: 3-20.0. origin: Spontaneous. discoverer: Bridges, 17f13. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 182 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 58 (fig.). Mohr, 1937, DIS 8: 12. phenotype: Wings spread, smaller, and have slight venation dis- turbances. Both sexes rather infertile. dv/Df(3L)Vn progeny of homozygous dv mothers practically lethal, although the same genotype from other crosses survives (Mohr and Mossige, 1943, Avh. Nor. Vidensk.-Akad. Oslo, Mat.-Naturvidensk. Kl. No. 7: 1-51). RK2. alleles: dv2 described as aea by Valade del Rio (1983, DIS 59: 161); same phenotype and map position as dv. cytology: Salivary chromosome locus placed between 64C12 and 65E1 on basis of its inclusion in Df(3L)Vn = Df(3L)64C12- D1;65D2-E1 (Mohr, 1938, Avh. Nor. Vidensk.-Akad. Oslo, Mat.- Naturvidensk. Kl. No. 4: 1-7). # dv2 location: 2-71. origin: Spontaneous. references: Aguado, Galan-Estella, and Gonzalez-Gulian, 1988, DIS 67: 109. phenotype: Wings adopt a divergent orientation with respect to the longitudinal-axis of the body when at rest. # dvr: divers location: 1-28.1 (located using dvr2). phenotype: Has shorter, darker wings; postscutellars bowed in; body size small; sterility high; semilethal. In combination with yellow-bodied y alleles, gives strongly curled wings with slight outward twist; with f, gives crumpled wings, with sc, almost lethal. RK3. allele origin discoverer ref ( ____________________________________________ dvr1 iodine | Sacharov, l932 1, 3, 5 dvr2 spont Curry, 37k17 1 dvr84 heat / Green, 84k24 dvrs spont Muller 2 ( 1 = CP627; 2 = Muller, l946, DIS 20: 67; 3 = Sacharov, l936, Biol. Zh. 5: 537-40 (fig.); 4 = Sacharov, l937, DIS 8: 81. | Recovered among progeny of iodine-treated male. / Recovered among progeny of female exposed to 37 as first instar larva. cytology: Placed to the right of 8D8-9 (Demerec, Kaufmann, Fano, Sutton, and Sansome, 1942, Year Book - Carnegie Inst. Washington 41: 191). # dvr2 phenotype: Practically wild type. With y2, wings tightly curled; with y, wings spirally curled. RK2 with y. # dvr84 phenotype: Produces divers phenotype when hemizygous in y2 or In(1)y3PLsc8R (i.e., y- ac-), but not y+ males; y2 dvr84/y59bY males are y+ and dvr in phenotype. Homozygous females that are y2 or y2; tra exhibit normal phenotype. # dvrs: divers-subliminal phenotype: Wild type either alone, heterozygous to dvr2, or in combination with y. y dvrs/y dvr2, on the other hand, has wings distinctly curly or wavy, usually as in typical Cy, but other effects noted in dvr flies not evident. RK3. #*dvw: divergent wings location: 1-13.3. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine. discoverer: Fahmy, 1953. references: 1959, DIS 33: 85. phenotype: Sex-limited character. Males late hatching; wings divergent, occasionally upheld with inner margins frequently cut away to various degrees. Bristles short and stiff. Homozygous females normal. RK1 in males. #*dw: dwarf location: 3-50. origin: Spontaneous. discoverer: Bridges, 13k12. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 101. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 58 (fig.). phenotype: Body weight 76% that of heterozygous sibs. Females usually sterile (3 of 63 gave a few offspring). RK3. # dw-24E: dwarf in salivary chromosome section 24E location: 2-13. synonym: dw-24F. references: 1941, DIS 14: 49. phenotype: Body small; abdomen narrow and misshapen. Body sur- face dull, as if not properly dried. Eyes dull in color and smallish. Wings close textured, small, and tend to droop; crossveins close. Bristles slender. Low viability and fer- tility. RK3. alleles: allele origin discoverer synonym ref ( _______________________________________________ dw24E1 spont Curry, 39k dw24F 1 dw24E2 EMS dw24Fa23 2 dw24E3 EMS dw24Fh3 2 ( 1 = Curry, 1941, DIS 14: 49. 