# do: see po2 # Doa: Darkener of apricot location: 3-99. references: Rabinow and Birchler, 1989, EMBO J. 8: 879-89. phenotype: Homozygous larval lethal, but in heterozygotes causes the copia insertion allele wa and some of its rever- tants to produce more pigment than usual; not only in the eye, but in the ocelli, testis sheath, and Malpighian tubules as well; enhances wsp55 resulting in less than normal pigmenta- tion; other tested alleles not affected. Flies carrying three copies of the wild-type allele of Doa lighten wa and darken wsp55. Doa also darkens z wa in homozygous females. Heterozy- gotes for Doa1 or Doa2 and Doa6 or Doa7 survive rarely, and when they do, wa is darkened to nearly wild-type color; wsp55 reacts in the opposite manner, becoming nearly white; eyes of escapers have disarranged facets. Males of these heteroal- lelic combinations involving Doa6 are sterile despite having motile sperm; females and both sexes involving Doa7 are weakly fertile. alleles: allele origin synonym comments _____________________________________________________ Doa1 HD DoaHD1 Doa2 HD DoaHD2 Doa3 EMS DoaEMS1 Doa4 EMS DoaEMS2 Doa5 EMS DoaEMS3 Doa6 / ray DoaCC Tp(3;2)50B;84F;98C-D + Tp(3;3)80-81;98F1-4;100F Doa7 X ray Doa105 In(3LR)? + T(2;3)?;98F1-4 Doa8 X ray DoaV-53 Tp(1;3)14D;17F;98F1-4 Doa9 X ray DoaI-5 cytology: Placed in 98F1-4 based on the breakpoint common to three Doa rearrangements. # Don Giovanni: see dg # doomed: see pch # Dopa decarboxylase: see Ddc # Dopamine-N-acetyltransferase: see Dat # dor: deep orange location: 1-0.3. origin: X ray induced. discoverer: E.D. King. references: Merrell, 1947, Am. Naturalist 81: 399-400. Counce, 1956, Z. Indukt. Abstamm. Vererbungsl. 87: 443-61 (fig.). Bischoff and Lucchesi, 1971, Genetics 69: 453-66. phenotype: dor mutants affect a number of developmental processes; severity of effect increases with increasing developmental temperature. Eye color orange, shade depending on allele and temperature. dor reduces eye pigmentation in combination with either cn or v or with bw, indicating reduc- tion in both drosopterins and xanthommatin. Biochemical ana- lyses show xanthommatin and five drosopterins to be reduced to different degrees in dor; levels, but not relative propor- tions, change according to temperature of development (Counce, 1957, Experientia 13: 354; Puckett and Petty, 1980, Biochem. Genet. 18: 1221-28). Reciprocal transplantation experiments show that eye color is autonomous (Hadorn and Counce). dor females produce no progeny in crosses to dor males at 25, although some allelic combinations able to produce progeny at 18; and a few dor/+ daughters are produced in crosses to + males. Germ-line clones homozygous for the lethal allele dor28 produce collapsed eggs (Perriman, Egstrom, and Mahowald, 1989, Genetics 121: 333-52). The lethal embryos produced by dor mothers reach gastrulation or beyond (Hildreth and Lucchesi, 1967, Dev. Biol. 15: 536-52; Counce, 1969, DIS 44: 101-82). Maternal effect shown to be germ line autonomous by both ovarian (Garen and Gehring, 1972, Proc. Nat. Acad. Sci. USA 69: 2982-85) and pole-cell transplantation (Marsh, van Deusen, Wieschaus, and Gehring, 1977, Dev. Biol. 56: 195-99). Maternal lethal effect rescuable by injections into preblastoderm embryos of cytoplasm from unfertilized eggs of normal females (Garen and Gehring, 1972); dor+ substance present during early stages of vitellogenesis but not detected in yolk of cellular blastoderm embryos (Marsh et al., 1977). Abnormalities of dor cells in culture eliminated by extracts of normal post- but not pregastrulation embryos (Kuroda, 1977, Dev. Growth Differ. 19: 57-66). dor males show variable extents of gonadal dysgenesis depending on culture conditions and genotypic background; abnormalities range from failure of testes to attach to genital ducts to failure of one attached testis to elongate (Lucchesi, Counce, and Hildreth, 1968, J. Exp. Zool. 168: 437-50). Viability and longevity of dor homozygotes and hemizygotes variably reduced depending on allele and temperature; dorl larvae develop melanotic pseudo- tumors (Stark, 1918, J. Exp. Zool. 27: 509-29; Oftedal, 1953, Z. Indukt. Abstamm. Vererbungsl. 