# d: dachs location: 2-31.0. origin: Spontaneous. discoverer: Morgan and Bridges, 12k22. references: Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 216 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 212 (fig.), 223. phenotype: Similar to fj. Tarsi four jointed instead of five jointed owing to failure of joint formation between second and third tarsal segments (Tokunaga and Gerhart, 1976, Genetics 83: s76); joint remnants sometimes persist beneath the cuti- cle (Held, Duarte, and Derakhshanian, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 145-57). Legs short and held close to body. Femur, tibia, and tarsae foreshortened [Tokunaga and Gerhart; Mikuta and Mglinetz, 1979, Genetika (Moscow) 15: 624-32]. Probability of failure of joint formation pro- portional to degree of foreshortening of second tarsal segment (Tokunaga and Gerhart). Joint failure phenotype can extend into d/+ tissue adjacent to d/d clones (Tokunaga and Gerhart). Number of longitudinal rows of bristles in second basitarsus unaffected, but number of bristles per row reduced (Held, 1979, Wilhelm Roux's Arch. Dev. Biol. 187: 105-27). Leg effects enhanced by ssa and ssaB (Villee, 1945, Genetics 30: 26-27). Wings smaller than wild type, narrowed, with L2 and L3 joined near anterior crossvein; distance between crossveins smaller and crossveins sometimes absent. Angle between L2 and L5 greater than normal. Eyes small and rough. Posterior scutellar bristles erect. Viability erratic. Fre- quently sterile. Enhances transforming effects of AntpNs (Mikuta and Mglinetz, 1979) and pb; labial legs in d; pb flies show failure of joint formation [Kaurov, 1978, Genetika (Mos- cow) 14: 306-12]. RK2. # dl: see Df(2L)d D: Dichaete From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 127. # D: see Lvp-D # D: Dichaete location: 3-40.7. origin: Spontaneous. discoverer: Bridges, 15a3. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 127 (fig.). phenotype: Wings extended uniformly at 45 from body axis and elevated 30 above (occasionally sharply downcast and dragging). Alulae missing. Dorsocentrals and some other bristles reduced in number (Sturtevant, 1918, Carnegie Inst. Washington Publ. No. 264; Plunkett, 1926, J. Exp. Zool. 46: 181-244). Head often deformed or split in postvertical region. Halteres turned down. Homozygous lethal. Nearly lethal in combination with eyD (Sobels, Kruijt, and Spronk, 1951, DIS 25: 128). Partially suppressed by sc alleles that remove postverticals (sc, sc4, sc6, sc7) but not by others (sc2, sc5) (Sturtevant). Classifiable in triploids. RK2A. alleles: D3 and DE less severe derivatives of D (CP627). D4 X ray induced, associated with T(2;3)21D;70-71 (Craymer, 1980, DIS 55: 197). cytology: Inseparable from In(3L)D = In(3L)69D3-E1;70C13-D1 (Bridges in Morgan, Bridges, and Schultz, 1937, Year Book - Carnegie Inst. Washington 36: 301). Tentatively placed in 70C13-D1 based on breakpoint common to In(3L)D and T(2;3)D4. # da: daughterless (C. Cronmiller and T.W. Cline) location: 2-41.5. origin: Spontaneous. discoverer: Bell. references: Bell, 1954, Genetics 39: 958-59. Colainne and Bell, 1968, DIS 43: 155. Sandler, 1972, Genetics 70: 261-74. Mange and Sandler, 1973, Genetics 73: 73-86. Mason, 1973, DIS 50: 93. Sandler, 1975, Israel. J. Med. Sci. 11: 1124-34. Cline, 1976, Genetics 84: 723-42. Bownes, Cline, and Schneiderman, 1977, Wilhelm Roux's Arch. Dev. Biol. 181: 279-84. Sandler, 1977, Genetics 86: 567-82. Watanabe and Yamada, 1977, Jpn. J. Genet. 52: 9-14. Cline, 1978, Genetics 90: 683-98. Picologlou, Bell, and Rogler, 1978, Genetica 48: 201-06. Cline, 1980, Genetics 96: 903-26. Cline, 1983a, Dev. Biol. 95: 260-74. Cline, 1983b, Genetics 104: s16-17. Cline, 1984, Genetics 107: 231-77. Cronmiller and Cline, 1986, Dev. Genet. 7: 205-21. Cronmiller and Cline, 1987, Cell 48: 479-87. Gergen, 1987, Genetics 117: 477-85. Muir and Bell, 1987, Genetica 72: 43-54. Brand and Campos-Ortega, 1988, Wilhelm Roux's Arch. Dev. Biol. 197: 457-70. Caudy, Grell, Dambly-Chaudiere, Ghysen, Jan, and Jan, 1988a, Genes and Dev. 2: 843-52. Caudy, Vassin, Brand, Tuma, Jan, and Jan, 1988b, Cell 55: 1061-67. Cronmiller, Schedl, and Cline, 1988, Genes and Dev. 2: 1666- 76. Dambly-Chaudiere, Ghysen, Jan, and Jan, 1988, Wilhelm Roux's Arch. Dev. Biol. 197: 419-23. Murre, McCaw, and Baltimore, 1989a, Cell 56: 777-83. Murre, McCaw, Vassin, Caudy, Jan, Jan, Cabrera, Buskin, Hauschka, Lassar, Weintraub, and Baltimore, 1989b, Cell 58: 537-44. phenotype: da+ performs multiple roles during development. Maternally supplied da+ is required in female embryos as a positive activator of the gene, Sex-lethal (Sxl), the key binary switch gene for the sex determination pathway. Also, da+ expression is required in the somatic gonad of adult females for proper egg membrane formation, and hence for the survival of all progeny regardless of their sex. Embryonic expression of da+ is required in both sexes for the formation of the peripheral nervous system (PNS) and parts of the cen- tral nervous system (CNS). And, during larval and/or pupal stages, da+ may be required for the growth and/or differentiation of cells that form the adult cuticle. Amorphic alleles (da2, da3, da5, etc.) are recessive lethals, with a lethal period which is predominantly embryonic (Cronmiller and Cline, 1987; Caudy et al., 1988a). In addi- tion, the hypomorphic allele, da1 (originally called da), is hemizygous [da1/Df(2L)da-] lethal (Mange and Sandler, 1973), and da1 homozygotes die when they undergo the first half of embryonic development at 29 (Cline, 1976). Death appears to be a consequence of dosage compensation defects (Cline, 1983a; Gergen, 1987). Viability of da1 homozygotes is improved by the presence of extra X or Y heterochromatin in either the paren- tal female or her progeny (Sandler, 1972; Mason, 1973). Temperature-sensitive lethality of the da1 zygotic lethal effect is not affected by the Sxl genotype (Cline, 1980). da+ is not required in the germline, since da-(da2/da3) pole cells produce fertile gametes; however, mitotic recombination failed to yield significant da-(da2 or da3) somatic clones, suggest- ing da+ may be essential during epidermal development (Cron- miller and Cline, 1987). Embryos, homozygous for lethal da alleles, have a reduced CNS, lack all peripheral neurons, and have no external sensory structures (Caudy et al., 1988a). Adult flies heterozygous for a deletion of the achaete-scute (ASC) genes and simultaneously heterozygous for Df(da) (also da2/+ or da5/+) exhibit characteristic bristle defects (Dambly-Chaudiere et al., 1988). Hemizygosity for da+ reduces the number of supernumerary bristles in Hw mutants (Dambly- Chaudiere et al., 1988). In addition to its zygotic phenotype, da1 exhibits two separable maternal effects. There is a female-specific mater- nal effect: At 22 and 25, homozygous da1 females produce no daughters, while at 18, they produce approximately 20% as many daughters as sons (Cline, 1976). At 29, da1 displays a sex- nonspecific maternal effect. Homozygous females are reversi- bly sterile; they lay eggs that show little or no development (Cline, 1976). Sterility of da1 females at high temperature results from a defect in the somatic gonad rather than in the germline, since da- germ cells in