# dg: Don Giovanni (J.C. Hall) location: 1- (between y and cv). origin: Spontaneous in Canton-S stock. discoverer: Gailey. references: Gailey, Jackson, and Siegel, 1984, Genetics 106: 613-23. Gailey and Siegel, 1989, Anim. Behav. 38: 163-89. phenotype: Males not conditioned by courtship of fertilized females, apparently because they fail to elicit the appropri- ate cues from them (Gailey and Siegel, 1989); this means, further, that after a dg male courts a fertilized female, a wild-type male will not show the usual depressed courtship of this female; yet if the fertilized female is first courted by a wild-type male, a dg male will exhibit depressed courtship of her; females fertilized by dg males do not effectively modify subsequent courtships directed at them by any male type (Gailey and Siegel, 1989). dg males can, in general, learn, i.e. also in artificial test situations such as those using shocks and odorants (Siegel, Hall, Gailey, and Kyriacou, 1984, Behav. Genet. 14: 425-52) or involving females to which quinine is applied (Ackerman and Siegel, 1986, J. Neurogenet. 3: 111-23). #*dg-a: degenerated spermatheca location: 3-75.5. origin: Spontaneous. discoverer: Collins, 21a. references: Wexelsen, 1928, Genetics 13: 389-400 (fig.). phenotype: Adult females show degeneration and pigmentation of epithelial cells of spermathecae 24 hr or more after eclosion. Viability and fertility good. Penetrance 100%. RK3. # dgl: double glazed location: 2-{51}. references: McGill, Chia, Karp, and Ashburner, 1988, Genetics 119: 647-61. cytology: Placed in 34C4-35C5 based on its inclusion in the Sco transposition. # dh: see eg2 #*dhm: dark hairy margins alleles: 3-43.2 (proximal to th). origin: Spontaneous. references: Barker and Hollingdale, 1970, DIS 45: 39. phenotype: Wings darker than wild type, have hairy margins and thick veins; increased numbers of abdominal and scutellars bristles. Viability and fertility good. other information: l(3)DTS5 may be allelic to dhm (Ashburner). # Dhod: Dihydroorotate dehydrogenase alleles: 3-48.0 (no recombinants with pp among 11,618 offspring of heterozygous mothers). references: Rawls, Chambers, and Cohen, 1981, Biochem. Genet. 19: 115-27. Porter and Rawls, 1984, Mol. Gen. Genet. 193: 27-32. phenotype: Likely to be the structural gene for dehydroorotate dehydrogenase, which catalyzes the fourth enzymatic step of de novo pyrimidine biosynthesis [DHOdehase (EC 1.3.3.1)]. Homoz- ygotes for null alleles display less than 3% normal levels of enzyme activity; heterozygotes have half-normal levels; flies with three normal alleles show increased levels. Enzyme appears to be monomeric; no interallelic complementation among null alleles. Enzyme activity located in outer surface of inner mitochondrial membrane in other species; also mitochon- drial in Drosophila. Homozygotes for null alleles exhibit wing truncation, irregular lengths and distribution of hairs on wing margin, deformed posterior legs, and female sterility, as seen in r and r-l. Viability normal. Phenotype suppressed, but enzyme level not restored, by su(r). Null mutants suppress eye mottling characteristic of r-l in doubly mutant genotypes. alleles: A naturally occurring variant designated Dhodlow pro- duces but 25% of normal DHOdehase activity. Twelve EMS- induced null or nearly null alleles are designated Dhod1 through Dhod12. Dhod2 and Dhod12 are hypomorphic, exhibiting weak wing effects and female fertility. In addition, Dhod13 and Dhod14 were X ray induced by Vincent (originally desig- nated DhodV7 and DhodV10); the former was associated with In(3R)Dhod13 = In(3R)85A;89B. Dhod15 induced by hybrid dys- genesis as DhodC2. cytology: Placed in 85A4-5 based on its inclusion in the region of overlap of Df(3R)V2 = Df(3R)84E6-9;85A3-5 and Df(3R)G1 = Df(3R)85A4-5;85A6-11; coordinates -49 to +19 (Jones and Rawls, 1988, Genetics 120: 733-42). molecular biology: Included in a 145-kb walk carried out by Jones and Rawls (0 coordinate chosen as the proximal end of the initiating lambda clone, with positive values to the right). A putative 0.8-kb P insertion associated with Dhod15 located between coordinates 14.4 and 14.9 kb; the inversion associated with Dhod13 is broken at 14 kb. Genomic sequence hybridizes to a 1.5-kb transcript that is most abundant in early embryos, moderately abundant in mid embryos, mid pupae and adults; lowest in mid-larval stages; some stages display a 1.6-kb transcript as well; transcribed from right to left. Partial sequence shows homology to bacterial DHOdehase in the 3 end but no discernable homology in the 5 end (Jones, Kirk- patrick, and Rawls, 1989, Mol. Gen. Genet. 219: 397-403). #*di: dimorphos location: 1- (near spindle attachment). origin: Spontaneous. discoverer: Harnly, 32d10. references: 1935, J. Exp. Zool. 72: 75-99 (fig.). 1940, DIS 13: 49. phenotype: Specific lengthener of vg wings, especially in males (di; vg female much like vg). At higher temperatures, eyes small and rough, and wings of both sexes approach wild type. RK2 in vg male. # dib: disembodied location: 3-12. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). phenotype: Homozygous lethal; no differentiation of cuticle and head skeleton. alleles: Three. dib1, dib2, and dib3, isolated as 10F, 10K, and 10L. cytology: Placed in 62D-64C; uncovered by terminally-deficient segregant from T(2;3)D11 = T(2;3)?;64B-C but not covered by Dp(3;Y)H141 = Dp(3;Y)61B;62D. # dibro: see frdi # dic: dicephalic location: 3-46.0. origin: Spontaneous. references: Lohs-Schardin, 1982, Wilhelm Roux's Arch. Dev. Biol. 191: 28-36 (fig.). phenotype: A semidominant maternal-effect mutant with low penetrance. Homozygous dic females and, to a lesser extent, dic/+ heterozygotes exhibit variable numbers of abnormal fol- licles and abnormal oocytes. During vitellogenesis, the oocyte occupies a position in the middle of or lateral to the nurse cells rather than posterior to them; the fifteen nurse cells distribute themselves into two clusters, one at each end of the follicle, instead of remaining together anteriorally, as normally occurs. The larger cluster tends to be located anteriorly. One or several nurse cells may become detached from remainder of cyst [Frey, Sander, and Gutzeit, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 388-93 (fig.)]. Pole- cell transplantation experiments show that the dic phenotype results if either the germ line or the soma or both are homoz- ygous for dic (Frey and Gutzeit, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 527-31). Chorionic respiratory processes irregular in shape and frequently point toward oviduct rather than germarium, as usually occurs. Eggs of dic females form micropyle at both ends, and they are less uniform in size and more irregular in shape than eggs from normal females. Embryonic development restricted to eggs of nearly normal shape. Blastoderm appears normal but no pole cells form. Head furrows and head lobes seen at both ends of embryo. Embryos secreting larval cuticle display (1) anterior denticle belt patterns at both ends, (2) a single abnormal polarity gradient, or (3) posterior pattern elements at both ends; seg- ment showing polarity switch varies. The relative frequencies of these three classes agree with hypothesis that the two ends of the egg develop independently with P (anterior develop- ment) = 0.9 for both ends. # Dichaete: see D # dichaete-beadex-lethal: see dbl # Difl: Drosophila-interferon-like-protein location: 3-{27}. discoverer: Garen. phenotype: Homologous to mouse (2 interferon. cytology: Localized to 67A8-10 by in situ hybridization. # dihedral: see eg2 # Dihydroorotate dehydrogenase: see Dhod # dil: dilute location: 2-57. origin: Spontaneous. discoverer: Bridges, 32f22. phenotype: Dilutes bw to pale yellowish brown and wee, we2, and wbl to paler grades. RK3. #*dil-3: dilute in chromosome 3 location: 3- (not located). discoverer: Bridges, 15l9. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 151. phenotype: Eye color like maroon, overlaps wild type. RK3. #*dil-wa: dilutor of white-apricot location: 3- (not located). discoverer: Weinstein. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 218. phenotype: Lightens wa. RK3. # dilute: see dil # dilute in chromosome 3: see dil-3 # dilute ocelli: see po2 # Dilute-1: see bwV29l # Dilute-2: see bwV30k1 # Dilute-3: see bwV30k10 # Dilute-4: see bwV30k12 # Dilute-5: see bwV30k13 # Dilute-6: see bwV30k18 # dilutor of white-apricot: see dil-wa # diminutive: see dm # Dimethylnitrosoamine demethylase: see Dmnd # dimorphos: see di #*Din: Dinty location: Unknown; associated with a rearrangement. origin: X ray induced. discoverer: Braver, 55a. references: 1955, DIS 29: 70. Pollock, 1963, DIS 38: 50, phenotype: In male and heterozygous female, central portion of vein L2 interrupted. Posterior supra-alar bristles absent in 95-99% of females and 97-99.5% of males. Anterior postalar bristles absent in 6-11% of females and 2-6% of males. Wings divergent. Viable and fertile in male and heterozygous female; homozygous lethal. RK2. cytology: Associated with T(1;2;3)Din = T(1;3)3C;63A + T(2;3)39D-73A. # Dint-1: see wg # Dinty: see Din # Dip-A: Dipeptidase-A location: 2-55.2 (based on 74 pr-cn recombinants). origin: Naturally occurring polymorphism. references: Voelker and Langley, 1978, Genetica 49: 233-36. Ohnishi and Voelker, 1981, Biochem. Genet. 19: 75-85. phenotype: Structural gene for dipeptidase A [DIP-A (EC 3.4.14.?)], a dimeric molecule based on the formation of hybrid enzymes in heterozygotes for electrophoretic variants. Enzyme molecular weight estimated at approximately 117,000 daltons by gel filtration (Leigh Brown). Substrate specificities determined by Laurie-Ahlberg (1982, Biochem. Genet. 20: 407-24). The only Drosophila peptidase with glycyl-L-isoleucine-ase activity. Occurs at high levels in the larval midgut. alleles: In order of increasing anodal migration in 12% starch gel electrophoresis designated Dip-A2, Dip-A4, and Dip-A6. Null alleles superscripted nNC1, nNC2, nGB1, nGB2, and nGB3 recovered from natural populations (Voelker, Langley, Leigh Brown, Ohnishi, Dickson, Montgomery, and Smith, 1980, Proc. Nat. Acad. Sci. USA 77: 1091-95). Dip-AnGB2/Dip-AnGB3 shows partial complementation producing Dip-A2 migration rate (Barkhart, Montgomery, Langley, and Voelker, 1984, Genetics 107: 295-306). cytology: Placed in 41A at heterochromatic-euchromatic junction of 2R based on its inclusion in Df(2R)M-S24, in which no loss of euchromatic bands can be detected; the locus is not included in Df(2)M-S28 or Df(2)M-S210, the latter of which has been shown to be deficient for the majority of 2R hetero- chromatin. # Dip-B: Dipeptidase B location: 3-53.6 (Laurie-Ahlberg, 1982). references: Ohnishi and Voelker, 1981, Biochem. Genet. 19: 75-85. phenotype: Structural gene for dipeptidase B [DIP-B(EC 3.4.14.?.)], which is virtually monomorphic in natural popula- tions but which differs in electrophoretic mobility from dipeptidase-B variants in D. simulans. Substrate specifici- ties determined by Laurie-Ahlberg (1982, Biochem. Genet. 20: 407-24). alleles: Dip-B4 is the common allele; Dip-B6, a slow variant, and Dip-BloNC25, a nearly null allele, isolated from natural populations (Laurie-Ahlberg, 1982). cytology: Localized to 87F13-88C2 based on the absence of D. melanogaster enzyme from hybrids between D. melanogaster and D. simulans when the melanogaster genome carries Df(3R)red3l = Df(3R)87F12-14;88C1-3. # Dip-C: Dipeptidase-C location: 3-{50-51}. references: Ohnishi and Voelker, 1981, Biochem. Genet. 19: 75-85. phenotype: Structural gene for dipeptidase C [DIP-C(EC 3.4.14.?.)], for which no genetic variants are known but which differs in electrophoretic mobility from dipeptidase-C in D. simulans. Specific for dipeptides with carboxy proline (Laurie-Ahlberg, 1982, Biochem. Genet. 20: 407-24). cytology: Localized to 87B6-9 based on the presence of the D. melanogaster enzyme in hybrids between D. melanogaster and D. simulans when the melanogaster genome carries Df(3R)T45 = Df(3R)86;87B5-6 but not when it carries Df(3R)E-079 = Df(3R)86F1-2;87B8-10. None of the three lethal complementa- tion groups (e180 and 280, e227, and e078) also defined by those two deficiencies is associated with Dip-C function. # Dipeptidase-A: see Dip-A # Diphenol oxidase: see Dox # Dipp: Defective in phototaxis plasticity (J.C. Hall) location: 1-not mapped. references: Willmund and Ewing, 1982, Anim. Behav. 30: 209-15. Willmund, Emanns, Eusmann, and Ross, 1984, J. Insect Physiol. 30: 431-36. phenotype: Fails to display long-lasting modification of visual responses (e.g., light/dark choices) that are usually induced by exposure to strong blue light; prolonged depolarizing aft- erpotential (PDA) of photoreceptor cells, usually induced by such exposure, decays rapidly in the dark, unlike wild type, in which PDA is stable; in optomotor behavior, Dipp1 still shows some responses to moving stimuli after PDA induced, whereas Dipp2, as does wild type, has such responses switched off by induction of PDA. alleles: Possibly two mutant alleles, Dipp1 and Dipp2. other information: The two mutations here do not complement, given their dominance; yet, they have not been mapped meioti- cally, so they could be non-allelic. # dipp-: defective in phototaxis plasticity (J.C. Hall) origin: Induced by ethyl methanesulfonate. references: Willmund, Emanns, Eusenmann, and Ross, 1984, J. Insect Physiol. 30: 431-36. Speck, Mutz, Ohl, and Spatz, 1984, J. Insect Physiol. 30: 437-40. phenotype: A series of sex-linked non-complementing, mutants with similar phenotypes. Homozygotes fail to display long- lasting decrement in visual response (i.e., light-dark choices) that are usually induced by exposure to strong blue light; prolonged depolarizing afterpotentials of photo recep- tors occur normally; other aspects of physiological phenotype described in individual entries, which follow. # dipp-3 location: 1-(not localized; said not to be mappable to a single X-chromosome interval). phenotype: Photoreceptors show subnormal sensitivity, in elec- troretinogram recordings, after blue light exposure followed by dark adaptation. ERG responses to flickering light (400 or 600 nm) suggest that the two central photoreceptors in each facet are abnormal in their response (Speck, Mutz, Ohl, and Spatz, 1984, J. Insect Physiol. 30: 437-40). Fast phototaxis responses show subnormal sensitivity after some kinds of pre- treatment. # dipp-4 location: 1-(v-centromere). phenotype: Photoreceptors show somewhat aberrantly high sensi- tivity, in electro-retinogram recordings, to various wave lengths of light. ERG light-on transient smaller than normal (Speck, Mutz, Ohl, and Spatz, 1984, J. Insect Physiol. 30: 4337-40). Fast phototaxis responses show subnormal sen- sitivity after exposure to blue light followed by dark adapta- tion. # dipp-5 location: 1-(cv-f). phenotype: ERG response to flickering light normal (Speck, Mutz, Ohl, and Spatz, 1984, J. Insect Physiol. 30: 437-40). Fast phototaxis responses show subnormal sensitivity after exposure to blue light followed by dark adaptation. # dipp-6 location: 1-(not localized; no recombinants from y cho cv v f /dipp-6 exhibit normal phenotypes as if several factors responsible for mutant behavior of dipp-6 strain. phenotype: Photoreceptors show subnormal sensitivity, in elec- troretinogram recordings, after blue light exposure followed by dark adaptation. Fast phototaxis generally defective. Mutant females exhibit defective mating kinetics (Willmund and Ewing, 1982, Anim. Behav. 30: 209-15). # dipp-7 location: 1-(cv-v). phenotype: Photoreceptors show subnormal blue-green light sen- sitivity, in electroretinogram recordings, after blue light exposure followed by dark adaptation. Fast phototaxis gen- erally defective. # dipp-8 location: 1-(cv-f). phenotype: Fast phototaxis generally defective. # Dipr: see rn #*dis: distorted eye location: 1-23. origin: Recovered among progeny of natural-gas-treated fly. discoverer: Mickey, 49b5. references: 1951, DIS 25: 74. phenotype: Whole or part of eye roughened. Sometimes bristles absent or doubled. Wings may be roughened with nicked margins and plexus veins. Expressivity variable. RK3. cytology: Salivary chromosomes appear normal. # Disabled: see Dab # discless: see dsl # disco: disconnected (J.C. Hall and H. Steller) locus: 1-53.1. discoverer: K. Fischbach and M. Heisenberg. references: Steller, Fischbach, and Rubin, 1987, Cell 50: 1139-53 (fig.). Dushay, Rosbash, and Hall, 1989, J. Biol. Rhythms 4: 1-27. Zerr, Hall, Rosbash, and Sibicki, 1990, J. Neurosci. 