85: 408-22) and midgut occlusion (Russell, 1940, J. Exp. Zool. 84: 363-79), dying in late third instar (Bischoff and Lucchesi, 1971). dor/dorl lethal at 29 (Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Bar- itcheva, Gorelova, and Zhimulev, 1980, Chromosoma 81: 281- 306). dor in combination with ry, ry2 (Lucchesi, 1968, Genet- ics 59: 37-44) and car (Nash, 1971, DIS 47: 73) causes lethality in pupal stage. Recovery of gynandromorphs with dor car male sectors less than in controls; bilateral gynandro- morphs not observed, but distribution of male tissue resem- bles that of control (Grell, 1976). dor behaves as a sem- ilethal in combination with pd and with cn bw (Lucchesi, 1968). alleles: Mutants can be arranged in a linear sequence of increasing strengths; heterozygotes between different pairs of alleles show intermediate phenotypes; no evidence of interal- lelic complementation (Bischoff and Lucchesi, 1971). Recombi- national mapping by Bischoff (1973, DIS 50: 172) established the order illustrated. dor3 dor12 dor17 dor1 dor15 dor4 dor16 dor6 ___________________________________________ | | | | | | Genetic fine structure map of the deep orange locus. allele origin discoverer synonym ref ( comments ____________________________________________________________________ dor1 X ray E. D. King 12 viable, male sterile; eyes orange at 25 dor2 dor17A dor3 spont Hildreth, 61e dor61e 7 viable, male sterile; eyes pale orange at 25 dor4 EMS Lefevre dor66g 9 viable, male fertile; eyes dark orange at 25 dor5 EMS dor69e 5 viable, male fertile; eyes red-orange at 25 dor6 EMS dor69L1 5 viable, male sterile; eyes orange at 25 *dor7 EMS dorB dor8 spont Bridges l(1)7, dorl 6, 12 lethal dor9 EMS Alikhanian l(1)76, dorl2 2 lethal dor10 EMS H. Lewis dorl3 11 lethal dor11 EMS dorl69B 5 lethal dor12 EMS dorl69F 5 lethal dor13 EMS dorl69J 5 lethal dor14 EMS dorl69K3 5 lethal dor15 EMS dorl69L1 5 lethal dor16 EMS dorl69L2 5 lethal dor17 EMS dorl69L3 5 lethal dor18 EMS dorl69L4 5 lethal dor19 EMS l(1)t81 1, 3, 4 lethal dor20 EMS l(1)t128 1, 3, 4 lethal dor21 EMS l(1)t141 1, 3, 4 lethal dor22 EMS l(1)t187 1, 3, 4 lethal | dor23 EMS l(1)t257 1, 3, 4 lethal dor24 EMS Pak l(1)t470 1, 3, 4 lethal dor25 X ray Lefevre l(1)A44 10 lethal dor26 X ray Lefevre l(1)HC221 10 lethal; T(1;2)2B11;22B dor27 X ray Lefevre l(1)RA17 10 lethal dor28 EMS Lefevre l(1)VE915 8 lethal ( 1 = Aizenzon and Belyaeva, l982, DIS 58: 3-7; 2 = Ardashni- kov, 1941, Dokl. Akad. Nauk SSSR 30: 344-46; 3 = Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbetova, Kramers, and Zhimu- lev, 1982, DIS 58: 184-90; 4 = Belyaeve, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelove, and Zhimulev, 1980, Chromosoma, 81: 281-306; 5 = Bischoff and Lucchesi, 1971, Genetics 69: 453-66; 6 = Bridges, 1916, Genetics 1: 149; 7 = Hildreth, 1963, DIS 37: 48; 8 = Lefevre; 9 = Lefevre, 1970, DIS 45: 32; 10 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 11 = Lewis, 1954, J. Exp. Zool. 126: 235-75; 12 = Merrell, 1947, Am. Nat. 81: 399-400. | When the salivary glands of homozygotes for dor22, an allele that causes death in the third larval instar with no signs of ecdysone induction, were incubated with ecdysterone, the development of puffs was restored (Biyasheva, Belyaeva, and Zhimulev, 1985, Chromosoma 92: 351-56). cytology: Tentatively placed in 2B11-12 by Lefevre [1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Franciso, Vol. 1a, pp. 31-66; 1981, Genetics 99: 461-80]. However, 2B4-8 (Rayle and Hoar, 1969, DIS 44: 69) and 2B6-7 (Belyaeva et al., 1980) have also been proposed. # dorsal: see dl dorsal-longitudinal-muscle-defective: see dlmd #*double: double location: 1-0. origin: Spontaneous. discoverer: Bridges, 1918. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 224. phenotype: Postvertical bristles doubled. Wings very small. Viability somewhat low. RK3. # Double Bar: see BB # double glazed: see dgl # Double Infrabar: see BiBi # double sex: see dsx # Doubler: see Dp(1;1)BsRMG # doughnut: see dn dow: downy From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 64. # dow: downy location: 1-8.0. origin: Spontaneous. discoverer: Bridges, 36c28. phenotype: Bristles very short and slender, nearly as small as ss. Males entirely sterile; testis shape normal. Sper- miogenesis arrested shortly after meiosis; nebenkern formation abnormal; spermatids degenerate after slight elongation [Kiefer, 1973, Genetic Mechanisms of Development (F.H. Ruddle, ed.). Academic Press, New York, London, and San Francisco, pp. 47-102]. Spermatocyte nuclei exhibit reduced amounts of Y-chromosome-dependent structures (Kiefer, 1973). Viability good. RK2. # Dox-A1: Diphenol oxidase A1 subunit location: 2-{80.6}. references: Deng and Rizki, 1988, Genome 30, Suppl. 1: 192. phenotype: Enzyme detectable in embryos at ten hours and remains throughout development and adult life. A1 band more intense than those of subunits A2 and A3. alleles: Monomorphic in D. melanogaster, but two bands present in D. melanogaster X D. simulans hybrids. cytology: Placed in 55A based on its inclusion in Df(2R)PC4 = Df(2R)55A;55F and Df(2R)Pcl11B = Df(2R)54F6-55A1;55C1-3 but not Df(2R)Pcl-W5 = Df(2R)55A-B;55C. as detected in D. melano- gaster X D. simulans hybrids. Bc and Phox occupy the same cytological interval. # Dox-A2: Diphenol oxidase A2 subunit location: 2-53.9. synonym: l(2)37Bf+. references: Pentz, Black, and Wright, 1986, Genetics 112: 823-41. Pentz and Wright, 1986, Genetics 112: 843-59. Wright, 1987, Adv. Genet. 