wild-type ovaries produce normal eggs which support full viability of sons (Cronmiller and Cline, 1987). The female-specific maternal effect has a temperature- sensitive period which includes the last 60 hr of oogenesis and the first 3 hr of development (Cline, 1976). This maternal effect is also observed in crosses of da1 females to D. simu- lans males (Watanabe and Yamada, 1977). The female-lethal maternal effect is autonomous to the germline, as demonstrated by transplantation of da1, or da2/da3 pole cells into + hosts (Cline, 1983b; Cronmiller and Cline, 1987). Female zygotes from da1 mothers at 25 die as embryos. Such lethal female embryos show consistent abnormalities in midgut formation, and in about 50% of the abnormal embryos, shortening of the germ band fails, while anus and posterior spiracles open on the dorsal surface behind the head segments (Counce). Female embryos from da1 mothers also show consistent defects in the CNS, which is either reduced in width or shows abrupt bends or twists; abnormally formed gut often extends into the CNS (Caudy et al., 1988a). The majority of daughters of da1 moth- ers surviving at 18 are morphologically abnormal, often miss- ing structures from one or more imaginal discs or abdominal histoblasts, and frequently with duplication of structures (Cline, 1976). Though it was reported that daughters of homozygous da1 females could be rescued by cytoplasmic injection (Bownes et al., 1977), the apparent rescue was subsequently found to result from nonspecific effects that may have slowed the early development of females who are on the threshold of surviving (Cline, 1984; see also Muir and Bell, 1987). Gynandromorphs can survive the lethal maternal effects, but there is no localized lethal focus. Diplo-X tissue develops abnormally alongside normally developing haplo-X tissue. Survival of the mosaics and their average fraction of diplo-X tissue increases with decreasing temperature (Cline, 1976). The da1 maternal effect masculinizes escaper daughters that are homozygous for mle (Cline, 1984) and masculinizes triploid intersex (XXAAA) progeny (Cline, 1983a). Females heterozygous for Sxl alleles that lead to male development develop as sterile males, mosaic intersexes, or sterile females (depend- ing on the Sxl allele), when produced by da1 mothers (Cline, 1984). The da1 female lethal maternal effect is unaffected by tra or dsx (Bell, 1954; Colainne and Bell, 1968). However, daughters of da1/da1 mothers are almost fully rescued by a single zygotic dose of SxlM1 and to a limited degree by a duplication for Sxl+ (Cline, 1978). Conversely, zygotic Sxl- enhances the da maternal effect. Females with reduced Sxl dose (Sxl-/+) fail to survive from da1/da1 mothers at the semipermissive 18 (Cline, 1978). A strong dominant da maternal effect [da1/+, Df(2L)da/+, or da2/+ mothers] is observed when female progeny are doubly heterozygous for Sxl- and sis-a- (Cline, 1986, Genetics 113: 641-63; Cronmiller and Cline, 1986, 1987). The maternal effect of da1 is made semidominant also by E(da) (cis or trans to da1) in the mother (Mange and Sandler, 1973; see also Cline, 1980). The zygotic da+ dose itself does not affect expression of Sxl+ sex determination function (Cronmiller and Cline, 1986). alleles: allele origin synonym ref ( comments molecular data _____________________________________________________________________________ da1 spont 1 (=da); viable; 900 bp insertion of temperature sensitive middle repetitive hypomorph; strong DNA in untranslated daughterless maternal leader effect above 22; lethal with Df or amorphic alleles; lethal at 29 da2 EMS 2 apparent amorph; normal Southern recessive lethal; lethal with da1, Df, or other lethal alleles da3 EMS 2 apparent amorph; normal Southern recessive lethal; lethal with da1, Df, or other lethal alleles da4 HD daA73 6 recessive lethal 500 bp deletion da5 EMS daIIB31 3 recessive lethal; lethal normal Southern with da1, Df or other lethal alleles da6 EMS 5 apparent amorph da7 HD daPa 4 viable; reduced P element insertion viability with da1; in untranslated partially complements leader da1 female lethal maternal effect; lethal with da2, da3, Df, or da5 da8 X ray daX9.3 6 recessive lethal 5' end rearrangement da9 X ray daX80 5, 6 (= In(2L)da9); inversion breakpoint recessive lethal within gene da10 X ray daX136 6 recessive lethal 4 kb deletion da11 X ray daX251 6 (= T(2;3)da11); translocation; recessive lethal breakpoint within gene ( 1 = Bell, 1954, Genetics 39: 958-59; 2 = Cronmiller and Cline, 1987, Cell 48: 479-87; 3 = Caudy, Grell, Dambly- Chaudiere, Ghysen, Jan, and Jan, 1988, Genes Dev. 2: 843- 52; 4 = Cronmiller, Schedl, and Cline, 1988, Genes Dev. 2: 1666-76; 5 = Brand and Campos-Ortega, 1988, Roux's Arch. Dev. Biol. 197: 457-70; 6 = Caudy, Vassin, Brand, Tuma, Jan, and Jan, 1988, Cell 55: 1061-67. cytology: Placed in 31E based on localization by in situ hybridization of da7 P-element insertion (Cronmiller, Schedl, and Cline, 1988). molecular biology: The genomic region was cloned by transposon tagging from da7 (Cronmiller, Schedl, and Cline, 1988) and by chromosome walking (Caudy et al., 1988b). Approximately 30-kb walks were restriction mapped; the da transcription unit was localized by the demonstration of altered transcripts on Northern blots of da1 and da7 RNAs and by mapping rearrange- ments of several mutant alleles within a 6-kb genomic region. Two transcripts are detected by Northern analysis, 3.2 and 3.4-3.7 kb; both transcripts are present in male and female adults and at all stages of development [including unfertil- ized eggs (Cronmiller)], although the smaller transcript is enriched in unfertilized eggs and in 0-2.5 hr embryos. cDNA sequence analyses revealed a single intron, approximately 1.5 kb, located upstream of the initiating AUG. The inferred amino acid sequence predicts a protein of 710 aa, with a molecular weight of 74,000 daltons. From the amino acid sequence, the da protein is a member of the Helix-Loop-Helix family of DNA binding proteins. Within this family, the most extensive sequence similarity exists between da and the human kE2 enhancer binding protein, E12, where the two proteins are 78% identical over 93 amino acids (Murre et al., 1989a). In vitro, da protein and E12 form heterodimers and bind to DNA (Murre et al., 1989b). The predicted da protein also includes two short (27 aa) regions of similarity to the bcd protein, one being the His-Pro repeat that is also present in prd. # da: see dar # Dab: Disabled location: 3-{44}. synonym: dab. references: Gertler, Bennett, Clark, and Hoffmann, 1989, Cell 58: 103-13. phenotype: A dominant enhancer of the lethal phenotype of geno- types deficient in Abl function. Abll/Abl-, which ordinarily survive to late pupal or adult stages, die as late embryos or early larvae with abnormal CNS development when heterozygous for Dab mutants or deficiencies; such Dab or Dab- heterozy- gotes are normal in the presence of Abl+. Double mutant embryos, Abl- Dab-, are lethal and have few or no proper long- itudinal or commissural axons in the CNS. Homozygous Dab- in the presence of Abl+ results in reduced survival with inter- mediate levels of CNS disruption. alleles: Two ethyl-methanesulfonate-induced alleles, Dab1 and Dab2, isolated