10: 2749-62. phenotype: Compound eyes are disconnected from optic ganglia in most mutant individuals, but approximately 5-10% have superfi- cially normal eye-brain connections. Photoreceptor cells ini- tially present but degenerate progressively with age; axons of photoreceptor cells which are still present form plexus beneath the eye. Focus of gene function fate maps to a point well anterior to the focus of either the eye or optic lobe (Fischbach). Adult defect arises as consequence of a defect in the larval visual nerve (Bolwig's nerve) which fails to connect with its target cells in the central nervous system; subsequently, owing to loss of the pioneer function of Bolwig's nerve, retinular axons fail to innevate their target cells in the developing optic lobes leading to massive degeneration of the optic ganglia during the early pupal stages (Steller and Rubin). Slight disarray of embryonic peripheral nervous sys- tem detectable; occasional errant neurons seen. Developing CNS appears normal, but adult brain is abnormal in that cer- tain lateral neurons, which normally express per are either absent or do not express per (Zerr et al.). Larval reacts normally to all stimuli except light. All alleles display significantly reduced viability; death occurs in late pupal stages as pharate adults. In tests of circadian rhythms, eclosion and adult locomotor activity are essentially arrhythmic (Dushay et al.). Cyclical expression of per pro- tein, which normally occurs in eyes and brain, is fairly robust in disco, whether eyes connected to the brain or not (Zerr et al.); hence this eye rhythm may be autonomous, i.e., given absence of CNS neuronal staining in mutant adults. alleles: Four ethyl-methanesulfonate-induced alleles: disco1 (Fischbach) and disco2, disco3 and disco4 (Steller); all alleles show reduced viability. cytology: Placed in 14B3-4 on the basis of its being included in Df(1)82c3k = Df(1)14B3-4;14E but not Df(1)80g7d = Df(1)14B3-4;14C6-8; not covered by Dp(1;2)r+75c = Dp(1;2)14B13;15A9;35D-E. Dp(1;4)r+ and Dp(1;4)80g7d cover disco-induced arrhythmicity (Dushay et al.). other information: Not allelic to bss or eas, two closely linked behavioral mutants in 14B4-13; order = disco eas bss. # Discolored: see bwV2 # disconnected: see disco # discs absent, small, or homeotic: see dash # discs large: see dlg1 # disembodied: see dib # dishevelled: see dsh # dispersed: see dsp # displaced: see dd # displacedlike: see ddl # disrupted: see dsr # diss: see nonA # Distal into proximal: see rn # Distalless: see Ba # distorted eye: see dis # disturbed segmentation: see dss # divergent: see dv # divergent wings: see dvw # divers: see dvr #*dk: dark location: 3- (not located). discoverer: Clausen, 20g. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 235. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 223. phenotype: Eye color maroon. Overlaps wild type. RK3. #*dkb: dark bubbly location: 2- (to the left of vg). discoverer: Bridges, 38d25. phenotype: Thorax has dark bubbly longitudinal streak. RK3. # dke: dark eye location: 2-73. origin: Spontaneous. discoverer: Bridges, 38c11. phenotype: Eye color soft, dull, and dark, like sf. sf/dke is wild type. RK2. # Dke: Darkened eye location: 2- (not located). origin: X ray induced. discoverer: Hendrix, 1963. references: 1964, DIS 39: 58. phenotype: In heterozygotes, eye facets roughened with black- spotted pigmentation, varying from light spotting near margin of eye to heavy pigmentation covering one-half of the eye. A bleached area sometimes appears adjacent to the pigmentation. Effect usually symmetrical. Homozygous lethal. RK3. cytology: Salivary chromosomes appear normal (Peacock). #*dkl: darker legs origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1954. synonym: thl-d: thick legs darker. references: 1959, DIS 33: 85. phenotype: Extra pigment in body and legs. Legs slightly shor- tened, especially in female. Wings small and divergent. Eye shape altered. Viability good in both sexes; female fertility reduced. RK3. # dl: dorsal location: 2-52.9. synonym: mat(2)dorsal. references: Nusslein-Volhard, 1979, Symp. Soc. Dev. Biol. 37: 185-211 (fig.). 1979, INSERM Symp. 10: 69-82 (fig.). Nusslein-Vollard, Lohs-Schardin, Sander, and Cremer, 1980, Nature 283: 474-76. Anderson and Nusslein-Volhard, 1984, Pattern Formation (Mala- cinski and Bryant, eds.). Macmillan, New York, pp. 264-89 (fig.). Steward and Nusslein-Volhard, 1986, Genetics 113: 665-78. phenotype: Embryos produced by homozygous dl females form nor- mal cellular blastoderm but at gastrulation develop into yolk-filled tube of dorsal hypoderm. Hair pattern of cuticle characteristic of dorsal hypoderm; ventral structures, such as denticle belts, lacking. Normally, dorsal infoldings occupy entire circumference of embryo. Evidence of anterior- posterior differentiation includes possible mouth armature structures anteriorly, small spiracles posteriorly, and orien- tation of hairs. The periodicity of stripes of ftz expression in pre gastrulation embryos, as revealed by antibody staining, displays the pattern normally characteristic of the dorsum circumferentially in embryos produced by dl females (Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32. Embryos produced by dl/dl and dl/Df(2L)TW137 indistinguish- able, suggesting dl to be amorphic. Penetrance complete; expression constant. Embryos of dl2 females lack all struc- tures normally derived from the ventral half of the egg, including mesoderm, endodermal gut, ventral nervous system, and ventral hypoderm. dl1 and to a lesser extent dl2, females produce embryos with reduced capacity for neurogenesis in response to an absence of dl function (Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 317-26). dl germ line dependent; homozygous germ-line clones produce dorsalized embryos (Schupbach and Wieschaus, 1986, Dev. Biol. 113: 443-48). Embryos of dl/+ females produced at 29 develop into compara- tively normal-looking larvae; they mainly lack internal organs, such as mesoderm and parts of the anterior and poste- rior gut; often ventral hypoderm including denticle belts reduced; phenotype sensitive to genetic background. At 22, dl/+ females produce normal embryos. Developmental fate of ventrally located cells on cellular blastoderm apparently shifted to that of more dorsally located cells. The phenotype of embryos produced by dl/dl females partially rescued by the injection of wild-type cytoplasm but not RNA (Santamaria and Nusslein-Volhard, 1983, EMBO J. 2: 1695-99; Anderson and Nusslein-Volhard, 1944, Nature 34: 225-27). Developmental profiles show transcript to be present only in ovaries and pre-cellular-blastoderm stages of embryogenesis. In situ hybridization indicates that ovarian transcript accu- mulates in nurse cells from stage 5 to 11; number of tran- scripts per genome equivalent in these polytene cells remains low and constant until stage 10, at which time there is a dramatic increase in the relative numbers of transcripts. After a lag of one or two nuclear divisions, transcript begins to accumulate in the oocyte; by stage 12 there is little detectable transcript in the nurse cells. It appears as though the nurse-cell transcript is transferred to the oocyte and thus to the embryo; transcript seems to be uniformly distri- buted in stage 14 oocytes (Steward, Ambrosio, and Schedl). dl protein is uniformly distributed throughout cytoplasm of early embryo; in the syncytial blastoderm a gradient of expression is achieved by the graded transport of dl protein into nuclei, with the highest nuclear concentrations found ventrally; protein remains cytoplasmic dorsally. Maternal dor- salizing mutants prevent nuclear localization and ventralized embryos show dorsal as well as ventral nuclear localization (Steward, Zusman, Huang, and Schedl, 1988, Cell 55: 487-95; Rushlow, Han, Manley, and Levine, 1989, Cell 59: 