24: 127-222. phenotype: The structural gene for the A2 component of phenol oxidase, which utilized diphenol substrates. Developmentally regulated; levels low until just prior to pupariation; dramatic rise to maximum at puparium formation, followed by reduced, but still high, levels throughout pupal stage, again decreasing at eclosion (Geiger and Mitchell, 1966, J. Insect Physiol. 12: 755-65). Heterozygotes for lethal alleles show reduced diphenol oxidase activity; homozygotes die as first instar larvae; dead larvae do not turn black. One homozygous Dox-A21 escaper reaching pharate adult stage was liberated from the pupa case; it was chalk white, devoid of any cuticu- lar pigment; cell lethal; no homozygous clones observed for any of the lethal alleles. alleles: Most alleles are larval lethals; Dox-A2mfs1 homozy- gotes are also lethal, but hemizygotes display 60% normal adult viability and, although diphenol oxidase activity is normal, females and males are sterile. allele origin discoverer synonym ref ( comments _____________________________________________________________________________ Dox-A21 EMS + / ray Wright l(2)7402 1 100-bp intragenic deletion Dox-A22 EMS + / ray Wright l(2)7409 1 1.1-kb intragenic deletion Dox-A23 EMS + / ray Wright l(2)7416 1 Dox-A2mfs1 EMS + / ray Wright mfs(2)7601 2 Hemizygote viability = 60% of expected. Male and female sterile. Homozygous lethal. Dox-A25 EMS + / ray Cecil l(2)B8 ( 1 = Pentz, Black, and Wright, 1986, Genetics 112: 823-41; 2 = Wright, Black, Bishop, Marsh, Pentz, Steward, and Wright, 1982, Mol. Gen. Genet. 188: 18-26. cytology: Localized to a region between 14.3 and 16.8 kilobases long in 37B10-13 between the right-hand breaks of Df(2L)hk-UC1 and Df(2L)OD15. molecular biology: Genomic clone isolated in a chromosome walk through the Ddc region. The 1.7 kb transcription unit is pro- cessed to an 1.66 kb mRNA which encodes a basic protein of 56 kD made up of 494 amino acids. A single mRNA is present at varying levels throughout development. # Dox3 location: 2- [placed between rdo and M(2)36F by Rizki; however, placed to the right of pr by Pentz and Wright]. discoverer: Rizki. references: Rizki and Rizki, 1985, Genetics 110: s98. Rizki, Rizki and Bellotti, 1985, Mol. Gen. Genet. 201: 7-13. phenotype: Apparently the structural gene of the A3 component of phenol oxidase. alleles: Electrophoretic variants exist. cytology: Placed in 36D1-E4 based on its location in the region common to Df(2L)H20 = Df(2L)36A89;36E3-4 and Df(2L)M-HS5 = Df(2L)36D1-E1;36F1-37A1. However, placed to the right of 37D1-2 by Pentz and Wright based on the failure of the follow- ing overlapping deficiencies to delete it: Df(2L)H20 = Df(2L)36A7-10;36E4-F1, Df(2L)TW203 = Df(2L)36E4-F1;37B9-C1, and Df(2L)TW130 = Df(2L)37B9-C1;37D1-2 (Wright, 1987, Adv. Genet. 24: 127-222). # dp: dumpy location: 2-13.0. references: Carlson, 1959, Genetics 44: 347-73 (fig.). Southin and Carlson, 1962, Genetics 47: 1017-26 (fig.). Grace, 1980, Genetics 94: 647-62. phenotype: dp alleles have variable effects on wing length and shape and on the thoracic cuticle. Presence of wing phenotype indicated by o = oblique in the allelic designation and of thoracic phenotype by v = vortex or cm = comma. The wing effect is an oblique truncation affecting the margins of the first and second posterior cells in weak alleles and reducing wings to approximately half normal length in extreme geno- types, where the truncation is more nearly perpendicular to the long axis of wing. Margins remain intact; angle between veins L2 and L5 increased, and intercrossvein distance decreased. Phenotype resembles rudimentary. Thoracic pheno- type comprises five types of hypodermal irregularities: first vortices, second vortices, commas, pre-episternal pits, and posterior invagination; all five have the form of pits, erup- tions, or raised pits of the cuticle (Metcalfe, 1970, Genetics 65: 627-54). First vortices are hypodermal pits or eruptions located posterolaterally on the scutum; they disrupt the acrostichal rows, resulting in surrounding whorls of micro- chaete. Second vortices are located anterolaterally on the scutum and resemble first vortices morphologically. Commas are comma-shaped depressions at the anterior margin of the scutum. The pre-episternal pit is in the pre-episternal plate immediately anterior to the sternopleural chaetae, which some- times exhibit disturbed orientation (Metcalf, 1969, DIS 44: 91). The posterior