as M2 and M29, mimic the effects of Dab defi- ciencies; not allelic to l(3)73Bc. cytology: Placed in 73B2-3 based on the enhanced Abl phenotype of Abll1/Df(3L)st100.62 = Df(3L)72F3-7;73B3 but not Abll1/Df(3L)st-j7 = Df(3L)73A1-2;73B1-2 (Henkemeyer, Gertler, Goodman, and Hoffmann, 1987, Cell 51: 821-28). # dachs: see d # dachsous: see ds # dal: daughterless abnormal oocyte like alleles: 2-44 (not separated from abo). references: Sandler, 1977, Genetics 86: 567-82. phenotype: External phenotype normal. Shows reduced survival in heterozygous combination with deficiency. Maternal effect embryonic lethal with relative survival of sons less than that of daughters. Maternal effect more severe at 25 than at 19. Maternal effect reduced by presence of Y or Xh in zygotes. Presence of dal+ allele increases survival of offspring of abo mothers. cytology: Placed in 31F-32E based on inclusion in Df(2L)J-der- 39 = Df(2L)31A-B;32E but not Df(2L)J27 = Df(2L)31B-D;31F or Df(2L)Mdh-1J = Df(2L)30D-F;31F. other information: Complements abo, hup, and wd2. #*dar: darky location: 1-0 (no crossovers with sc in 547 flies). origin: X ray induced. discoverer: Fahmy, 1956. synonym: da; preoccupied. references: 1959, DIS 33: 84. phenotype: Small, heavily melanized flies. Sometimes wings curl upward. Male sterile; viability about 15% wild type; late eclosing. RK2. #*dark: darkener of white-eosin location: Autosomal. discoverer: Bridges, 13i23. references: 1916, Genetics 1: 148. 1919, J. Exp. Zool. 28: 347. phenotype: Specific partial suppressor of we. RK3. # dark: see dk # dark body: see db # dark bubbly: see dkb # dark carmine: see dcm # dark eye: see dke # dark eye: see sf32e # dark hairy margins: see dhm # dark red brown: see drb # Darkened eye: see Dke # Darkener of apricot: see Doa # darkener of white-eosin: see dark # darker legs: see dkl # darker legs: see thld # darky: see dar # dash: discs absent, small, or homeotic (A. Shearn) location: 3-47.6. discoverer: Shearn. references: Shearn, Rice, Garen, and Gehring, 1971, Proc. Nat. Acad. Sci. USA 68: 2594-98. phenotype: Homozygotes lethal at prepupal-pupal stage; imaginal discs described as homeotic, with the second leg and the wing discs described as like engrailed. Disc and cell autonomous. alleles: allele synonym ___________________ dash1 dashIII-10 dash2 dashXVI-18 dash3 dashGTK117 dash4 dashGTN402 dash5 dashRD317 dash6 dashRE418 dash7 dashRF327 dash8 dashRF605 dash9 dashRL031 dash10 dashRZ426 dash11 dashRZ606 dash12 dashSP1017 dash13 dashVD11 dash14 dashV234 dash15 dashVD238 dash16 dashVE238 dash17 dashjVF101 dash18 dashVS356 dash19 dashVS393 dash20 dashVT367 dash21 dashjVU215 dash22 dashVV183 dash23 dashVZ406 dash24 dashWA160 # Dash: see Abl # Dat: Dopamine-N-acetyltransferase location: 2-107 (within 0.17 unit to the left of sp). references: Maranda and Hodgetts, 1977, Insect Biochem. 7: 33-43. Huntley, 1978, Ph.D. Thesis, University of Virginia. Marsh and Wright, 1980, Dev. Biol. 80: 379-87. phenotype: The structural gene for dopa N-acetylase (EC 3.2.1.5). Molecular weight 2.9 x 104 daltons. Biochemi- cal characterization by Maranda and Hodgetts (1977). Marsh and Wright (1980) argue from developmental profile that enzyme level not coordinately controlled with that of dopa decarboxy- lase and not hormonally regulated. alleles: Datlo specifies an enzyme with low activity and rela- tive thermolability. Dat+/Datlo enzyme level intermediate between those of the two homozygous genotypes. cytology: Placed in 60B1-10 based on the failure of Df(2R)Px = Df(2R)60B8-10;60D1-2, which includes sp, to delete the locus and on dosage effects of segmental aneuploidy constructed using T(Y;2)A160 = T(Y;2)60B-C and T(Y;2)H137 = T(Y;2)60D (Huntley, 1978). # daughterless: see da # daughterless abnormal oocyte like: see dal # db: dark body location: 3-45. references: Chovnick and Talsma, 1966, DIS 41: 58. phenotype: Body color darker than normal. Male rarely sur- vives, dies in late pupal stage as pharate imago. Female weakly fertile. RK2. alleles: allele origin discoverer comments _________________________________________________________ db1 spont male lethal, female viable db2 ENU Belote both sexes lethal db4 ENU Belote both sexes viable db5 ENU Belote male lethal, female viable db83e X ray Belote male lethal, female viable db83l X ray Belote male lethal, female viable db4 viable in heterozygous combination with db1, db5, and deficiencies for db; however male lethal in combination with db2 (Belote). db2 complements other lethals in vicinity and may be an antimorphic allele (Belote). cytology: Placed in 73C2-D1 by deficiency analysis (Belote). other information: Possibly allelic to du. # dbl: dichaete-beadex-lethal location: 1-23.0. origin: I-factor induced. references: 'llison, 1981, Mol. Gen. Genet. 183: 123-29. phenotype: Produces a phenotype resembling the double mutant Bx/+; D/+ at 20; lethal at 25. other information: Reverts at frequency between 10-3 and 10-2. # DCg1: see Cg25C # dcm: dark carmine location: 1- (between y and w). origin: Spontaneous. references: Aguado, Galan-Estella, and Gonzalez-Gulian, 1988, DIS 67: 109. phenotype: Eye color dark carmine. dcm;st eyes orange. # Dcx: see In(3LR)CxD # DcxF: see In(3LR)DcxF #*dd: displaced location: 1-24.3. discoverer: Bridges, 31d7. phenotype: Antennae sunken into shortened head; eyes also deformed. Females often sterile. RK2. cytology: Locus lies between 7C4 and 8C2 (Demerec, Kaufmann, Fano, Sutton, and Sansome, 1942, Year Book - Carnegie Inst. Washington 41: 191). Further restricted to 7F through 8C2 on the basis of its genetic location to the right of oc which is in 7F-8A. # dd3: see ddl # Ddc: Dopa decarboxylase (T.R.F. Wright and J. Hirsh) location: 2-53.9+ (.025 centimorgans to the right of hk at 53.9 and .002 centimorgans to the right of amd). discoverer: Wright, 1974. references: Wright, Bewley, and Sherald, 1976, Genetics 84: 287-310. Wright, Beerman, Marsh, Bishop, Steward, Black, Tomsett, and Wright, 1981, Chromosoma 83: 45-58. Wright, Black, Bishop, Marsh, Pentz, Steward, and Wright, 1982, Mol. Gen. Genet. 188: 18-26. phenotype: Structural gene for dopa decarboxylase [DDC, 3-4- dihydroxy-L-phenylalanine-carboxylase (EC 4.1.28)] which catalyzes the decarboxylation of dopa to dopamine (Lunan and Mitchell, 1969, Arch. Biochem. Biophys. 132: 450-56) and 5- hydroxytryptophan to serotonin (5-hydroxytryptamine) but not tyrosine to tyramine (Livingstone and Tempel, 1983, Nature 303: 67-70). Native DDC isolated from mature larvae is a homodimer with subunit molecular weight 54 kd (Clark, Pass, Venkataraman, and Hodgetts, 1978, Mol. Gen. Genet 162: 287- 97). Distinct DDC isoforms are generated in the CNS and hypo- derm by alternate splicing of the Ddc primary transcript; the CNS isoform differs by the addition of 35 amino acids at the amino terminus (Morgan, Johnson, and Hirsh, 1986, EMBO J. 5: 3335-42). The predicted subunit molecular weights of these are 57.1 and 53.4 kd, respectively. DDC requires pyridoxal- 5-phosphate for activity and is strongly inhibited by heavy- metal ions and the sulfhydryl reagent, N-ethylmaleimide. Ini- tial velocity constants determined by Black and Smarrelli (1986, Biochim. Biophys. Acta 870: 31-40). The dopamine pro- duced by DDC is necessary to effect sclerotization of the cuticle, being further metabolized both to N-acetyldopamine and N-|-alanyldopamine, which after oxidation to their respec- tive quinones, crosslink cuticular proteins. Thus in adults and white prepupae more than 90% of the DDC activity is located in the epidermis (Lunan and Mitchell, 1969; Scholnick, Morgan, and Hirsh, 1983, Cell 34: 37-45). Some DDC activity (~5%) is found in the central nervous system of white prepupae and adults where it produces the neurotransmitters dopamine and serotonin [Wright, 1977, Amer. Zool. 17: 707-21; Living- stone and Tempel, 1983; White and Valles, 1985, Molecular Basis of Neural Development (Edelman, Gell, and Cowan (eds.). John Wiley and Sons, N.Y., pp 547-63]. The limited amounts found in the ovaries (Wright, Steward, Bentley and Adler, 1981, Dev. Genet. 