1165-77; Steward, 1989, Cell 59: 11179-88; Roth, Stein, and Nusslein- Volhard, 1989, Cell 59: 1189-1202). alleles: allele origin synonym ref ( comments __________________________________________________________ dl1 EMS 1 dl2 EMS 2 hypomorphic allele; temperature sensitive dl3 EMS 7 dl4 EMS 7 dl5 EMS 5 hypomorphic allele dl6 EMS 5 dl7 EMS dl8 EMS 5 dl9 EMS dl103 7 dominant allele dl10 EMS dl160 7 dominant allele dl11 EMS dl7607 7 dominant allele dl12 X ray dlH 4, 5 In(2L)36C;37B dl13 X ray dlT 4, 5 In(2L)21E-F;36C dl14 EMS dlB10 7 dominant allele dl15 X ray dlI5 5 dl16 EMS dlO11 7 dominant allele dl17 EMS dlPZ 3, 7 temperature sensitive dl18 EMS dlQD 3, 7 hypomorphic allele dl19 EMS dlQF 3, 7 hypomorphic allele dl20 EMS dlQI 3 hypomorphic allele dl21 EMS dlSC 3, 7 hypomorphic allele dl22 EMS dlSG 3, 7 hypomorphic allele dl23 EMS dlU5 7 dominant allele dl24 EMS dlD4 6 dominant allele dl25 EMS dlD5 6 dominant allele dl26 EMS dlD6 6 dominant allele dl27 EMS dlD7 6 dominant allele ( 1 = Nusslein-Volhard, 1979, Symp. Soc. Dev. Biol. 37: 185- 211; 2 = Nusslein-Volhard, 1979, INSERM Symp. 10: 69-82; 3 = Schupbach and Wieschaus, 1989, Genetics 121: 101-17; 4 = Steward, McNally, and Schedl, 1984, Nature 311: 262-65; 5 = Steward and Nusslein-Volhard, 1986, Genetics 113: 665- 78; 6 = Szabad, Erdelyi, Hoffmann, Szidonya, and Wright, 1989, Genetics 122: 823-35; 7 = Tearle and Nusslein- Volhard, 1987, DIS 66: 209-26. cytology: Placed in 36C2-D1 based on its inclusion in Df(2L)TW137 = Df(2L)36C2-4;37B9-C1 but not Df(2L)VA18 = Df(2L)36C4-D1;36F-37A. Further confined to 36C by breakpoints common to In(1)dlH and In(1)dlT. molecular biology: Genomic clone isolated by Steward, McNally, and Schedl (1984, Nature 311: 262-65). A 14 kb transcription unit encodes a 2.8 kb poly-adenylated transcript; transcrip- tion proceeds from right to left; transcript contains two and probably three introns, a 1 kb intron down stream from a 5 kb intron. A 2.3 HindIII-SstI restriction fragment from the 3' exon contains the breakpoints of both In(2)dlH and In(2L)dlL (Steward, Ambrosio, and Schedl, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 223-38). The cDNA sequence indicates that the dorsal protein has 678 amino acids and a molecular weight of 75,450 daltons; the NH2 terminal portion of the conceptual amino-acid sequence reveals a high level of homology with the c-rel proto-oncogene. The C-terminal portion has regions in common with N and en (Steward, 1987, Science 238: 692-94; 1989, Cell 59: 1179-88; Rushlow, Han, Manley, and Levine, 1989, Cell 59: 1165-77). other information: Expression of twi prevented in embryos pro- duced by dl females (Thisse, Stoetzel, El Messal, and Perrin- Schmidt, 1987, Genes Dev. 1: 709-15). # dl: see dpl Dl: Delta From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 197. # Dl: Delta location: 3-66.2. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 197-201 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 75 (fig.). Vassin and Campos-Ortega, 1987, Genetics 116: 433-45. Alton, Fechtel, Terry, Miekle, and Muskavitch, 1988, Genetics 118: 235-45. phenotype: A haplo-insufficient member of the group of neuro- genic genes originally described on the basis of its dominant phenotype. Several classes of alleles designated by Vassin and Campos-Ortega based on the phenotype of heterozygous adults: Amorphic and strong hypomorphic alleles display wing veins widened at their junctions with the margin to form delta-like structures; in addition, they show irregular thickening of vein 2, and wings frequently held in divergent attitude; fusion of ommatidia may give rise to disruptions in regular hexagonal array of eye facets; ocelli are slightly enlarged; additional bristles are present on head, thorax, and abdomen; homozygotes die as embryos. Rare antimorphic alleles display the above phenotype in exaggerated form with irregular widen- ing of all longitudinal wing veins, enlarged deltas, regularly divergent wings, smaller rougher eyes, larger and often fused ocelli, and further increase in the numbers of extra bristles; in addition, tarsal joints 2 to 4, but not 5 are fused; homoz- ygotes are embryonic lethals. Rare recessive alleles show low levels of survival as homozygotes or trans heterozygtoes with more severe alleles; survivors usually display a less extreme version of the phenotype exhibited by heterozygotes for amorphic alleles; however, some combinations are wild type in appearance and others (e.g., the antimorphs) are lethal. The embryonic lethality of homozygotes displays the typical neuro- genic phenotype with neural hyperplasia accompanied by epider- mal aplasia; most or all cells of the neurogenic ectoderm recruited into the neurogenic pathway. Transplantation of homozygous Dl pole cells demonstrate Dl expression during oogenesis (Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32). Dl classed as non-autonomous in that single cells from the neurogenic ectoderm of Dl- embryos are capable of giving rise to both neural and epidermal derivatives when transplanted into the neurogenic region of wild-type embryos, suggesting that Dl- cells are capable of responding normally to information from neighboring cells (Technau and Campos- Ortega, 1987, Proc. Nat. Acad. Sci. USA 84: 4500-04). Tran- scription in cellular blastoderm seen in the ventrolateral neurogenic ectoderm, with a ventral-to-dorsal gradient of expression, corresponding to the gradient of neurogenic capa- bilities of the neurogenic ectoderm. During gastrulation a metameric pattern of expression appears, disappears, and reap- pears; as development proceeds complicated spatial and tem- poral specificities of expression ensue (Vassin et al., 1987). Interactions with other neurogenic mutations complex; Dl mutations suppress the spl-enhancing effect of E(spl) (Shepard, Boverman, and Muskavitch, 1988, Genetics 122: 429- 38) and the expression of Ax (Siren and Portin, 1989, Genet. Res. 54: 23-26); severe alleles fail to survive in heterozy- gotes with E(spl) loss-of-function alleles [Lehmann, Dietrich, Jimenez, and Campos-Ortega, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 226-29 (fig.)] especially when E(spl) is mater- nally inherited. Expression of Dl/+ observed to be partially suppressed by duplications for E(spl)+ (Vassin, Vielmetter, and Campos-Ortega, 1985, J. Neurogenet. 2: 291-308), yet, de la Concha, Dietrich, Weigel, and Campos-Ortega (1988, Genetics 118: 499-508) report that extra doses of E(spl)+ enhance the neurogenic phenotype of Dl-. Dl/+ and Dl- phenotypes are suppressed by heterozygous and homozygous deficiencies for H, respectively. For example, H2 is able to suppress the pheno- typic effects of Dl9P, either in Dl9P/+ or in Dl9P/Dl9P geno- types; Dl9P/Dl9P is cell lethal in both the eye and the cuti- cle; Dl9P H2/Dl9P H2 cells, on the other hand, develop nearly normally (Dietrich and Campos-Ortega, 1984). Expression of Dl enhanced by duplications for N+ or H+, and three doses of Dl+ enhance expression of N- and neu-, but reduce the severity of the mam- phenotype. de la Concha, et al. have incorporated many of these observations into a model of neurogenic-gene interaction. Dl alleles interact synergistically with certain Minutes, producing extreme phenotypes and drastically lowered viability (Schultz, 1929, Genetics 14: 366-419); DlOf enhances spaCat (Tsukamoto, 1956, DIS 30: 79). alleles: allele origin discoverer synonym ref ( comments ______________________________________________________________________________ Dl1 spont Bridges, 18k30 3, 4 *Dl2 spont Bridges, 20h13 3 Dl3 spont Bridges, 24l10 1, 3, 4 *Dl4 spont Bridges, 26g28 4 Dl5 X ray R.L. King, 32d 1, 3, 4 Dl5F EMS Nusslein- 5F102 1, 6, 7, 9 Volhard *Dl6 X ray Schultz, 33a5 3, 4 Dl6B EMS Nusslein- 6B37 1, 6, 7, 9 temperature-sensitive | Volhard Dl6L EMS 7 Dl7 X ray Schultz, 33a7 3, 4 *Dl7p Panshin, 1935 3, 4 T(3;4) Dl8 3 Dl9 1, 3, 5 moderate allele Dl9D EMS Nusslein- 9D27 1, 6, 7, 9 extreme allele Volhard Dl9K EMS Nusslein- 9K23 1, 6, 7, 9 weak allele Volhard Dl9M EMS Nusslein- 9M46 1, 6, 7 extreme allele Volhard Dl9P EMS Nusslein- 9P39 1, 6, 7 extreme allele Volhard Dl9Q EMS Nusslein- 