invagination occurs between the laterotergite plate and the metanotum (Metcalf, 1969); dif- ferent alleles exhibit different combinations of these traits. Musculature attached to disturbed regions of the cuticle often degenerates (Metcalfe, 1970). Some alleles show reduced body size and small weak legs (dph, dpobw females, dpolv/dpov). Phenotypic expression enhanced by increased temperature during development; wing and thorax effects show dominance when heterozygotes exposed to increased temperatures at 12-16 and 8-10 hr of pupal life, respectively (Blanc and Child, 1940, Physiol. Zool. 13: 65-72). Normal larvae fed 6-azauracil produce adults with oblique phenocopies; 6-azauracil feeding suppresses dp (Rizki and Rizki, 1965, Science 150: 222-23), su(r) enhances the oblique phenotype (Stroman, 1974, Hereditas 78: 157-68). The four genotypes studied [dpo2, dpovN, dpv2, and dpv; e(dpv)] show increased orotate phosphoribosyl transferase activity during third larval instar and enhanced incorportion of labeled glucose into chitin (Blass and Hunt, 1980, Mol. Gen. Genet. 178: 437-42). Many alleles are lethal when homozygous; they are identified by l in the allelic designation. Lethal stages vary among alleles, e.g., dpolv is embryonic lethal; dplv1, and dplvI die at the egg-larval boun- dary; dplm homozygotes die primarily at larval ecdysis between the first and second larval instar with some death at hatching and at ecdysis of second-instar larvae; dpobm homozygotes die mostly at hatching but a few die during first and second lar- val instars (Metcalfe, 1971, Genet. Res. 17: 173-83). In Me/+ heterozygotes, many dp alleles show a dominant oblique effect when heterozygous for dp+ and dp; dpv is an exception (Carlson, 1959). dpv homozygotes normal; show thoracic phenotype only if third chromosomes homozygous for e(dpv). alleles: One, two, or three of the phenotypic attributes of dp (o, l, or v) may be expressed in an allele, and alleles are classified according to which attributes they exhibit; the information is generally included in the superscript designa- tion; the order olv is roughly in accord with map order. As a rule, the heteroallelic combination of any two alleles exhi- bits only phenotypic features common to the two alleles [e.g., dpo/dpv is normal, and dpov/dplv exhibits thoracic but not wing abnormalities (Carlson, 1959)]. Partial complementations between some pairs of olv and l or lv alleles are exceptions to this rule (Carlson, 1959; Grace, 1980). Identified alleles are tabulated below. allele origin ( synonym ref | _________________________________________ o alleles _________________________________________ dpo spont 1 dpo2 5 dpo3 *dpo33 dpoA2 dpoA4 *dpo50C dp50C 1 dpo51e UV 1 dpobm X ray 1 *dpobw spont dpbw 1 dpodef spont dpdef 1 dpoDG6 5 dpoDG33 5 dpoDG41 5 *dpoDG53I 5 dpoDG56 5 dpoem2 EMS 6 dpoem9 EMS 6 dpoem10 EMS 6 dpoem11 EMS 6 dpoh13 X ray 10 dposz66 EMS 10 *dpou UV 1 _________________________________________ l alleles _________________________________________ dpl20 dplDG82 NMU 4, 5 dplDG83 NMU 4, 5 dplDG85 dplDG91 dplb1 EMS 10 dplh40 X ray 10 dplh41 X ray 10 dplm UV dplHM52f 5 dplMi spont dplM57f 8 dplsz31 EMS 10 dplsz46 EMS 10 _________________________________________ v alleles _________________________________________ *dpcm spont 1 dvv spont 1 dpv2 spont 1 dpv7 EMS dpvem3 EMS 6 dpvM spont 1 dpvsz4 EMS 10 dpvW spont 1 _________________________________________ ol alleles _________________________________________ dpol spont dpL 1 dpol4 dpolAS dpLS 1 dpLSch dpolb20 X ray 10 dpolb27 EMS 10 dpolb42 EMS 10 dpolCS19 ICR170 dpolCS41 ICR170 dpolCS50 ICR170 dpolCS80 ICR170 3 dpolCS109 3 dpolDG9 NMU 4 dpolem1 EMS 6 dpolem8 EMS 6 dpolem9 EMS 6 dpolh6 X ray 10 dpolh8 / X ray 10 dpolh9 / X ray 10 dpolh10 / X ray 10 dpolh12 / X ray 10 dpolh20 / X ray 10 dpolh21 / X ray 10 dpolM UV dpLM 1 dpT51b dpolsz24 / X ray 10 dpolXAS1 _________________________________________ ov alleles _________________________________________ dpcm2 spont 1 dpov1 spont dp 1, 9 dpovCB1 dpov7 dpov51f dp51f dpov51h spont 1 *dpov52b spont 1, 9 dpovDG2 5 dpovDG27 dpovDG30 5 dpovDG35 5 dpovDG37 5 dpovDG55 dpovDG61 dpovdr spont dpdr 1 dpovh dph 9 dpovJ96 ` / ray 7 dpovN X ray dpNov 1 _________________________________________ lv alleles _________________________________________ dplv1 spont dplvCB1 1, 5 dptx dplv2 dp2 dplv44 X ray dplv51e UV dpTH51e dplvb21 EMS 10 dplvCS24 ICR170 dplvCS35 ICR170 3 dplvCS36 ICR170 dplvCS38 ICR170 dplvCS42 5 dplvCS43 ICR170 dplvCS51 ICR170 dplvCS58 ICR170 dplvCS67 ICR170 dplvCS78 ICR170 3 dplvCS81 ICR170 dplvCS105 ICR170 dplvDG1 5 dplvDG3 NMU 4 dplvDG5 NMU 4 dplvDG7 5 dplvDG10 dplvDG12 dplvDG13 dplvDG14 dplvDG16 dplvDG23 dplvDG24I dplvDG38 5 dplvDG39 