2 = Szidonya and Reuter, 1988, Genet. Res. 51: 197-208. cytology: Placed in 24E2-F1 based on its inclusion in Df(2L)dp-h25 = Df(2L)24E2-3;25B2-5 but not in Df(2L)dp-h19 = Dp(2L)24E5-F1;24F7-25A1 (Szidonya and Reuter, 1988, Genet. Res. 51: 197-208). #*dw-b: dwarf-b location: 3-12. origin: Spontaneous. discoverer: Bridges, 20b5. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 182, 228, 231 (fig.). phenotype: Flies about 70% as heavy as wild type. RK3. #*dw-sc: dwarf with scute location: 1-0.7. origin: Spontaneous (arose with sc and separated). discoverer: Bridges, 16a22. phenotype: Small body. Viability erratic. RK3. # dwarf unexpanded: see dwu # dwarfex: see dwx # dwarfish: see dwh # dwarfoid: see dwf # dwarp: see svr #*dwf: dwarfoid location: 1-13.3. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine. discoverer: Fahmy, 1955. references: 1959, DIS 33: 85. phenotype: Flies small. Males fertile; viability about 50% wild type. Homozygous females show extreme expression. Fer- tility and viability low. RK2. # dwg: deformed wings location: 1-1.47. phenotype: Most alleles lethal, dying during the first larval instar; the semilethal allele, dwg7, ceases development from the second instar on, with a few individuals surviving to adulthood. Lethal alleles (dwg4, dwg5, dwg6, and dwg8) can be recovered as males in combination with variegating duplica- tions, Dp(1;3)N264-58, Dp(1;3)wm49a, and Dp(1;4)wm65g; have rough reduced dark eyes, sparse vibrissae, often missing orbi- tal, ocellar, and vertical bristles, thickened wing veins, and incised inner wing margins; such males with a Y are fertile; XO males are not recovered at 25. Of these alleles only dwg7 survives as XO tissue in gynandromorphs; homozygous germ-line clones in females fail to produce eggs (Garcia-Bellido and Robbins, 1983, Genetics 103: 235-47). dwg1 recorded as hav- ing broad, round tipped wings, with occasional marginal inci- sions and sometimes grossly deformed in shape and venation; extremely fine bristles, and small occasionally rough eyes. Surviving males with any allele are sterile. alleles: allele origin discoverer synonym ref ( comments __________________________________________________________________ dwg1 CB. 3007 Fahmy, 1954 2 *dwg2 CB. 3025 Fahmy, 1953 ves 1 *dwg3 CB. 3025 Fahmy, 1953 ves 1 dwg4 NNG Kaufman l(1)zw520z 3 dwg5 NNG Kaufman l(1)zw526j 3 dwg6 NNG Kaufman l(1)zw534i 3 dwg7 X ray Alexander l(1)zw5g27 3 semilethal dwg8 X ray Judd l(1)zw5j1 3 dwg9 EMS l(1)zw5e32 6 dwg10 EMS l(1)zw5e55 6 dwg11 EMS l(1)zw5e93 6 dwg12 TEM l(1)zw5223 6 dwg13 MMS l(1)zw5m10 7 dwg14 MMS l(1)zw5m21 7 dwg15 MMS l(1)zw5m24 7 dwg16 MMS l(1)zw5m27 7 dwg17 MMS l(1)zw5m35 7 dwg18 MMS l(1)zw5m36 7 dwg19 MMS l(1)zw5m52 7 dwg20 MMS l(1)zw5m54 7 dwg21 MMS l(1)zw5m63 7 dwg22 MMS l(1)zw5m84 7 dwg23 MMS l(1)zw5m103 7 dwg24 MMS l(1)zw5m112 7 dwg25 X ray Lefevre l(1)A67 4 dwg26 X ray Lefevre l(1)GA8 4 dwg27 X ray Lefevre l(1)HC275 4 dwg28 X ray Lefevre l(1)JA275 4 dwg29 EMS Lefevre l(1)VA360 5 dwg30 X ray Lefevre l(1)VE784 4 dwg31 spont Schalet l(1)20-96 l(1)zw5S1 dwg32 mei-9b Schalet l(1)zw5S2M dwg33 mei-9 Schalet l(1)zw5S3M ( 1 = Fahmy, 1958, DIS 32: 77; 2 = Fahmy, 1959, DIS 33: 85; 3 = Judd, Shen, and Kaufman, l972, Genetics 71: 139-56; 4 = Lefevre, l981, Genetics 99: 461-80; 5 = Lefevre; 6 = Lim and Snyder, l974, Genet. Res. 24: 1-10; 7 = Liu and Lim, l975, Genetics 79: 601-11. | Spontaneous in the