1, 7 temperature-sensitive Volhard Dl10 spont Curry, 37k30 3 weak allele Dl10G EMS 7 Dl11 spont Bridges, 36f11 1, 3, 5 moderate allele Dl13 spont Bridges, 38d4 1, 3, 5 weak allale Dl14 spont Curry, 40d6 1, 3, 5 weak allele Dl33 X ray Oliver, 33a3 3 *Dl55k EMS Clark 4 DlB Schultz, 1933 3, 4, 9 In(3R)90B1-2;92A1-2 DlB29 EMS 8 DlB107 EMS Vassin 9 antimorphic allele | DlBE21 EMS Muskavitch 1 moderate allele DlBE23 EMS Muskavitch 1 weak allele DlBE24 EMS Muskavitch 1 weak allele DlBE26 EMS Muskavitch 1 recessive hypomorph DlBE30 EMS Muskavitch 1, 2 weak allele DlBE31 EMS Alton 1, 2 recessive hypomorph DlBE32 EMS Alton 1, 2 weak allele DlBE33 EMS Alton 1, 2 recessive hypomorph DlBE34 EMS Alton 1, 2 recessive hypomorph DlBE35 EMS Alton 1, 2 recessive hypomorph DlBE36 EMS Alton 1, 2 recessive hypomorph DlBE37 EMS Alton 1, 2 recessive hypomorph DlBE38 EMS Alton 1, 2 weak allele DlBE39 EMS Alton 1, 2 weak allele DlBX1 X ray Muskavitch 1 weak allele DlBX2 X ray Muskavitch 1 strong allele deletes locus DlBX3 X ray Muskavitch 1 strong allele DlBX4 X ray Muskavitch 1 moderate allele DlBX5 X ray Muskavitch 1 moderate allele DlBX6 X ray Muskavitch 1 moderate allele DlBX7 X ray Muskavitch 1 weak allele DlBX8 X ray Muskavitch 1 recessive hypomorph DlBX9 X ray Muskavitch 1, 5a moderate allele DlBX10 X ray Muskavitch 1 strong allele; 114.6 to 123.1 kb DlBX11 X ray Muskavitch 1, 5a strong allele DlBX13 X ray Muskavitch 1 strong allele DlBX14 X ray Muskavitch 1 moderate allele; 96.0 to 103.7 kb DlBX32 X ray Terry 1, 5a moderate allele DlBX35 X ray Terry 1 moderate allele; partially deletes locus DlBX38 X ray Terry 1 moderate allele; partially deletes locus DlBX39 X ray Terry 1 strong allele DlBX40 X ray Terry 1, 5a strong allele; 114.6 to 123.1 kb DlBX41 X ray Terry 1, 5a moderate allele; 108.9 to 114.6 kb DlBX43 X ray Terry 1, 5a moderate allele DlBX44 X ray Terry 1 moderate allele DlBX45 X ray Terry 1, 5a moderate allele; 96.0 to 103.7 kb DlBX46 X ray Terry 1, 5a recessive hypomorph; 95.7 to 108.9 kb DlCE1 EMS Muskavitch 1 strong allele DlCE2 EMS Muskavitch 1 moderate allele DlCE3 EMS Muskavitch 1 moderate allele DlCE4 EMS Muskavitch 1 weak allele DlCE5 EMS Muskavitch 1 strong allele DlCE6 EMS Muskavitch 1 strong allele DlCE7 EMS Muskavitch 1 moderate allele DlCE8 EMS Muskavitch 1 weak allele DlCE9 EMS Muskavitch 1 moderate allele DlCE10 EMS Muskavitch 1 moderate allele DlCE11 EMS Muskavitch 1 weak allele DlCE12 EMS Muskavitch 1 strong allele DlCE13 EMS Muskavitch 1 moderate allele DlCE14 EMS Muskavitch 1 moderate allele DlCE15 EMS Muskavitch 1 weak allele DlCE16 EMS Muskavitch 1 moderate allele DlCE21 EMS Muskavitch 1 moderate allele DlCE23 EMS Muskavitch 1, 5a strong allele; 114.6 to 123.1 kb DlCE33 EMS Muskavitch 1, 5a strong allele; 114.6 to 123.1 kb DlCE34 EMS Muskavitch 1, 2 weak allele DlCE37 EMS Muskavitch 1 moderate allele DlCE43 EMS Muskavitch 1, 5a recessive hypomorph; 98.6 to 101.6 kb *DlCf-3 spont Imaizumi Cf-3 3, 4 DlCS20 spont Muskavitch 1 moderate allele; 95.5 to 96.8 kb DlE50-2 6, 9 antimorphic allele DlFE1 EMS Jimenez 6, 9 extreme allele DlFE2 EMS Jimenez 6, 9 extreme allele DlFE3 EMS Jimenez 6, 9 extreme allele DlFE4 EMS Lehman 6, 9 weak allele DlFE7 EMS Jimenez 6, 9 extreme allele DlFE9 EMS Jimenez 6, 9 extreme allele DlFE17 EMS Jimenez 6, 9 extreme allele DlFE26 EMS Jimenez 6, 9 extreme allele DlFE27 EMS Vassin 9 severe allele DlFE28 EMS Vassin 9 severe allele DlFE29 EMS Vassin 9 severe allele DlFE30 EMS Vassin 9 antimorphic allele DlFE31 EMS Vassin 9 severe allele DlFE32 EMS Vassin 9 antimorphic allele DlFE33 EMS Vassin 9 intermediate allele DlFE35 EMS Vassin 9 intermediate allele DlFE36 EMS Vassin 9 weak-to- severe allele DlFE37 EMS Vassin 9 weak-to- severe allele DlFE38 EMS Vassin 9 severe allele DlFE39 EMS Vassin 9 intermediate-to- severe allele DlFE40 EMS Vassin 9 severe allele DlFE41 EMS Vassin 9 intermediate-to- severe allele DlFE43 EMS Vassin 9 weak-to-inter- mediate allele DlFE45 EMS Vassin 9 weak-to-inter- mediate allele DlFE46 EMS Vassin 9 intermediate allele DlFE47 EMS Vassin 9 intermediate allele DlFX1 X ray Jimenez 6, 9 extreme allele DlFX4 X ray Campos-Ortega 6, 9 extreme allele DlFX5 X ray Campos-Ortega 6, 9 extreme allele DlFX6 EMS Lehman 6, 9 extreme allele *DlFX7 EMS Lehman 6, 9 extreme allele DlFX8 X ray Lehman 6, 9 DlH22 spont Tanaka 35d28 3 DlHD9 HD Artavanis- 1, 5a recessive hypomorph Tsakonas 98.6 to 101.6 kb DlHD40 HD Artavanis- 1, 5a recessive hypomorph Tsakonas 95.7 to 108.9 kb DlHD62 HD Artavanis- 1, 5a moderate allele Tsakonas 95.5 to 96.8 kb DlHD82 HD Artavanis- 1, 5a weak allele Tsakonas 98.6 to 101.6 kb DlI79 EMS IL79N 6, 7, 9 DlII13 X ray Schrons II13 8, 9 Tp(3;3)88F5-9; 91A3-8;92A1-2 DlKE1 EMS Vassin 9 intermediate allele DlKE2 EMS Vassin 9 weak-to-inter- mediate allele DlKE3 EMS Vassin 9 severe-to- intermediate allele DlKE4 EMS Vassin 9 intermediate allele DlKE6 EMS Vassin 9 weak allele DlKE7 EMS Vassin 9 severe allele DlKE8 EMS Vassin 9 severe allele DlKE12 EMS Vassin 9 intermediate allele DlKE13 EMS Vassin 9 intermediate allele DlKE14 EMS Vassin 9 weak-to-inter- mediate allele DlKE15 EMS Vassin 9 severe allele DlKE48 EMS Vassin DlKE49 EMS Vassin DlKE50 EMS Vassin DlKE50-2 EMS Jurgens extreme allele DlKE51 EMS Vassin DlKE52 EMS Vassin DlKE53 EMS Vassin DlKE54 EMS Vassin DlKE55 EMS Vassin DlKE56 EMS Vassin DlKE57 EMS Vassin DlKE58 EMS Vassin DlKE59 EMS Vassin DlKE60 EMS Vassin DlKE61 EMS Vassin DlKX1 X ray Vassin 9 severe allele DlKX2 X ray Vassin 8, 9 severe allele DlKX3 X ray Vassin 8, 9 severe allele DlKX6 X ray Vassin 8, 9 severe allele DlKX7 X ray Vassin 8, 9 severe allele DlKX8 X ray Vassin 9 severe allele DlKX13 X ray Vassin 9 severe allele DlKX14 X ray Vassin 8 DlKX15 X ray Vassin 8, 9 severe allele DlKX19 X ray Vassin 8, 9 severe allele DlKX22 X ray Vassin 9 severe allele *Dll spont Bridges, 38c10 l(3)D1 3, 4 *DlM spont L.V. Morgan, 36k 3 *DlN spont Kikkawa 3 *DlOf spont Tsukamoto, 1956 4 DlP-B55 P 8 DlP-N P 8 Dlr spont L.V. Morgan *Dl6 3 Dlroe 6, 9 extreme allele Dlroex X ray Jurgens roXM3 6, 9 extreme allele Dlru EMS ru-41 6 extreme allele DlSp spont Knust 8, 9 In(3R)92A1-2;92A12-13 Dlvi1 | EMS Vassin via1 9 recessive hypomorph | Dlvi2 | EMS Vassin via2 9 recessive hypomorph | Dlvi3 | EMS Vassin via3 9 recessive hypomorph | DlX Stern, 1932 1, 3, 5 extreme allele DlX8 9 extreme allele DlX18 / Jurgens 6, 9 extreme allele DlXT XTU1 6 extreme allele ( 1 = Alton, Fechtel, Kopczynski, Shepard, Kooh, and Muscav- itch, 1989, Dev. Genet. 10: 261-72; 2 = Alton, Fechtel, Terry, Mickle, and Muscavitch, 1987, Genetics 118: 235-45; 3 = CP552; 4 = CP627; 5 = Craymer, 1980, DIS 55: 197; 5a = Kopczynski, Alton, Fechtel, Kooh, and Muscavitch, 1988, Genes Dev. 2: 1723-35; 6 = Lehmann, Jimenez, Dietrich, and Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 62-74; 7 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26; 8 = Vassin, Bremer, Knust, and Campos-Ortega, 1987, EMBO J. 6: 3431-40; 9 = Vassin and Campos-Ortega, 1987, Genetics 116: 433-45. | Phenotypes described more fully below. / Associated with T(2;3). cytology: Placed in 92A2 based on its inclusion in both Df(3R)Bxd110 = Df(3R)91D;92A2 and Df(3R)Dl-KX12 = Df(3R)92A2;92A4. molecular biology: Two chromosomal walks carried out in the region (Vassin, Bremer, Knust, and Campos-Ortega, 1987, EMBO J. 6: 3431-40; Kopczynski, Alton, Fechtel, Kooh, and Muska- vitch, 1988, Genes Dev. 2: 1723-35); coordinate 0 of the Kopczynski et al. walk is at approximately -20 kb on the Vas- sin et al. walk; in both coordinate systems, positive values extend to the left. Lesions associated with Dl mutations found between 75 and 100 kb on the Vassin et al. coordinates and between 95 and 127 kb on that of Kopczynski et al.; probes from this region identify two major transcripts of 4.5 or 4.6 and 5.4 kb; in addition, Kopczynski et al. report four minor transcripts. Probing of cDNA with genomic restriction frag- ments indicate that both major transcripts comprise four exons spread over 25 kb of chromosomal DNA. The smaller transcript is found in ovaries and in 0-2 hour embryos and is presumably maternal in origin; the larger one accumulates maximally in 2-6 hour