dplvDG49 5 dplvDG50 5 dplvDG51 dplvDG57 5 dplvDG58 5 dplvDG65 NMU dplvDG66 dplvDG67 dplvDG72 dplvDG78 NMU dplvDG81 dplvem1 EMS 6 dplvem2 EMS 6 dplvem4 EMS 6 dplvh37 X ray 10 dplvI spont dpTh 1 dpThI dptxI dplvx1 X ray 8 dplvx2 X ray 8 dplvx3 X ray 8 dplvx4 X ray 8 dplvx5 X ray 8 dplvx18 X ray 8 _________________________________________ olv alleles _________________________________________ dpD X ray 1 dpolv dpT 1 *dpolv2 dpT2 1 *dpolv54d UV 1 *dpolv55b spont dpT55b 1 *dpolv55c UV dpT55C 1 *dpolv57g UV dpT57g 1 dpolv101 dpolv6m X ray 1 dpolva22 - EMS 10 dpolvb12 EMS 10 dpolvCG112 ICR170 dpolvCS3 ICR170 dpolvCS8 ICR170 dpolvCS24 ICR170 dpolvCS28 ICR170 dpolvCS39 ICR170 dpolvCS69 ICR170 3, 5 dpolvCS93 ICR170 dpolvCS95 ICR170 dpolvCS100 ICR170 dpolvCS103 ICR170 5 dpolvCS108 ICR170 5 dpolvCS112 ICR170 *dpolvD spont dpTD 1 dpolvDG10 dpolvDG20 NMU 4 dpolvDG27 NMU 4, 5 dpolvDG32 dpolvDG34 dpolvDG44 dpolvDG45 dpolvDG46 dpolvDG59 dpolvDG61 NMU 4, 5 dpolvDG62 NMU 4 dpolvDG63 dpolvDG72 dpolvDG75 dpolvem4 EMS 6 dpolvem5 EMS 6 dpolvem6 EMS 6 dpolvem7 EMS 6 dpolvem8 EMS 6 dpolvem9 EMS 6 dpolvem10 EMS 6 dpolvem11 EMS 6 dpolvh2 X ray 10 dpolvh3 X ray 10 dpolvh4 X ray 10 dpolvh5 X ray 10 dpolvh7 / X ray 10 dpolvh11 X ray 10 dpolvh14 X ray 10 dpolvh17 / X ray 10 dpolvh18 X ray 10 dpolvh22 / X ray 10 dpolvh26 / X ray 10 dpolvh27 X ray 10 dpolvh29 X ray 10 *dpolvH spont dpH 1 dpolvHC3 dpolvHC39 NMU 4, 5 dpolvHC59 5 dpolvHC69 dpolvHC234 *dpolvM spont dpTO 1 dpdvM516 5 *dpolvP heat dpTP 1 dpolvR X ray dpRf 1 dpolvS neutrons dpTSch 1 *dpolvSn spont dpTs 1 dpolvsz28 EMS 10 dpolvW spont dpTW 1 dpolvx1 X ray 8 dpolvx2 X ray 8 dpoldx3 X ray 8 dpolvx4 X ray 8 dpolvx5 X ray 8 _________________________________________ dominant alleles _________________________________________ dpD3 dpD4 _________________________________________ unclassified alleles _________________________________________ *dp49 X ray 1 *dp53 spont 1 *dp61d X ray 1 dpCA2 X ray 11 dpCA5 X ray 11 dpCA6 X ray 11 *dpG spont 1 dpw1 1 dpw2 1 dpw3 dpw8 dpw18 ( UV = ultraviolet; EMS = ethyl methanesulfonate; NMU = nitrosomethylurea; ICR-170 = 2-methoxy-6-dichloro-9- 3(3-[ethyl-2-cloroethyl]aminopropylamino)acridine dihydro- chloride. | 1 = CP627; 2 = Carlson and Southin, 1962, Genetics 47: 321-36; 3 = Grace, 1966, DIS 41: 83; 4 = Grace, 1970, Mut. Res. 10: 489-96; 5 = Grace, 1980, Genetics 94: 647-62; 6 = Jenkens, 1970, DIS 45: 38; 7 = Kotarski, Pickert, and MacIntyre, 1983, Genetics 105: 371-86; 8 = Meyer, 1970, DIS 45: 147; 9 = Sederoff, 1967, Nature 216: 1348-49; 10 = Szidonya and Reuter, 1988, Genet. Res. 51: 197-208; 11 = Velissariou and Ashburner, 1980, Chromosoma 77: 13-27. / Also display dominant suppression of variegation presumably owing to effect on Su(var)2-3. ` Associated with T(Y;2,4)J96; variegated-type position effect. - Shows a fully penetrant oblique phenotype; the few homozy- gous survivors show strong oblique-vortex phenotype with blistered wings; lethal in combination with other lethal dp alleles. dpo: dumpy-oblique From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 65. dpov: dumpy-oblique vortex Edith Wallace, unpublished. cytology: 25A1-2 (Velissariou and Ashburner, 1980, Chromosoma 77: 13-27) or 25A3-4 (Roberts and Broderick, 1982, Genetics 102: 74-89). T(Y;2;4)J96 = T(Y;2;4)25A2-3 shows Y-suppressed dp position effect (Kotarski, Pickert, and MacIntyre, 1983, Genetics 105: 371-86). other information: Recombination between alleles belonging to the same or different phenotypic classes allows construction of genetic map with clusters of discontinuously distributed alleles; o and olv alleles found in several clusters, other phenotypic classes confined to a single cluster. # Dp: see Dr # dpl: duplicated legs location: Not located. origin: Derived from ethyl-methanesulfonate-treated flies. synonym: dl. references: Mglinetz, 1979, Ontogenez 10: 602-08. Mglinetz and Ivanov, 1980, Ontogenez 11: 277-85. phenotype: Some 6.7% of the flies of this strain show dupli- cated tarsi and in some instances tibiae; primarily involves mesothoracic legs. Distribution of bristles on leg and its duplicate agree with polar coordinate model (French, Bryant, and Bryant, 1976, Science 193: 969-81) of regeneration and duplication initiated in region of cell death. Phenotype resembles that of heat-pulsed su(f)lts726. Produces dupli- cated antennal legs in combination with ssak, and both leg and its duplicate four jointed in combination with fj (Mglinetz, 1980, Ontogenez 11: 542-44). No genetic analysis reported. # dpp: decapentaplegic (W.M. Gelbart) location: 2-4.0. discoverer: E. Novitski (original ho mutation). R. Tung and W. Gelbart (original multi-disk dpp mutation). synonym: ho, blk, shv, DPP-C, Hin-d, Tg. references: Spencer, Hoffmann, and Gelbart, 1982, Cell 28: 451-61 (fig). Segal and Gelbart, 1985, Genetics 109: 119-43 (fig). Irish and Gelbart, 1987, Genes Dev. 1: 868-879 (fig). St. Johnson, Hoffman, Blackman, Segal, Grimalia, Padgett, Irick, and Gelbart, 1990, Genes Dev. 4: 1114-27. phenotype: dpp is a complex locus affecting numerous develop- mental events. Mutations fall into three major genetic and phenotypic groupings: called shortvein (shv), Haplo- insufficiency (Hin) and imaginal disk-specific (disk). Each group maps to a different region of the dpp gene. Hin-region mutations have two distinguishing features: they are defective in normal dorsal-ventral patterning of the embryo, and they generally fail to complement mutations of the shv and disk types. shv-region mutations all show recessive defects in longitudinal wing vein formation. disk-region mutations exhi- bit pattern deletions in the adult epidermal derivatives of the imaginal disks. The phenotypes of most shv/disk heterozy- gotes suggest partial or full complementation of the shv and disk lesions. Within each of the three major groupings, several phenotypic classes of alleles have been identified. Complementation between certain combinations of dpp alleles is transvection sensitive (Gelbart, 1982, Proc. Nat. Acad. Sci. USA 79: 2636-40). The genetic properties of the several classes of dpp muta- tions are outlined below. For a given class, the prototypical recessive phenotypes are inferred from examinations of trans heterozygotes for two different alleles of that class. This procedure obviates possible complications due to the frequent association of dpp mutations with gross chromosomal rearrange- ments. Particular allelic combinations may deviate from the prototypical descriptions. Hin-region emb: Embryonic lethal mutation. Homozygous viable, but reces- sive lethal in combination with hin-r alleles, and, in the latter background, exhibits the same weakly ventralized pheno- type as hin-r homozygotes. Completely complements all shv- and disk-region mutations. The sole emb allele is associated with a small deletion in Hin-region. Hin: Haplo-insufficient mutations. Hin/+ heterozygotes exhibit dominant embryonic lethality with the same weakly ventralized phenotype as hin-r homozygotes. Dominant lethality is rescued by duplication of dppHin+. Homozygotes are defective in gas- trulation and die as embryos with completely ventralized cuti- cle. In general, Hin alleles do not complement any other dpp mutations. However, Hin alleles associated with small dele- tions or point mutations exhibit transvection effects in heterozygotes with small deletions or insertions in the shv and disk-regions. Hin mutations are considered the null alleles of the dpp gene. Hin alleles are associated with breakpoints, small deletions or point mutations in the Hin- region. Hin-Df: Haplo-insufficient mutations which are behave identi- cally to breakoint Hin mutations, except that Hin-Df lesions are gross deletions removing the entire dpp gene and adjacent vital loci. hin-r: Recessive mutations behaving as milder versions of the Hin lesions. In homozygotes, hin-r mutations exhibit embryonic lethality with weak ventralization effects (identical to emb/hin-r or Hin/+ heterozygotes). All hin-r mutations engender temperature-sensitive mutant phenotypes when heterozygous with shv- and disk-region mutations. Phenotypes elicited in heterozygotes with small deletions, or insertions in the shv and disk regions are transvection sensitive. All hin-r mutations are cytologically normal and show no altera- tions in their restriction maps. Some have been associated with point mutations in the Hin-region. shv-region shv-lc: Recessive larval-lethal shortvein alleles which com- plement all disk-region mutations. Exhibit mutant phenotypes in heterozygotes with all shv, Hin, and hin-r mutations. Muta- tions generally associated with rearrangement breakpoints. shv-lnc: Recessive larval-lethal shortvein alleles which do not complement disk-region mutations. Also exhibit mutant phenotypes in heterozygotes with all shv, Hin, and hin-r muta- tions. Mutations generally associated with rearrangement breakpoints. shv-p: Recessive shortvein alleles surviving at least to pharate adult. Only two alleles are known; one (s11) is adult viable; exhibits strong venation defects, and variable head capsule defects, including loss of palps, and misarranged vibrissae. Allelic to all shv, Hin, and hin-r mutations. Com- plement all disk-region mutations. Both alleles are associated with rearrangement breakpoints. shv-w: Recessive viable and fertile shortvein alleles exhibit- ing only venation defects. Associated with small deletions of the