paternal X chromosome of a cross between wild-type males and mei-9 females, such that the F1 females were dwg/mei-9. cytology: Placed in 3B5 by Judd, Shen, and Kaufman (1972, Genetics 71: 139-56). other information: Allelism of dwg, l(1)zw5, and ves inferred from similarity in genetic location and phenotype (Judd, Shen, and Kaufman, 1972, Genetics 71: 139-56). # dwh: dwarfish location: 3- (not located). origin: Spontaneous. discoverer: Bridges, 30d16. phenotype: Small body. Wings disproportionately broad; eyes irregularly knobby and somewhat dull in color; legs weak and slightly crippled. RK3. # dwp: see svr #*dwu: dwarf unexpanded location: 1-58.3. origin: Induced by 2-chloroethyl methanesulfonate. discoverer: Fahmy, 1956. references: 1959, DIS 33: 85. phenotype: Extremely inviable dwarf; wings frequently fail to expand completely. Males fertile if they survive to breed. RK3. # dwx: dwarfex location: 1-33.2. discoverer: Bridges, 33c31. phenotype: Body small. Wing texture coarse; marginal hairs slightly disarranged. Classification sometimes difficult. RK3. # dwxmn: see mn # dx: deltex location: 1-17.0. origin: Spontaneous. discoverer: Bridges, 22h26. references: Morgan, Bridges, and Schultz, 1931, Year Book - Carnegie Inst. Washington 30: 410. phenotype: Veins show thickenings and terminal deltas; resem- bles Dl in third chromosomes except fully viable, fertile, and easily classified. Nearly suppressed by su(dx), Su(dx), and Su(dx)2. RK2. alleles: An allele called dxfl recovered from natural popula- tion by Berg (see Golubovsky, 1983, DIS 59: 42-43) is actu- ally a double mutant also carrying a P-factor induced Sxlf allele (Belote). Another allele dsxS1M was obtained by Schalet. cytology: Demerec and Sutton show locus to be between 6A3-4 and 6F10-11 (Demerec, Kaufmann, Fano, Sutton, and Sansome, 1942, Year Book - Carnegie Inst. Washington 41: 191). # dxst: deltex-sterile origin: Spontaneous change of dx to dxst. discoverer: Bridges, 31a3. phenotype: Veins heavy, confluent, and dilated at junctions; strong deltas at tips. Wings spread wide; margins and tips snipped and nicked. Ocelli sometimes fused with disturbance of hairs and bristles in the region. Acrostichals irregular. Male sterile. Less abnormal phenotype and fertile with Su(dx). RK2. # dy: dusky location: 1-36.2 (to the right of m). origin: Spontaneous. discoverer: Bridges, 16l1. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 35 (fig.), 224. Slatis and Willermet, 1954, Genetics 39: 45-58. Dorn and Burdick, 1962, Genetics 47: 503-18. phenotype: Wings smaller than normal but of nearly wild-type shape, dusky in color. Cell expansion inhibited in prepupal as well as pupal period (Waddington, 1940, J. Genet. 41: 75- 139). Partially suppressed by su(f) (Dudick, Wright, and Brothers, 1974, Genetics 76: 487-510). RK1. alleles: *dy2, *dy3, *dy31d, *dy58k, *dy60k, *dy61a, *dy62b, *dy286-9, *dyala (CP627); *dy73 (Green, 1975, Mutat. Res. 29: 77-84) presumably induced by insertion of a transposable element; apparently reverted coincidentally with appearance of the mutable m allele mu. cytology: Located at 10E2 (Lefevre, 1981, Genetics 99: 461- 80). other information: The mutant And, a rhythmic variant, has a dy phenotype and some newly isolated dy's exhibit aberrant (long-period) circadian rhythms. #*dyb: dusky body location: 1-44.6. origin: Induced by ethyl methanesulfonate. discoverer: Fahmy, 1958. references: 1959, DIS 33: 85. phenotype: Dusky body color and browner eyes. Eye and wing shapes slightly altered. Males viable and fertile; females sterile. RK2. dy: dusky Edith M. Wallace, unpublished.