embryos. Conceptual amino acid sequence indicates a protein of 832 amino acids which contains a signal sequence (residues 1-25), an extracellular domain, which included nine EGF-like repeats (residues 26-595), a transmembrane domain (residues 596-617), and an intracellular domain (residues 618-832); it also contains five consensus asparagine-linked glycosylation sites at residues 98, 137, 167, 421, and 649 (Kopczynski et al.). # Dl6B phenotype: Like Dl1 except that severity of phenotype in homoz- ygous embryos temperature sensitive. At 18 there is patchy neuralization of cephalic and ventral ectoderm; expression more severe at 25 and extreme at 29. Temperature-sensitive period between pole-cell formation and mesodermal segmenta- tion. Clone of ommatidia homozygous for Dl6B, normal when reared under permissive conditions; in flies raised at 29C, however, ommatidial pattern severely disturbed, producing scarring of the eye surface; ommatidia appear larger than nor- mal and interommatidial bristles missing; homozygous mutant facets contain more than a normal complement of retinula cells-up to 13; cytodifferentiation apparently normal. Cutic- ular clones exhibit elaboration of extra bristles at bristle- forming sites [Dietrich and Campos-Ortega, 1984, J. Neuro- genet. 1: 315-32 (fig.)]. # DlB107 phenotype: The most severe antimorphic allele (Vassin and Campos-Ortega, 1987). All components of the phenotype of heterozygosity for a Dl deletion are present in a drastically increased manner in heterozygotes for DlB107 (or for DlFE30 or DlFE32). All wing veins are irregularly widened, veins 3 and 5 being broadened along their whole lengths (same for vein 2 in DlFE30 and DlFE32) and are occasionally incised posteriorly; the deltas formed at the wing margins are larger and the wings are held spread with complete penetrance. The eyes are smaller and rougher. There is also a severe disturbance of the normal bristle pattern on the head, thorax, and abdomen owing to a further increase in the number of bristles. The ocelli are larger and often fused together, thus forming a half circle. Finally, tarsal segments 2 to 4 are fused, but segment 5 is never found to be affected. # Dlvi: Delta viable phenotype: Three alleles survive as homozygotes (Vassin, and Campos-Ortega, 1987). Slight delta-like thickenings at poste- rior tips of wing veins 2, 3, 4 and 5; roughening of eye. Dlvi homozygotes also show shortening and frequent fusion of tarsal segments. A few homozygous embryos fail to hatch, showing patchy neuralization in cephalic and ventral territories. Dlvi/+ normal. Trans heterozygotes with dom- inant alleles show extreme wing, eye, and tarsal abnormali- ties; Dlvi1 lethal in combination with DlF30, DlF32 DlE50-2, and DlB107 (Vassin, and Campos-Ortega, 1987). # dlg1: discs large location: 1-34.82. synonym: l(1)10Bf. references: Stewart, Murphy, and Fristrom, 1972, Dev. Biol. 27: 71-83. Gateff, 1978, Biol. Rev. 53: 123-68. 1978, Science 200: 1448-59. Kiss, Szabad, and Major, 1978, Mol. Gen. Genet. 164: 77-83. Perrimon, 1988, Dev. Biol. 127: 392-407. Woods and Bryant, 1989, Dev. Biol. 134: 222-35. phenotype: Late larval lethal; prolonged larval stages with bloated larvae attempting pupariation around day 15; some cuticular tanning, but no adult cuticular structures formed. During early larval development, the imaginal discs are smaller than those of normal larvae of the same age and are misshapen, but as the larvae continue to survive after the normal pupariation time, the discs continue to grow. They become large, amorphous, and solid, containing three times the normal numbers of cells at ten days of age; they also experi- ence substantial cell death. By eleven days, wing and haltere discs may fuse; also first and second leg discs fuse with ven- tral ganglion of the CNS; great enlargement of optic lobes of brain also takes place. Discs, but not brains, transplanted into adults grow rapidly displaying invasive growth; they do not differentiate when transplanted into larvae for metamor- phosis. Homozygous tissues do not survive, nor do gynandro- morphs (one with male abdominal tissue vs. 66 expected). It is possible to produce homozygous germ-line clones (Perrimon). dlg1 embryos generated from such clones display defects in morphogenesis and neurogenesis; most tissues are defective; partial rescue achieved by a paternal dlg1+ contribution, in the form of either a normal X or a v+Y. alleles: allele origin discoverer synonym ref ( comments ________________________________________________________________________ dlg11 X ray Lefevre l(1)L11 4, 6 dlg1/dlg2 lethal at 18 dlg12 X ray Lefevre l(1)HF321 5, 6 temperature sensitive; 5.5 kb insert near 5 end | dlg13 X ray Lefevre l(1)N17 5 In(1)10B10-11;10D5-6 dlg14 X ray Lefevre l(1)RA16 5, 6 dlg4/dlg2 lethal at 18 dlg15 EMS Geer l(1)v55 2, 6 complements dlg12, dlg17, and dlg113; late pupal lethal dlg16 EMS Geer l(1)v59 2 dlg17 EMS l(1)d.lg.-1 6, 7 null allele XI-2 dlg18 EMS Gateff l(1)bwn 1 late pupal lethal dlg19 EMS l(1)l.pr.2 3 dlg110 ENU Voelker l(1)M15 8 dlg111 ENU Voelker l(1)M24 8 dlg112 ENU Voelker l(1)M30 8 dlg113 ENU Voelker l(1)M35 6, 8 complements dlg118 dlg114 ENU Voelker l(1)M52 6, 8 dlg14/dlg2 lethal at 18 dlg115 X ray l(1)G3 9 dlg116 l(1)G6 9 dlg117 l(1)M1 9 dlg118 EMS Perrimon l(1)1P20 6 complements dlg12 and dlg113; late pupal lethal dlg119 DEB Perrimon l(1)565 6 dlg19/dlg12 lethal at 18 ( 1 = Gateff, 1977, DIS 52: 4-5; 2 = Geer, Lischwe, and Mur- phy, 1983, J. Exp. Zool. 225: 107-18; 3 = Kiss, Szabad, and Major, 1978, Mol. Gen. Genet. 164: 77-83; 4 = Lefevre, 1971, Genetics 67: 497-513; 5 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 6 = Perrimon, 1988, Dev. Biol. 127: 392-407; 7 = Stewart, Murphy, and Fristrom, 1972, Dev. Biol. 27: 71-83; 8 = Voelker, Wisely, Huang, and Gyurko- vics, 1985, Mol. Gen. Genet. 201: 437-45; 9 = Zhimulev, Pokholkova, Bgatov, Umbertova, Solovjeva, Khudyakov, and Belyaeva, 1987, Biol. Zentralbl. 106: 699-720. | More complete description following molecular biology. cytology: Placed in 10B8 based on its inclusion in Df(1)DA622 = Df(1)10B8;10D2 but not Df(1)m13 = Df(1)10B8;11A3-5. molecular biology: Region contained in a 60-kb walk initiated from the junction fragment of Df(1)m13. A 5.1 kb putative dlg1 cDNA clone isolated (Woods and Bryant); it hybridizes to genomic fragments extending over 25 kb; antisense probe detects five different mRNA species in Northern blots; these species altered or absent in various dlg1 mutants; the direc- tion of transcription is from left to right. Late third instar larvae have transcripts to 6.0 and 5.5 kb; they are reduced in two-day pupae and a 1.9 kb transcript appears; it disappears in three-day pupae and the 6.0 and 5.5-kb species become more abundant and a 5.0-kb species appears. Adult females show five distinct mRNA species of 6.0, 5.5, 5.0, 4.0 (ovary specific), and 1.9 kb; only the two largest bands are seen in adult males. 0-4 hour embryos contain the 5.0 and at lower level the 5.5 kb transcripts; at 6-12 h these levels reduced and the 6.0 kb RNA appears; all species are barely detectable at end of embryogenesis; 5.5 and 6.0-kb species appear in the first larval instar becoming abundant in the third instar. # dlg12 phenotype: Homozygotes fail to survive when raised at 25; when raised at 18 however, 37% survival attained; hemizygous females show 65-70% survival at 18, but are also lethal at 25. Survival at 18 nearly complete in heterozygotes with dlg15 and dlg118, and survival at 25 is 4% and 95% respectively. Embryos produced by matings between surviving dlg12 flies raised at 18 show but 4% hatchability at 18, and such crosses are com- pletely sterile at 25; however in crosses of homozygous dlg1+2 females to dlg1+ males, rescue of heterozygous daughters nearly complete at either 18 or 25 and is somewhat reduced at 29. Abnormal embryos produced by dlg12 females show failure of dorsal closure, and head involution. The maternal effect of dlg1 is germ-line specific, since embryos produced by homozy- gous clones in heterozygous mothers are indistinguishable from those produced by homozygous mothers (Perrimon, 1988, Dev. Biol. 127: 392-407). # dlg2 location: 1-24.9. origin: Induced by ethyl methanesulfonate. synonym: l(1)d.lg.