2: 223-35) and proventriculus (Wright and Wright, Proc. Int. Congr. Genet., 15th, 1978, Part I, p. 615) are localized in associated neural ganglia (Konrad and Marsh, 1987, Dev. Biol. 122: 172-85). Five peaks of DDC activity evident during development: at the end of embryogenesis, the two larval molts, pupariation, and eclosion (Marsh and Wright, 1980, Dev. Biol. 80: 379-87; Kraminsky, Clark, Estelle, Gietz, Sage, O'Conner, and Hodgetts, 1980, Proc. Nat. Acad. Sci. USA 77: 4175-79). The largest peak, which occurs at pupariation, is induced by a coincident ecdysone peak of the molting larvae (Marsh and Wright, 1980) and has been shown to be attributable to a rapid increase in translatable DDC mRNA following administration of 20-0H-ecdysone (Kraminsky et al., 1980). Ecdysone induces Ddc expression in the mature larval epidermis within two to four hrs (Karminsky, et al., 1980; Clark, Doctor, Fristrom, and Hodgetts, 1986, Dev. Biol. 114: 141-50). Since cycloheximide addition is sufficient to largely abolish this induction, it appears that this response is an indirect action of ecdysone. A different response of Ddc to ecdysone occurs in cultured imaginal discs; Ddc induc- tion occurs only subsequent to withdrawal of the hormone (Clark et al., 1986). Most mutations in Ddc are homozygous or hemizygous lethal. The effective lethal phases of the first eight lethal alleles, Ddcn1-Ddcn8, were almost identical. As hemizygotes over Df(2L)TW130 almost all mortality is late embryonic with actively moving larvae, exhibiting unpigmented cephalophar- yngeal apparatuses and denticle belts, unable to hatch. When homozygous there is a fairly uniform shift in effective lethal phases with mean mortalities from all eight alleles in the cross of Ddcn/CyO x Ddcn/cn bw being 13.6% embryonic, 14.1% larval, and 4.8% pupal (Wright and Wright, 1978). Many larvae hemizygous for lethal alleles, or homozygous deficient for Ddc, when mechanically released from the egg membranes, con- tinue development to the 3rd larval instar and to the pharate adult stage. Genotypes which produce individuals with drastically reduced DDC activities (~0.5-5% of wild type) exhibit an "escaper" phenotype characterized by incomplete pigmentation and sclerotization of the cuticle; developmental time can be pro- longed for as many as four or five days; puparia are easily scored showing melanization at each end of the greenish-gray pupa case; adults often die or get stuck in the food within 24 hr of eclosion; macrochaetae may be very thin, long, and straw-colored or colorless; the whole body remains light, i.e., doesn't take on its normal pigmentation; abdominal mark- ings are apparent but do not darken; upon aging a few hours wing axillae become melanized similar to the phenotype of sp, leg joints also become melanized perhaps due to the phenoloxi- dase wound reaction brought on by ruptures of weakened cuti- cle; flies walk on tibias rather than tarsi, but leg movements appear to be coordinated (Wright, Bewley, and Sherald, 1976). Genotypes that produce flies exhibiting the "escaper" pheno- type include heteroallelic intragenic complementing heterozy- gotes with less than 5% of the expected number of survivors (Wright, Bewley, and Sherald, 1976), hemizygotes of the ts allele Ddcts2 raised continuously at 22 or 25, or homozygotes for Ddcts1 or Ddcts2 exposed to the restrictive temperature 30 for 24- or 48-hour pulses at the end of the pupal stage (Wright). Ddc temperature-sensitive mutants have been reported to show reduced learning after a three-day period at the restrictive temperature (Tempel, Livingstone, and Quinn, 1984, Proc Nat. Acad. Sci. USA 81: 3577-81). However, these results cannot presently be reproduced by other investigators (see Tully, 1987, Trends in Neurosci. 10: 330-35; Hirsh, 1989, Dev. Genet. 10: 232-38). It is possible that this lack of repro- ducibility is due to the accumulation of genetic modifiers. In homozygous deficient larvae normally-serotonin-containing neurons lack immunologically detectable serotonin but display normal levels of uptake of exogenously supplied serotonin (Valles and White, J. Neurosci. 6: 1482-91). Further studies of these Ddc- larvae, on which catecholamine histofluorescence studies were performed, revealed novel neu- ronal subsets lighting up, which become fluorogenic earlier than the wild-type-like neurons in the mutant CNS (Budnik, Martin-Morris, and White, 1986, J. Neurosci. 6: 1482-91). Certain serotonin-containing nerve fibers in developing larvae are still able to reach their normal targets in Ddc- animals (which therefore are intrinsically serotonin-minus), but there is anomalous extra branching associated with the incoming fibers (Budnik, Wu, and White, 1989, J. Neurosci. 9: 2866- 77). Ddc mosaics generated by crossing a transduced Ddc+ insert into R(1)wvC (Gailey, Bordne, Valles, Hall, and White, 1987, Genetics 115: 305-11). Such adult mosaics used to reveal no absolute requirement of DDC in any particular por- tion of epidermis or CNS, but there was low recovery of gynan- dromorphs with large Ddc- patches. Larval mosaics show that DDC-positive neurons always contain serotonin, but some serotonin-positive cells (which were near DDC+) have no detectable enzyme protein; hence, the serotonin phenotype can be nonautonomous (Valles and White, 1990). In addition to the naturally occurring alleles, DdcRE, DdcRS, and Ddc+4, which are described separately, three sur- veys of natural populations for Ddc variants have been reported. Estelle and Hodgetts (1984, Mol. Gen. Genet. 195: 434-41) measured DDC levels in 109 strains isogenic for second chromosomes isolated independently by Bewley (1978, Biochem. Genet. 