shv-region. Venation phenotype allelic to all shv, Hin, and hin-r mutations. shv-w/Hin, and shv-w/hin-r mutant pheno- types are transvection sensitive. Only two alleles are known; both are associated with small deletions in the shv-region. Tg: A dominant gain-of-function allele in which the tegula on the wing appears duplicated. Tg/+ wings are held out and down. Distinct in phenotype from heldout (d-ho) homozygotes. Tg completely complements all dpp mutations. The dominant effects of Tg can be reverted by superimposing shv, Hin, or hin-r mutations on the Tg chromosome. The one Tg allele is associated with a rearrangement breakpoint in or near the shv-region. disk-region disk-blk: Recessive viable and fertile allele in which the only mutant phenotype is loss of 80-90% of ommatidia in eye; hence this allele was designated blink by Sparrow (unpub- lished). Exhibits mutant eye phenotypes in heterozygotes with disk-III, disk-V, Hin, and hin-r mutations. Can exhibit transvection effects. The one disk-blk allele is associated with a small deletion within the disk-region. disk-ho: Recessive viable and fertile alleles in which the only mutant phenotypes are heldout wings and loss of the Sc25 on the dorsal base of the wing. Heldout phenotype displayed in heteroyzgotes with all disk-region mutations except d-blk, and with Hin and hin-r mutations. Can exhibit transvection effects. In addition to the one mutant allele listed here, which is associated with a small deletion within the disk- region, several cytologically normal disk-ho alleles have been associated with mobilization of hobo mobile elements residing in the disk-region. disk-II: Recessive viable alleles. Homozygotes exhibit reduc- tions in wing blade, haltere and male genitalia. Elicit mutant phenotypes in heterozygotes with all disk-region mutations except d-blk, and with Hin and hin-r mutations. Mildest class of disk-region alleles associated with rearrangement break- points. disk-III: Recessive viable alleles. Homozygotes exhibit multi- ple pattern abnormalities in epidermis of head, thorax, and terminalia. Structures absent or reduced include labial palps, arista, eye, wing blade, capitellum of haltere, tarsal claws, male terminalia, and female analia. Elicit mutant phenotypes in heterozygotes with all disk-region mutations, and with Hin and hin-r mutations. Intermediate class of disk-region alleles associated with rearrangement breakpoints. disk-V: Recessive early pupal lethal alleles. Homozygous lar- vae have greatly reduced imaginal disks. Elicit mutant pheno- types in heterozygotes with all disk-region mutations and with Hin and hin-r mutations. Most severe class of disk-region alleles associated with rearrangement breakpoints. t: Recessive larval-lethal alleles. Allelic to all disk, Hin, and hin-r mutations. The only two known alleles of this class behave identically to disk-V lesions, except for the earlier recessive lethal period. Tentatively classified as part of the disk-region. These two mutations are associated with break- points which map between the two tRNAtyr genes residing at the Hin-disk-V boundary. Hence the t designation is used to describe these alleles. alleles: allele class origin cytology _______________________________________________________________________ dppd-blk d-blk hobo + dppd-ho d-ho spont + *dppd-ho40 d-II X ray In(2L)21D4-E1;22E2-3 dppd1 d-III hobo In(2L)22E2-3;22F2-3 dppd2 d-III X ray In(2L)22F1-2;28B *dppd3 d-III X ray T(2;3)22E3-F1;85B-D dppd5 d-II X ray + dppd6 d-III X ray In(2L)22F1-3;24F2-6 dppd7 d-III X ray T(2;3)22F1-2;80F dppd8 d-III X ray In(2L)22A1-2;22F1-2 dppd9 d-III X ray T(2;3;4)22F2-23A1;41A; 57E-F;64F;80B;101 dppd10 d-III X ray In(2L)22E4-F1;23E2-4 dppd11 d-III X ray Tp(2;2)22F1-2;29C;32C-D;39B dppd12 d-V X ray In(2L)22E2-3;22F2-3 dppd13 d-V X ray Tp(2;2)22F1-2;24C1-2;37F;40 dppd14 d-V X ray Df(2L)22E4-F2;22F3-23A1 dppd15 d-III X ray T(1;2)20;22F1-2 dppd16 d-III X ray T(Y;2)Y;22F1-2 dppd17 d-III X ray In(2L)22F1-3;27E dppd18 d-III X ray In(2L)22F1-2;36C4-6 dppd19 d-III X ray Df(2L)22F2-3;22F3-4 dppd20 d-III X ray T(2;3)22F1-3;64D dppd21 d-V X ray Tp(2;2)22A2-3;22F1-2;52F dppd22 d-III X ray T(2;3)22F1-3;67E dppd23 d-III X ray In(2LR)22F1-2;41A dppd25 d-V X ray T(2;3)21F;22F1-3;72A-B;80F dppd26 d-V X ray In(2LR)22F1-2;47A1-4 dppd28 d-II EMS T(2;3)22F2-3;86E15-18 dppd29 d-V X ray T(2;3)22F2-3;87D1-2 dppd30 d-? ( X ray + dppd31 d-III EMS In(2LR)22F1-3;41C-D dppd33 d-V P Df(2L)22F1-2;23A1-2 dppd35 d-V X ray In(2LR)22F1-2;42A2-8 dppd36 d-III X ray In(2LR)22F1-3;35E dppd41 d-III / ray In(2LR)22F2-4;54F dppd42 d-V / ray In(2L)22F1-3;22F3-4 dppd44 d-V / ray T(2;3)22F1-2;80C dppd49 d-V / ray T(1;2)XS(?);22F dppd50 d-II / ray In(2LR)22F2-3;27C dppd52 d-V / ray