-2. references: Gateff, 1978, Biol. Rev. 53: 123-68. 1978, Science 200: 1448-59. phenotype: Imaginal disc neoplasm with invasive mode of growth. Brains enlarged, but do not display neoplastic growth. # Dll: see Ba # dlmd: dorsal-longitudinal-muscle-defective (J.C. Hall) location: 3-18 to 19 (approximately 8 cM. to left of h). origin: Induced by ethyl methanesulfonate. references: Wang, Keng, Hsu, and Tan, 1989, J. Neurogenet. 6: 27-39. phenotype: Flightless; wings held in normal position; walking, jumping, overall viability said to be normal; dorsal- longitudinal muscles (DLMs) degenerate, usually observed most readily at periphery of fibers; in degenerative areas, muscle Z lines disappear. DLM degeneration begins in late pupae, becoming more pronounced in newly eclosed adults (this pro- gressive atrophy quantified for four of the alleles in homozy- gous condition: 3, 14, 23, 26); physiology of giant-fiber nerve pathway (which in part ends at DLMs) is essentially nor- mal, though muscle-cell resting potential in mutant flies is lower than normal, and membrane excitability is accentuated. alleles: dlmd23, dlmd30, dlmd17, dlmd26, dlmd14, dlmd3, listed in order of decreasing penetrance for flightlessness, which ranges from 80-100%; also dlmd23/+ almost thoroughly flightless; other alleles, over +, lead to 50-70% adults unable to fly. other information: dlmd17 mutation was the only one mapped mei- otically; others said to be allelic by lack of inter se com- plementations in flight tests; dlmd23 seems not knowable as allelic, given its nearly complete dominance. # dlv: deltoid veins location: 1-25.9. origin: Induced by S-2-chloroethylcysteine. discoverer: Fahmy, 1957. references: 1959, DIS 33: 85. phenotype: Wings small, abnormal, with margin occasionally incised, and frequently either divergent or slightly upheld. Extra venation, especially at junctions between longitudinal and costal veins, giving Delta-like formations. In extreme cases, wings grossly deformed and blistered. Excess melaniza- tion throughout body. Eyes dark, small, and slightly rough. Total body size reduced. Both sexes viable and fertile. RK1. alleles: One allele induced by S-2-chloroethylcysteine. # Dly: Delayed recovery (W.B. McCrady) location: 3-52.7 (2.7 units to right of cu). origin: Natural population. discoverer: McCrady, 1959. references: McCrady and Sulerud, 1964, Genetics 50: 509-26. Clark, McCrady, and Fielding, 1979, Genetics 92: 503-10. phenotype: Recovery from CO2 exposure for 15 min at 14C of most Dly/Dly flies occurs between one and four hr, although many never recover, compared to less than 15 min for wild-type. Dly/+ flies recover between 15 min and one hr post-exposure. Percent of flies recovering decreases with increasing tem- peatures at time of exposure to CO2 and with length of expo- sure. Exposure of Dly/Dly flies to 28 during development res- cues them but not their Dly-bearing progeny from delayed recovery. Dly strains carry cytoplasmic factors which can transmit CO2 sensitivity by injection. Cytoplasmically transmissible factor reduced by successive backcrossing, but Dly strains remain CO2 sensitive. Dly strains show partial resistance to suprainfection by sigma virus. # dm: diminutive location: 1-4.0. origin: Spontaneous by insertion of gypsy (Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. USA 80: 1678-82). discoverer: Nichols-Skoog, 33j9. references: 1935, DIS 3: 10. phenotype: Bristles and body small and slender. Viability excellent. Females sterile. Oocyte cyst development abnor- mal; nurse-cell nuclei swell in stage 7, subsequently becoming pycnotic (King and Burnett, 1957, Growth 21: 263-80); cuboidal follicle cells covering developing oocyte in stage 8 fail to show normal growth and degenerate rather than becoming columnar (King and Vanoucek, 1960, Growth 24: 333-38). Chambers degenerate around stage 8; phenotype of homozygous dm less severe than that of dm/Df(1)dm (King and Vanoucek). RK1. alleles: *dm264-58 (CP627); dpls. cytology: 3D5 (Lefevre, 1981, Genetics 99: 461-80). # dmd: see pch # Dmnd: Dimethylnitrosamine demethylase location: 2-64.7. references: Waters, Shigemi, Simms, and Nix, 1984, Biochem. Biophys. Res. Comm. 123: 907-13. phenotype: Different strains differ with respect to presence or absence of this activity. cytology: Placed in 48A-49D. # Dmras64B: see Ras2 # dn: doughnut location: 3-50. origin: Spontaneous. references: Wallbrunn, 1942, DIS 16: 54. Wright, 1946, DIS 20: 68. phenotype: Eye of se dn has unpigmented spot (in middle or toward posterior) at emergence from puparium. Spot gradually darkens; after 2 days, eyes appear sepia. Difficult to detect with wild-type eye color, appears as slightly lighter red spot, which disappears after 2 days. Viability low; many die as pupae at 25. Viability nearly normal at 17 but character not detectable. Both sexes highly infertile; testes about one-third normal length. Spermathecae very small. External genitalia of both sexes often abnormal. RK3. # DNase-1: Deoxyribonuclease-1 location: 3-61.8 (based on 83 bx-sr recombinants). references: Grell, 1976, Genetics 83: s28-29. Detwiler and MacIntyre, 1978, Biochem. Genet. 16: 1113-34. phenotype: The structural gene for DNase 1, one of an estimated 7 or more DNase species (Boyd, 1964, Biophys. Biochem. Acta 171: 103-12). Active on native DNA at acid pH (optimum = 4.8) and in the presence of EDTA. Heterozygotes for electrophoretic alleles show two bands on gels indicating monomeric nature of enzyme. Activity of paternally inherited allele demonstrable in 0- to 1-hr embryos. Activity fluctu- ates during embryogenesis, is low during larval stages, rises precipitously just before pupation, and falls after eclosion (Detwiler and MacIntyre, 1978). DNase-1 activity isolated with lysosomal fraction of embryo homogenates (Detwiler and MacIntyre, 1980, Insect Biochem. 10: 255-63). Flies homozy- gous for hypomorphic allele are small with reduced viability; maturation of ovaries delayed for several days after eclosion; recombination normal (Grell, 1976). Homozygotes for the hypo- morphic allele DNase1lmn accumulate low-molecular-weight, low-thermal-stability DNA, especially in the ovaries; Feulgen-positive vesicles visible in maturing oocytes near chorionic appendages (Stone, Dower, Hauseman, Cseko and Seder- off, 1983, Can. J. Genet. Cytol. 25: 129-38). alleles: Naturally occurring alleles designated F, I, and S by Grell are probably same as those subsequently designated A, B, and C by Detwiler and MacIntyre (1980); we adopt F, I, and S. Young adult flies homozygous for DNase1F or DNase1I exhibit two bands on gels; DNase1S homozygotes show one (Grell, 1976). DNase1lo (Grell, 1976) induced by ethyl methanesulfonate is hypomorphic. Also mentioned by Detwiler and MacIntyre (1978, 1980) are three hypomorphic alleles isolated by J. Stone, including DNaselmh, and eight null alleles, including DNase1n324, isolated by Detwiler. cytology: Placed between 90C2 and 90F based on the absence of any electrophoretic allele on Df(3R)P14 = Df(3R)90C2-D1;91A2-3 or on the YP3D element of T(Y;3)B116 = T(Y;3)YL;90E (Detwiler and MacIntyre, 1978). other information: Hyperploidy for 30F-35BC and 67C-70C as well as 88C-91B caused greater than 50% increase in acid deoxyri- bonuclease activity (MacIntyre, 1974, Isozyme Bull. 7: 23). # DNase2 location: 3-45.9 (between st and in). references: Grell, 1976, Genetics 83: s28-29. phenotype: The structural gene for a deoxyribonuclease that is active on heat-denatured DNA at pH 8.5. Causes the appearance of two bands on polyacrylamide gels. Null allele without detectable phenotypic effect. alleles: A naturally occurring null allele designated DNase2n1 removes both bands. other information: There is evidence for two other alkaline deoxyribonuclease genes. One produces a band on denatured substrate at pH 8.5 and is localized to 3L on the basis of different mobilities in D. melanogaster and D. simulans (Grell, 1976). The other is located in 97F-100F based on increased alkaline DNase activity in hyperploids for