16: 769-75) from collections at Raleigh, NC, Bloomington, IN., and Webster Groves, MO. (WGM). Two (WGM) strains (including Ddc+4) had increased activities and two had reduced activities when compared with a Canton-S control. Marsh and Wright report DDC activities from twelve different wild-type strains maintained in laboratories for many years. Relative to Oregon-R (DdcC) females, they ranged from a low of 68% for Urbana males to a high for Canton-S females (180%) and males (130%) with most strains with activities between Oregon-R and Canton-S. Aquadro, Jennings, Bland, Laurie- Ahlberg, and Langley (1984, Genetics 107: s3) surveyed forty-six second chromosome lines isolated from five natural populations for restriction fragment variations in the 80kb region surrounding Ddc and for adult DDC activity. No con- sistent pattern of association between level of DDC activity and restriction site haplotype was apparent although the lines showed a two-fold variation in DDC activity. Two lines with 5kb and 1.5kb inserts within an intron and at the 5' end of Ddc showed normal adult DDC activities. The temperature-sensitive periods causing lethality for Ddcts2 homozygotes are primarily during embryogenesis and late in the third larval instar. Heat shocks, 30 for 24 or 48 hr, during metamorphosis do not increase lethality significantly but produce adults with the extreme "escaper" phenotype. DDC in extracts from adult Ddcts1 and Ddcts2 homozygotes is signi- ficantly more thermolabile than that from wild-type controls. DDC from Ddcts1/+ heterozygotes is much less labile showing a biphasic inactivation curve. Ddcts2/+ DDC is no more thermolabile than wild-type DDC (Wright, unpublished data). Genotypes with reduced levels of DDC activity, e.g. Ddcn5/Ddcn8 and Ddcn1/Ddcn8 with less than 4% DDC activity, are not more sensitive to dietary alpha methyl dopa nor are genotypes with increased levels of DDC activity more resistant (Marsh and Wright, 1986, Genetics 112: 249-65). In fact, the reverse may be true: reduced DDC, more resistant; increased DDC, more sensitive. alleles: The numbered superscripts of many of the alleles were previously preceeded by n to indicate null; the n's have been removed, but the numbers retained. allele origin discoverer synonym ref ( comments | ____________________________________________________________ Ddc1 EMS Wright l(2)E7 5 32.6 Ddc2 EMS Wright l(2)E57 5 53.3 Ddc3 EMS Wright l(2)E61 5 51.7 Ddc4 EMS Wright l(2)E126 5 31.1 Ddc5 EMS Wright l(2)E135 5 33.3 Ddc6 EMS Wright l(2)E17 5 28.4 Ddc7 EMS Wright l(2)E140 5 43.1 Ddc8 EMS Wright l(2)E143 5 39.6 Ddc9 EMS Wright l(2)214 5 51.2 Ddc10 EMS Wright l(2)247r 5 33.7 Ddc11 EMS + F Wright l(2)315 5 48.1 Ddc12 EMS + F Wright l(2)332 5 49.4 Ddc13 EMS + F Wright l(2)340 5 42.2 Ddc14 EMS + F Wright l(2)348 5 39.2 Ddc15 EMS + F Wright l(2)3543 5 53.0 Ddc16 EMS + F Wright l(2)405 5 32.0 Ddc17 / ray Wright l(2)esc4 5 53.5 Ddc18 / ray Wright l(2)esc6 5 50.5 Ddc19 EMS Wright l(2)605 5 50.5 Ddc20 EMS Wright l(2)617 5 31.0 Ddc21 EMS Wright l(2)628 5 50.0 Ddc22 EMS Wright l(2)634 5 37.4 Ddc23 EMS Wright l(2)637 5 30.7 Ddc24 EMS Nusslein- 5 39 Volhard Ddc25 EMS Nusslein- 5 42 Volhard Ddc26 EMS Nusslein- 5 54 Volhard Ddc27 / ray Cecil l(2)esc7 5 44 2.2kb deletion in Ddc Ddc28 / ray Cecil l(2)esc8 5 43 Ddc29 / ray Cecil l(2)esc9 5 39 Ddc30 EMS + Wright l(2)7411 5 30.5 / ray Ddc31 EMS + Wright l(2)7422 5 37.5 / ray Ddc32 EMS + Wright l(2)7423 5 23.5 / ray Ddc33 EMS + Wright l(2)7426 5 42.7 / ray Ddc34 EMS + Wright l(2)7443 5 78.5 / ray Ddc35 DEB Cecil l(2)esc10 5 29 Ddc36 EMS Brittnacher l(2)L3 5 37.5 Ddc37 EMS Brittnacher l(2)L6 5 24.0 Ddc38 EMS Brittnacher l(2)L8 5 50.0 Ddc39 EMS Brittnacher l(2)L15 5 29.0 Ddc40 DEB Cecil l(2)esc11 5 55 Ddc41 DEB Cecil l(2)esc12 5 49 Ddc42 DEB Cecil l(2)esc13 5 60 Ddc43 EMS Wright l(2)620 5 57.8; chromosome also lethal over l(2)37Ca DdcC spont Wright 3, 4 100 / DdcDE1 EMS Wright 1 / Ddclo1 EMS Wright l(2)651 5 76.5 hypomorph / DdcRE spont Sherald 3, 4 158 hypermorph / DdcRS spont Sherald 3, 4 141 hypermorph / Ddcts1 EMS Wright l(2)248 5 65.5 Ddcts2 EMS + F Wright l(2)308 5 52.3 Ddcts3 EMS Wright l(2)607 5 52.5 Ddcts4 EMS Wright l(2)652 5 43.7 Ddcts5 EMS Wright l(2)633 5 65.4 Ddc+4 spont Estelle 2 / ( 1 = Bishop and Wright, 1987, Genetics 115: 477-91; 2 = Estelle and Hodgetts, 1984, Mol. Gen. Genet. 195: 434- 41; 3 = Marsh and Wright, 1986 , Genetics 112: 249-65; 4 = Sherald and Wright, 1974, Mol. Gen. Genet. 133: 25-26; 5 = Wright, Black, Bishop, Marsh, Pentz, Steward, and Wright, 1982, Mol. Gen. Genet. 188: 18-26. | Specific DDC activity of newly eclosed adult CyO/Ddc hetero- zygotes expressed as a percentage of appropriate CyO/+ con- trols. / Expanded description below. cytology: In situ hybridization with cloned Ddc placed the Ddc gene in or very close to 37C1-2 (Hirsh and Davidson, 1981, Mol. Cell Biol. 1: 475-85). The distal breakpoint of Df(2L)VA17 breaks in 37C1,2 deleting the proximal part of the band (Wright et al., 1981), and at the DNA level this break- point is located in the first intron of Ddc deleting the 5' (proximal) exon (Gilbert, Hirsh, and Wright, 1984, Genetics 106: 679-94). The smallest deficiency that completely deletes Ddc is Df(2L)TW130. molecular biology: Ddc was cloned by a two-step screen, first screening for genes encoding hypodermally expressed mRNA's and then screening these clones by in situ hybridization (Hirsh and Davidson, 1981, Mol. Cell Biol. 1: 475-85). The sequence of Ddc and flanking DNA has been determined by the Hirsh and Marsh laboratories, as shown in the Genbank entries DRODDC and DRODDCG, respectively. (Primary references: Morgan et al., 1986; Eveleth, Geitz, Spencer, Nargan, Hodgetts, and Marsh, 1986, EMBO J. 5: 2663-72). Whereas these entries are in gen- eral agreement, there are several differences, including several that affect the predicted reading frames. The open reading frame given in DRODDC shows conservation with the periwinkle tryptophan hydroxylase sequence (Genbank entry CTRTPDC) in several regions, where the DRODDCG sequence indi- cates alternate reading frames. Ddc encompasses four exons, labelled A, B, C, and D, of which B, C, and D are protein encoding. The major mRNA encoded by Ddc is in the hypoderm, a 2.1-kb mRNA containing all four exons. As mentioned above, these mRNA's encode different DDC isoforms. A different pat- tern of Ddc exons is predicted in the exon B-C region by Eveleth et al., but these predictions are not consistent with the functional expression analyses in Morgan et al. (1986). Ddc and amd share high levels of sequence identity; their 3 ends are separated by a sequence of 2 kb, which contains another transcription unit (Eveleth and Marsh, 1986, Nucleic Acids Res. 114: 6169-83; Black, Pentz, and Wright, 1987, Mol. Gen. Genet. 209: 306-12). Using the same 7.5 kb Pst restriction enzyme fragment that straddles the Ddc gene but using different P element vector constructs, both Scholnick, Morgan, and Hirsh (1983, Cell 34: 37-45) and Marsh, Gibbs, and Timmons (1985, Mol. Gen. Genet. 