T(2;3)22F1-2;86A-B dppd54 d-II P + dppd55 d-III P + dppd60 d-III / ray In(2L)21E;22F dppd65 d-V / ray In(2L)22F;34C;40 dppd66 d-II / ray Dp(3;2)78F;80F;21E;22F1-2 dppd67 d-V / ray In(2LR)21F;22F dppd68 d-III / ray In(2LR)22F1-2;23D;51D dppd70 d-V / ray Tp(2;2)21D;22F;21A dppd71 d-III / ray T(2;3)22F1-2;101 dppd72 d-V / ray Tp(2;3)22F1-2;34B;81F dppd73 d-III / ray T(2;4)22F1-2;57A;101F dppd74 d-III / ray Tp(2;2)26A-B;29D-E;22F1-2 dppd75 d-V / ray In(2LR)22F1-2;58D dppd76 d-III / ray Tp(3;2) heterochromatin into 22F1-2 dppd77 d-V / ray T(2;3)22F1-2;80F dppd78 d-V / ray T(2;3)22F1-2;95A1-2 dppd79 d-V / ray Df(2L)22F1-2;22F4-23A1 dppd80 d-III / ray Dp(3;2)85D;86E into 22F1-2 dppd81 d-V / ray T(2;3;4)22F1-2;30C;80F;101A-F dppd82 d-III / ray + dppe87 emb EMS + dppH32 Hin-Df X ray Df(2L)22E3-F1;23A1-2 dppH34 Hin-Df X ray Df(2L)22E2-3;23A2-4 dppH37 Hin X ray + dppH38 Hin-Df / ray Df(2L)22A1-2;22F3 dppH39 Hin-Df / ray Df(2L)21E1-2;23A2-4 dppH40 Hin-Df / ray Df(2L)22E1;23A1 dppH43 Hin-Df / ray Df(2L)22B1-2;23A3-B1 dppH45 Hin-Df / ray In(2LR)22F1-3;52F | dppH46 Hin-Df / ray Df(2L)22F1-2;22F2-3(?) dppH47 Hin / ray + dppH48 Hin / ray + dppH51 Hin-Df / ray Df(2L)21F;23B1-2 dppH53 Hin-Df / ray Df(2L)22A1-2;23A3-7 dppH57 Hin / ray + dppH59 Hin-Df / ray Df(2L)22A;23A dppH61 Hin / ray + dppH62 Hin-Df / ray Df(2L)22B;22F dppH84 Hin-Df / ray Df(2L)22B;23A dppH85 Hin-Df / ray Df(2L)22E2-F1;23A dppH86 Hin / ray In(2L)22F;26C;35D-E dppH88 Hin EMS + dpphr4 hin-r EMS + dpphr27 hin-r EMS + dpphr56 hin-r / ray + dpphr89 hin-r EMS + dpphr90 hin-r EMS + dpps1 shv-w spont + dpps2 shv-lc X ray T(2;3)22F1-2;64E1-2 dpps3 shv-lc X ray T(3;2)22F1-2;40C;82A;92A5-8 dpps4 shv-lnc X ray In(2L)21B1-C1;22F1-2 dpps5 shv-lnc X ray In(2L)21E1-2;22F1-2 dpps6 shv-w X ray + dpps7 shv-lc X ray Tp(2)24E1-2;25A1-2 into 22F1-2 dpps8 shv-lnc EMS + dpps9 shv-lc / ray T(2;4)22F1-2;101 dpps10 shv-lc / ray + dpps11 shv-p / ray In(2L)22F1-2;31C-D dpps12 shv-lc / ray In(2L)22F1-2;24A dpps13 shv-lnc / ray T(2;3)22F1-2;93B8-10 dpps14 shv-lnc / ray T(2;4)22F1-3;IVS dpps15 shv-lc / ray In(2LR)22F1-2;59B dpps17 shv-lc / ray In(2LR)22F1-2;41A dpps18 shv-lnc / ray T(2;3)22F1-2;88E1-4 dpps19 shv-lnc / ray T(2;3)22F1-2;35B1-2;97B dpps20 shv-lc / ray In(2L)22B1-2;22F1-2 dpps21 shv-lnc / ray In(2L)22A1-3;22F1-2 dpps22 shv-p / ray In(2L)22F1-2;35C-D dpps23 shv-lc / ray + dpps24 shv-lc / ray T(2;3)22F1-2;59D;80F?;81F?;87C;88D;94D dpps25 shv-lnc / ray T(2;3)22F1-2;88E1-4 dpps26 shv-lc / ray T(1;2)1D;22F1-2 dpps27 shv-lc / ray + dpps28 shv-lc / ray Tp(2;?)22F1-2;24A1-2 -> chromocenter dppTg Tg X ray In(2L)21C;22F dppt24 t X ray In(2LR)22F1-2;58B dppt63 t / ray In(2L)22F;39C-D dpp58 unknown / ray + dpp64 unknown / ray Not done ( This mutation was induced upon dpphr4, complicating its mutant classification. | Broken in 22F of the normal distal 2L copy of dpp and in 22C of the Dp(2;2)dppd21 insertion into 52F. cytology: Localized to 22F1-2 based on common breakpoints of numerous mutant rearrangements and in situ hybridization of cloned dpp DNA. molecular biology: These phenotypic classes fall into discrete regions of the dpp map. The order of these groups on the chro- mosome from (distal to proximal) is: [shv-w, shv-p] shv-lc shv-lnc [Hin, hin-r] t disk-V disk-III disk-II disk-ho Several alternatively initiated and alternatively spliced transcripts encode a single 588-amino-acid long polypeptide which is a member of the transforming growth factor-| family of secreted factors (Padgett, St. Johnston, and Gelbart, 1987, Nature 325: 81-84). The open reading frame encoding the dpp polypeptide is contained in two exons located entirely within the Hin-region. Transcripts are localized dorsally at blasto- derm in the dorsal ectodermal region during early germ band elongation and in two stripes, one dorsal and one lateral dur- ing late germ band extension and germ band shortening. Also expressed in two blocks in the embryonic visceral mesoderm (St. Johnston and Gelbart, 1987, EMBO J. 6: 2785-91). For proper ontogeny of normal disk-region functions dpp is required and expressed just anterior to the A/P compartment boundary in imaginal disks (Posakony et al., 1990, submitted). # dpt: depilated location: 3- (not mapped). origin: Spontaneous. references: DeAngelis, 1972, DIS 49: 39. phenotype: Loss of thoracic and head bristles during first week of adult life. Hairs unaffected. Penetrance 100%; viability excellent. #*dpy: dumpoidy location: 3- (right arm near 90). origin: Spontaneous. discoverer: Villee, 40a. phenotype: Wings obliquely truncated and reduced in length; marginal vein intact. No vortices or whorls of bristles on thorax. Suppressed by Cy and Gla, made dominant by Me. Over- laps wild type slightly. RK2. # dq: see Ldq