198: 393-403) have effected germline transformation of Ddc+ DNA which rescues Ddc mutant homo- and hemizygotes. All except two of the total of 16 transformed strains examined showed approximately normal levels of DDC activity along with normal tissue and temporal expression of the transposed Ddc genes. One strain had the expected level of DDC activity at pupariation but unexpectedly low levels in both sexes of newly emerged adults, and the other strain gave elevated DDC activi- ties at all stages (Marsh, Gibbs, and Timmons, 1985). Of the two X-linked transformants, one was dosage compensated (Schol- nick, Morgan and Hirsh, 1983) and the other was not (Marsh, Gibbs and Timmons, 1985). P-element germline integration (Scholnick et al., 1983; Marsh et al., 1985) initially defined essential Ddc regulatory sequences to lie within 2.5 kb of 5 and 1 kb of 3 flanking DNA. These studies were extended by analyses of deletions (Hirsh, Morgan, and Scholnick, 1986, Mol. Cell Biol. 6: 4548-57; Scholnick, Bray, Morgan, McCormick, and Hirsh, 1986, Science 234: 998-1002) and by the detection of promoter sequences conserved between the Ddc genes from D. melanogaster and D. virilis (Bray and Hirsh, 1986, EMBO J. 5: 2305-11). These data indicate that sequences farther than 98 base pairs from the RNA transcription start site are not required for normal temporal regulation of Ddc expression in the hypoderm and implicate sequences between -106 and -38 as being neces- sary for this regulation. This region contains a number of sequence elements conserved between the two evolutionarily related Ddc genes. In a wild-type larval CNS (Beall and Hirsh, 1987, Genes Dev. 1: 510-20; Konrad and Marsh, 1987, Dev. Biol. 122: 172-85), Ddc is expressed in approximately 85 se- rotonergic neurons, and in another approximately 45 neurons previously identified as containing catecholamines (Budnick, Martin-Morris, and White, 1986, J. Neuroscience 6: 3682-91) which are presumably dopaminergic neurons. In addition, there is a low level of expression in a network consisting of a sub- set of glial cells (Beall and Hirsh, 1987). All cis elements necessary for neuronal expression of Ddc are contained within the 2,200 base pairs of Ddc 5 flanking sequences (Bray, John- son, Hirsh, Heberlein, and Tjian, 1988, EMBO J. 7: 177-88). At least two separate regions are required for normal expres- sion of Ddc in the CNS: a distal CNS-enhancer region, extend- ing from ~1000 to 1600 upstream of the transcription start point (Beall and Hirsh, 1987; Johnson and Hirsh, 1989, Genes Dev. 3: 676-86) and a small proximal element I, at -60 (Scholnick et al., 1986; Bray et al., 1988; Bray, Burke, Brown, and Hirsh, 1989, Genes Dev. 3: 1130-45). The distal enhancer contains most if not all of the information control- ling cell specificity of Ddc expression in the CNS (Johnson and Hirsh, 1989) whereas element I is required for Ddc expres- sion in all Ddc-expressing neurons. The protein NTF (Neurogenic-element-binding transcription factor) binds to the CNS-specific element I in the proximal promoter (Bray et al., 1988, 1989), and a number of binding factors are found within the distal enhancer (Johnson and Hirsh, 1989). NTF and the factor cf1a, which binds to dopamine-cell-specific regulatory elements in the distal enhancer, have been cloned (Bray et al., 1989; Dynlacht, Attardi, Admon, Freeman, and Tjian, 1989, Genes Dev. 3: 1677-88; Johnson and Hirsh, 1990, Nature 343: 467-70). cf1a encodes a POU homeodomain protein. # DdcC: Dopa decarboxylase-C origin: Made isogenic by homozygosing single first, second, and third chromosomes from the Oregon-R6 isogenic strain from Yale University. phenotype: DDC activity and resistance to dietary alpha methyl dopa in the normal range for Oregon-R derived stocks. This strain was put through the same genetic manipulations as DdcRE and DdcRS so it could serve as a valid control for those strains. cytology: Normal. # DdcDE1: Dopa decarboxylase Differential Expression 1 discoverer: K. Wade. references: Bishop and Wright, 1987, Genetics 115: 477-91. phenotype: Hemizygous adults (9% of expected eclose) exhibit an extreme "escaper" phenotype (see Ddc above) except macrochae- tae are normally pigmented suggesting that DdcDE1 is differen- tially active in the epidermis vis-a-vis the bristle-forming cells. Pupa cases of DdcDE1 homo- and hemizygotes are wild type. DDC activity in newly eclosed adult DdcDE1 homozygotes is 4.4 _ 0.2% and in hemizygotes is 0.6 _ 0.1% of wild-type controls. Homozygous late embryos have 4.8 _ 2.3% activity. In striking contrast homozygous white prepupae have 46.5 _ 2.8% DDC activity. However, central nervous systems dissected from these DdcDE1 homozygous white prepupae show a tissue specific difference having 4.8 _ 2.3% DDC activity compared to wild-type CNS. Specific DDC activity in DdcDE1 homozygotes ranges significantly more than two times DDC levels in DdcDE1/Df(2L)TW130 hemizygotes. DDC from DdcDE1 homozygotes, crawling third instar larvae and adults, is less thermostable in vitro in comparison to controls. Late DdcDE1/DdcDE1 embryos (16-20 hr) have no detectable mature 2.0 kb Ddc RNA and have reduced levels of the 2.3 kb RNA. The precise reason for the differential expression has yet to be established but is not due to posi- tion effect variegation (Bishop and Wright, 1987, Genetics 115: 477-91). DdcDE1 phenotype rescued by a 7.5kb transfor- mant of Ddc+ DNA. # Ddclo1: Dopa Decarboxylase low-1 discoverer: T.R.F. Wright. references: Wright, Black, Bishop, Marsh, Pentz, Steward, and Wright, 1982, Mol. Gen. Genet. 188: 18-26; phenotype: Some hemizygous adults exhibit the incomplete sclerotization "escaper" phenotype. Not temperature sensi- tive: hemizygotes being equally viable at 18, 25, and 30 (40- 56% of expected). DDC from Ddclo1 hemizygotes is not more thermolabile in vitro than that from wild type. Heterozygous Ddclo1/CyO have about 77% wild type specific DDC activity and Ddclo1 homozygotes have 15-30% activity. cytology: No visible aberration. No detectable difference in the DNA (>50bp). # DdcRE: Dopa decarboxylase-RE origin: Natural variant; Canton-S-like on the basis of restric- tion enzyme site polymorphisms. Originally reported as being EMS-induced in Oregon-R but probably a Canton-S contaminant. Made coisogenic with DdcC strain. discoverer: Sherald. references: Marsh and Wright, 1986, Genetics 112: 249-65. phenotype: Dual phenotype of elevated DDC activity and increased resistance to dietary alpha methyl dopa relative to Oregon-R derived controls (DdcC). Specific DDC activity of newly eclosed adults 158% and DDC crossreacting material (CRM) 156% of the DdcC control. LD50 for alpha methyl dopa is ~0.4 mM vs. ~0.2 mM for the DdcC control. Gene dosage studies with Ddc+ and l(2)amd+ demonstrate that increased resistance to alpha methyl dopa is not the result of increased DDC activity. Thus, the dual phenotype is inferred to arise from a coordi- nated increase in Ddc+ activity and l(2)amd+ activity produced either by accumulated changes in a genetic element (or ele- ments) in the close proximity to the Ddc and amd genes. cytology: No visible difference apparent: not a duplication at either the cytological level or at the DNA level. # DdcRS: Dopa decarboxylase-RS origin: Variant isolated from a sp2 bs2 stock. Made coisogenic with DdcC strain. discoverer: Sherald. phenotype: Dual phenotype of elevated DDC activity and increased resistance to dietary and methyl dopa relative to Oregon-R derived controls (DdcC). Specific DDC activity of newly eclosed adults 141% and DDC crossreacting material (CRM) 137% of the DdcC control. Interpretation of phenotype identi- cal to that for DdcRE. cytology: No visible difference apparent: not a duplication at either the cytological level or at the DNA level. # Ddc+4: Dopa decarboxylase +4 origin: Natural variant in a second chromosome extracted from a Webster Groves, Missouri (WGM) population and made isogenic using marked balancer chromosomes (Bewley, 1978, Biochem. Genet. 16: 769-75). references: Estelle and Hodgetts, 1984, Mol. Gen. Genet. 195: 434-41. phenotype: No visible phenotype: Ddc+4 overproduces DDC activity at embryonic hatching, the second to third instar molt, and at adult eclosion relative to a Canton-S control: 141%, 150%, and 118% respectively; in contrast, underproduces DDC at pupariation: 50%. These temporal differences are found in epidermis but not in neural tissues where DDC activi- ties are normal. DDC CRM at pupariation and adult eclosion are 49% and 140% respectively of Canton-S CRM. No difference was found in the electrophoretic mobility of non-denatured and denatured DDC molecules. DDC mRNA is 140%, 52%, and 148% of Canton-S at embryonic hatching, pupariation, and adult eclo- sion respectively indicating that the temporal phenotype is reflected in mRNA levels. molecular biology: Ddc+4 DNA was cloned and examined by acrylamide gel electrophoresis of restriction fragments. Six small restriction length polymorphisms and one restriction site polymorphism exist between Ddc+4 and Canton-S DNA. Five of these differences occur in the 5' untranslated leader sequence of the DDC mRNA or in the 4.5 kb of DNA upstream of the transcription start site. Some DNA sequence data have been acquired (Spencer and Hodgetts, unpublished data). # ddd: defective dorsal discs (A. Shearn) location: 3-18.0. origin: Induced by ethyl methanesulfonate. references: Shearn, Rice, Garen, and Gehring, 1971, Proc. Nat. Acad. Sci. USA 68: 2594-98. Wurst, Hersperger, and Shearn, 1984, Dev. Biol. 106: 147-55. Simcox, Wurst, Hersperger, and Shearn, 1987, Dev. Biol. 122: 559-67. phenotype: Homozygous larvae perish between the first larval instar and the prepupal stage; dorsal thoracic imaginal discs, i.e. of the pronotum, mesonotum, and metanotum reduced to 3% or less of normal size; all other imaginal discs develop normally. Mutant larvae support the growth of wild-type wing discs; mutant wing discs show very little development in wild-type larval. Mutant cells develop normally in wing discs that contain mixtures of mutant and wild-type cells, as pro- duced by nuclear or cellular transplantation into blastoderms or by somatic exchange. Mutant leg discs transplanted into wild-type hosts can transdetermine to wing development. Stu- dies of temperature-sensitive genotypes indicate that ddd+ product is not required for normal wing development during embryogenesis. No evidence for a maternal effect in either conditional mutants raised under permissive conditions and switched to restrictive temperatures or in germ-line- transplants of mutant cells into wild-type hosts. alleles: Thirteen alleles induced by ethyl methanesulfonate by Shearn. allele synonym comments __________________________________________ ddd1 l(3)LGA ddd2 l(3)RD310 ddd3 l(3)RG436 L3-P lethal ddd4 l(3)RY507 embryonic lethal ddd5 l(3)SA519 cold-sensitive allele ddd6 l(3)SI134 ddd7 l(3)UH5 ddd8 l(3)UH64 ddd9 l(3)VJ449 ddd10 l(3)VK97 ddd11 l(3)VU288 ddd12 l(3)VW100 ddd13 l(3)WB240 heat-sensitive allele cytology: Placed in 64D-E by segmental aneuploidy. #*ddl: displacedlike location: 1-27.2. origin: Induced by triethylenemelamine. discoverer: Fahmy, 1953. synonym: dd3. references: 1959, DIS 33: 84. phenotype: Frontal region with antennae sunken into shortened head. Eyes deformed. Thoracic bristles stiff and slightly shortened. Wings frequently misheld. Males sterile; viabil- ity slightly reduced. RK2. alleles: One X-ray-induced allele. #*de: deacon location: 1-56. origin: X ray induced. discoverer: Muller, 26l12. references: 1935, DIS 3: 29. phenotype: Body and wings narrow and rectangular. Eyes slightly flattened with oblique cast. RK3. other information: Possibly an allele of sl (1-53.5). #*De: Dented location: 2- (between dp and b). origin: X ray induced. discoverer: Belgovsky, 36c. references: 1937, DIS 8: 7. phenotype: In heterozygote, most flies show one or two indenta- tions on thorax at front. Homozygote has two smaller, sharper dents. Wings often raised. RK3. # deacon: see de # deadlock: see del # dec-1: defective chorion 1 location: 1-20.7 (based on 69 ct-oc and 93 ct-sn recombinants; combined data of Lineruth et al.). references: Gans, Audit and Masson, 1975, Genetics 81: 683- 704. Komitopoulou, Gans, Margaritis, Kafatos, and Masson, 1983, Genetics 105: 897-920. Lineruth and Lambertsson, 1985, Wilhelm Roux's Arch. Dev. Biol. 194: 436-39. Lineruth, Lambertsson, and Lindberg, 1985, Mol. Gen. Genet. 201: 375-78. Lineruth and Lambertsson, 1986, Mol. Gen. Genet. 205: 213-16. Bauer and Waring, 1987, Dev. Biol. 121: 349-58. phenotype: Females homozygous for dec-12 produce few eggs; chorion thin and fragile, often lost during ovoposition; dor- sal appendages much reduced, often absent; chorion appears vacuolated and permits uptake of neutral red. Mosaic studies with dec-12 demonstrate that it is a somatically active gene [Wieschaus, Audit, and Masson, 1981, Dev. Biol. 92-103 (fig.)]. Mature egg shell shows lack of organization within the endochorion and accumulation of electron dense material in the vitelline membrane of stage-14 egg chambers. No abnormal- ities detected in stage-10 oocytes. Three protein products of gene detected; the primary translation product of 130 kd found in stage-10 follicles; this appears to be quickly processed into an 85-kd product, which is in turn processed into a 67-kd protein in stage 13 and 14 egg shells (Bauer and Waring); these products measured as 92, 82, and 76 kd, respectively, by Lineruth and Lambertsson (1985). All three proteins absent in dec-1 mutants, and they vary coordinately in molecular weight in natural variant alleles. alleles: Three molecular-weight variants found among strains from natural populations; each variant affects all three forms of the gene product. The majority of strains are as character- ized: strains labeled Israel and Krasnodar produce slightly smaller polypeptides, and strains labeled Alma Ata, Frunze, and Shahrinau produce polypeptides that are even smaller (Lineruth, Lambertsson, and Lindberg, 1985, Mol. Gen. Genet. 201: 375-78). These wild-type alleles are designated dec-1+1, dec-1+2, and dec-1+3 respectively. allele origin discoverer synonym ref u( comments _______________________________________________________________________________ dec-11 EMS fs(1)A267 2 dec-12 EMS fs(1)A384 2, 4 protein products absent dec-13 EMS fs(1)A1336 2 dec-14 EMS fs(1)A1501 2, 4 proteins 25 kd larger than normal; complements Df(1)ct4b1, but not dec-1 mutants dec-15 EMS fs(1)K467 3 dec-16 EMS fs(1)K718 3 dec-17 EMS fs(1)K1090 3 dec-18 EMS fs(1)K1124 3 dec-19 EMS fs(1)K1232 3 dec-110 EMS fs(1)K1511 3 dec-111 EMS 11-549 5 dec-112 EMS 12-365 5 dec-113 EMS 12-403 4, 5 protein products absent dec-114 EMS 12-1873 5 dec-115 EMS 12-2514 5 dec-116 EMS 12-3512 5 dec-117 EMS 12-3907 5 dec-118 EMS 12-4860 5 dec-119 EMS 13-453 5 dec-120 EMS 14-963 5 dec-121 EMS 13C-57 5 dec-122 EMS 13C-73 4, 5 protein products absent dec-123 EMS 14A-114 5 dec-124 EMS 14E19 5 dec-125 EMS Vyse fs(1)A15 5 dec-126 EMS L. Girton fs(1)952 5 dec-127 EMS fs(1)107 1 dec-128 EMS fs(1)400 1 dec-129 EMS fs(1)410 1, 4 protein products absent dec-130 EMS fs(1)764 1 1.6-kb insert in 3.2 to 3.6 kb dec-131 EMS fs(1)1195 1 dec-132 EMS fs(1)2325 1 ( 1 = Bauer and Waring, 1987. Dev. Biol. 121: 349-58; 2 = Gans, Audit, and Masson, 1975, Genetics 81: 683-704; 3 = Komitopoulou, Gans, Margaritis, Kafatos, and Masson, 1983, Genetics 105: 897-920; 4 = Lineruth and Lambertsson, 1986, Mol. Gen. Genet. 205: 213-16; 5 = Mohler and Carroll, 1984, DIS 60: 236-41. cytology: Placed in 7C1-3 based on its inclusion in Df(1)ct4b1 = Df(1)7B2-4;7C3-4 but not in Df(1)ct268-42 = Df(1)7A5-6;7B8- C1. molecular biology: Region isolated in a chromosome walk from the proximal breakpoint of Df(1)ct4b1 (Hawley and Waring, 1988, Genes Dev. 2: 341-49); coordinate 0 placed at EcoRI site just proximal to above breakpoint with positive values extending to the left. Sequence from 0 to 6.6 kb (which includes ct4b1 breakpoint) is complementary to an abundant poly(A)+ RNA of 4.0 kb from stage-8 to stage-11 follicles and a less abundant one of 5.8 kb from stage-11 and stage-12 fol- licles. cDNA's indicate that both messages have a common tran- scription start site, share several small introns, and that transcription is from right to left. A segment is apparently spliced out of a large exon present in the 5.8-kb message to generate the 4.0-kb message, which contains sufficient coding capacity to encode the 130 kd protein. Df(1)ct4b1 removes the 3 end of the transcript beginning at approximately the site of the 4.0-kb RNA-specific splice donor. Preliminary sequence determination indicates a N-terminal signal sequence. A 200- base-pair deletion between coordinates 1.9 and 2.7 differen- tiates the Shahrinau from the Canton-S wild-type allele and accounts for the molecular weight differences between their protein products. # dec-2 location: 1-23.1. discoverer: D. Mohler. synonym: fs(1)C2. phenotype: Homozygous females rarely ovoposit. Eggs have thin chorion with thin respiratory appendages. cytology: Placed in 7E10-8A5. # decapentaplegic: see dpp # deep orange: see dor # defective: see df # defective chorion 1: see dec-1 # defective dorsal disc: see ddd # defective in phototaxis plasticity: see dipp # Defective in phototaxis plasticity: see Dipp # deflected wing: see dfw # Deformed: see Dfd # deformed antennae: see dfa # deformed eye: see dfi # deformed tergites: see dft # deformed wings: see dwg # degenerated spermatheca: see dg-a # del: deadlock (T. Schupbach) location: 2-{54}. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female-sterile; homozygous del1 females often have underdeveloped ovaries which seem to lack germ cells alto- gether. In some females a small number of developing egg chambers are found. These never develop beyond the first few stages of oogenesis. Females homozygous for del2 and del3 have normal numbers of developing egg chambers of all stages in their ovaries. The eggs produced by the females very fre- quently have fused dorsal appendages, or lack dorsal append- ages altogether, and remain unfertilized. alleles: del1 to del4 are isolated as WK, HN, PS, and WH, respectively. cytology: Placed in 37F5-39F1, since uncovered by Df(2L)TW65 = Df(2L)37F5-38A1;39E2-F1. # Delayed recovery: see Dly # Delta: see Dl # delta vein: see thvd # delta wing: see dta # deltex: see dx # deltoid veins: see dlv # den: denervated location: 2- {39}. references: de la Concha, Dietrich, Weigel, and Campos-Ortega, 1988, Genetics 118: 499-508. genetics: Loss-of-function of den+ results in considerable neural hypoplasia (Brand and Campos-Ortega). cytology: Located in 31B-D. # Dented: see De # Deoxyribonuclease-1: see DNase-1 #*dep: depressed location: 1-18. discoverer: Bridges, 13d. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 67 (fig.). phenotype: Wings turned down at tips, flat from side to side. Somewhat variable but does not overlap wild type. RK2. # depilated: see dpt #*depl: depressedlike location: 1-23. origin: Recovered among progeny of flies treated with Janus green. discoverer: Muller, 28e20. synonym: depr: depressed-roof. references: 1935, DIS 3: 29. phenotype: Wings droop at sides. Flies dark and weak; bristles fine. Viability variable, about 20% wild type. RK3. # depressed: see dep # depressedlike: see depl #*der: deranged location: 1-57.2. origin: Induced by triethylenemelamine. discoverer: Fahmy, 1953. references: 1958, DIS 32: 69. phenotype: Thoracic hairs deranged, many point toward midline. Wings usually obliquely upheld and twisted, bringing inner margins together. Overlaps wild type. Good viability in both sexes, but female fertility reduced. RK3. # DER: see Egfr det: detached From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 54. # det: detached location: 3-72.5. origin: Spontaneous. discoverer: Nichols-Skoog, 35k27. phenotype: Posterior crossveins detached from longitudinals at one or both ends and may be absent. Wings occasionally folded back under or folded flat at middle. Eyes sometimes rough and bulging. Wings slightly spread. Bristles tend to break; scu- tellars occasionally doubled. RK3. # Detached: see Dt # dev: devenir location: 3-40.9. origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1983. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Isolated as a dominant suppressor of Pc mutations. Associated with recessive larval lethality. Lowered survival and loss of humeral bristles in combination with D3 may indi- cate allelism with Dichaete, but it is difficult to ascertain. alleles: Two alleles induced by ethyl methanesulfonate. cytology: Placed in 70C2-D3 based on its inclusion within Df(3L)fz-CAL5 = Df(3L)70C2;70D3 and exclusion from Df(3L)fz- M21 = Df(3L)70D2-3;71E4-5. #*df: defective location: 1-32.5. origin: Spontaneous. discoverer: Bridges, 15l3. phenotype: Head bristles around ocelli missing. Viability poor. RK3. #*dfa: deformed antennae location: 1-13.9. origin: Induced by 2-chloroethyl methanesulfonate. discoverer: Fahmy, 1956. references: 1959, DIS 33: 84. phenotype: Wings short, broad, either convex or concave, and abnormally held. Eyes small, dark, and rough. Bristles short, stiff, and occasionally bent. Trident pattern more pigmented. Abnormal antennae and aristae. Males viable and fertile. Females sterile. RK2. # Dfd: see ANTC #*dfi: deformed eye location: 3- (near D). origin: Recovered among descendants of heat-treated flies. discoverer: Ives, 32c. synonym: rough III. references: Plough and Ives, 1934, DIS 1: 34. 1935, Genetics 20: 42-69. phenotype: Eyes roughish, reduced, and misshapen. Overlaps wild type. Female sterile; poorly viable. RK3. # deflected wing: see dfw # deformed antennae: see dfa #*dft: deformed tergites location: 1-33.7. origin: Induced by 2-chloroethyl methanesulfonate. discoverer: Fahmy, 1956. references: 1959, DIS 33: 84. phenotype: Small fly with small, slightly rough eyes. Wings slightly divergent or upheld, abnormally shaped with occa- sional incision of the inner margin. Bristles slightly thinner and shorter with one or both postscutellars frequently absent, and a dorsocentral occasionally missing. Abdominal segmentation deformed to various degrees; abdominal hairs fewer and deranged. Males poorly fertile; viability about 50% wild type. RK2. # degenerated spermatheca: see dg-a # dfw: deflected wing location: 1-21.6. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine. discoverer: Fahmy, 1955. references: 1959, DIS 33: 84. phenotype: Wings slightly divergent and upheld to various degrees, often twisted on their axes. Inner margins fre- quently incised; occasionally, wing membranes separated by fluid. Eyes slightly smaller. Males viable and fertile. Females sterile; viability reduced. RK2. alleles: One X-ray-induced allele.