that region (MacIntyre, 1974, Isozyme Bull. 7: 23); segmental aneuploidy failed to identify the other two regions as affect- ing DNase levels (MacIntyre, 1974). # dnc: dunce (R. Davis; J.C. Hall) location: 1-3.9 [about five-eighth the recombinational distance from w to ec (Salz, and Kiger, 1984, Genetics 108: 377-92); however, as it is adjacent to dm (1-4.0), it is assigned a map position of 3.9]. origin: Induced by ethyl methanesulfonate (all alleles except dncCK, which was X ray induced). discoverer: Byers. references: Dudai, Jan, Byers, Quinn, and Benzer, 1976, Proc. Nat. Acad. Sci. USA 73: 1684-86. Byers, Davis, and Kiger, 1981, Nature 289: 79-81. Davis and Kiger, 1981, J. Cell Biol. 90: 101-07. Salz, Davis, and Kiger, 1982, Genetics 100: 587-96. Davis and Kauvar, 1983, Adv. Cyclic Nucleotide and Protein Phosphorylation Res. 16: 393-402. Salz and Kiger, 1984, Genetics 108: 377-92. phenotype: Gene encodes a cAMP-specific phosphodiesterase. Mutants blocked or impaired in learning, with respect to several of the conditioning tests used on groups of flies or larvae or on individual adults, e.g., those involving odors and electric shocks or sugars (Aceves-Pina and Quinn, 1979, Science 206: 93-96; Tempel, Bonini, Dawson, and Quinn, 1983, Proc. Nat. Acad. Sci. USA 80: 1482-86; see also Aceves-Pina, Booker, Duerr, Livingstone, Quinn, Smith, Sziber, Tempel, and Tully, 1983, Cold Spring Harbor Symp. Quant. Biol. 48: 831- 40), visual stimuli (Folkers, 1982, J. Insect Physiol. 28: 535-39), or various elements of courtship (with respect to tests on mutant males or females, summarized by Hall, 1984, Dev. Genet. 4: 355-78); also, dncM14 males have reduced reproductive fitness after exposure to and courtship of imma- ture females, i.e. when mutant males are put, post training, with mixed female/young male populations (Gailey, Siegel, and Hall, 1985, Genetics 111: 795-804). dnc females display an increased frequency of mating; it is suggested that this could account for their 50% normal longevity (Bellen and Kiger, 1987, Genetics 115: 153-60). dnc males are not conditioned to avoid virgin females by sequestration with such females in the presence of quinine; wild type males are (Ackerman and Siegel, 1986, J. Neurogenet. 3: 111-23). dnc mutants apparently learn normally, or nearly so, in certain experi- ments but have abnormally short memory (e.g., Dudai, 1979, J. Comp. Physiol. 130: 271-75; Mariath, 1985, J. Insect Physiol. 31: 779-87); more specifically, modificatons of original shock-odor testing system reveal that dnc is defective in short term memory, with long-term memory similar to wild type (Tully and Quinn, 1985, J. Comp. Physiol. 157: 263-77); dnc/+ females also memory deficient (Dudai, 1983, Proc. Nat. Acad. Sci. USA 80: 5445-48). Whereas dnc adults seem normal in several general behaviors (Dudai et al., 1976), the mutant displays aberrant "centrophobic" behavior [i.e., transient avoidance of the center of an arena displayed by normal adults (Gotz and Biesinger, 1985, J. Comp. Physiol. 156: 319-27, 329-37)]. Mosaic studies suggest that the focus of dnc/+ function is the brain, even though some learning responses demonstrated by headless flies (Aceves-Pina, et al.). Sensory fatigue associated with an adult mechanosensory neuron, as measured by bristle stimulation, occurs more rapidly than nor- mal in dnc (allele not specified) (Corfas and Dudai, 1990, J. Neurosci. 10: 491-99). There is an increased number of mush- room-body axonal fibers in young adults expressing dnc1 or dncM11, which, unlike wild type, decreases over the next few days (Balling, Technau, and Heisenberg, 1987, J. Neurogenet. 4: 65-73). Mutations or deletions of the locus reduce or eliminate one form of cyclic AMP phosphodiesterase (EC 3.1.4.17) activity; caffeine, an inhibitor of this enzyme, decreases visual learning performance of normal adults and of dnc1 as well, suggesting that the biochemical effects of the drug and the mutation are not identical (Folkers and Spatz, 1984, J. Insect Physiol. 30: 957-65). The effects of dnc mutations on heat stability or Km of this activity indicate that the locus codes for this enzyme (Kauvar, 1982, J. Neu- rosci. 2: 1347-58; Davis and Kauvar); dnc variants also lead to increased levels of cyclic AMP (summarized by Davis and Kauvar, 1983), more specifically, such that most of the excess is in free (vs. bound) nucleotide; both fractions exist in whole-fly homogenates (Friedrich, Solti, Gyurkovicz, 1984, J. Cell. Biochem. 26: 197-203). dncM11 affects the level of phosphorylation of the regulatory subunit of the cyclic-AMP- dependent kinase (Devay, Pinter, Yalcin, and Friedrich, 1986, Neurosci. 18: 193-203). Levels of regulatory subunit of cAMP-dependent protein kinase tend to be higher than normal in dnc1 and dnc2 (Muller and Spatz, 1989, J. Neurogenet. 6: 95- 114). dncM11 flies exhibit increased levels of expression of copia (Yun and Davis, 1989, Nucleic Acids Res. 17: 8313-26). dnc alleles cause varying degrees of female sterility; oocytes of females homozygous for amorphic alleles rarely reach maturity, and for the most part are not oviposited; 90% of the few that are oviposited are fragile, lacking a chorion. That this phenotype is somatic in origin is demonstrated by the observation that homozygous germ-line clones produce mor- phologically normal eggs; some of these eggs undergo a few abortive nuclear divisions, but they never reach an identifi- able stage of oogenesis. The maternal-effect lethality par- tially suppressible by rut, which reduces adenylate cyclase activity. The earliest defect seen in the embryos produced by dnc rut females occurs soon after fertilization and affects DNA replication and mitosis, prevents nuclear migration, and leads to large polyploid nuclei; a later defect prevents cleavage nuclei from migrating into, or dividing in, the pos- terior region of the egg, affecting the developmental behavior or fate of blastoderm cells. The few surviving offspring of double-mutant females show frequent developmental abnormali- ties of the second and third thoracic, and the first five abdominal segments; these include deficiencies, duplications, and transformation of structures; some 15% of the daughters of such females lack one or both ovaries (Livingstone, Sziber, and Quinn, 1984, Cell 37: 205-15; Bellen, Gregory, Olsson, and Kiger, 1987, Dev. Biol. 121: 432-44; Bellen and Kiger, 1988, Roux's Arch. Dev. Biol. 197: 258-68). alleles: allele origin discoverer synonym phenotype _____________________________________________________ dnc1 EMS Byers dncDB38 hypomorph dnc2 EMS Byers dncDB hypomorph dncCK ( X ray hypomorph dncM11 | EMS Mohler fs(1)M42 amorph dncM14 EMS Mohler fs(1)M42 amorph dncML EMS amorph ( Associated with T(1;3)dncCK=T(1;3)3C-D4;63C. | dncM11 maps 0.04 map unit to the left of the other dnc alleles. Also, two molecularly defined "iso-alleles", resulting from transposon insertions at the locus that may have accompanied intragenic recombination events, have been characterized at high resolution (Pittler and Davis, 1987, Mol. Gen. Genet. 208: 325-28). cytology: Placed in 3C11-D4, with exons 1 and 2 at 3C11 and exons 3-13 in 3D4 (Chen, Malone, Beckendorf, and Davis, 1987, Nature 329: 721-24). Claimed to be uncovered by Df(1)N64i16 = Df(1)3C2-3;3D4-5, but not Df(1)N64j15 = Df(1)3C3-5;3D3-4 (Kiger and Golanty, 1977, Genetics 85: 609-22). molecular biology: Both cDNA and genomic DNA cloned and sequenced (Davis and Davidson, 1984, Mol. Cell. Biol. 4: 358-67; Chen et al.). Genomic DNA at the locus identified in part by intragenic recombination events and following RFLPs as markers (see Pittler, Salz, and Davis, 1987, Mol. Gen. Genet. 208: 315-24 for further information on such recombina- tion and putative gene conversion events). Gene comprises 13 exons, with exons 1 and 2 being separated from the remainder by an intron of 79 kb; this intron contains at least two and perhaps four genes, including Pig1 (transcribed from the oppo- site strand) and Sgs4 plus another developmentally regulated transcript (transcribed off the same strand as dnc); sam may also be encoded within the 79 kb intron (Chen, Malone, Becken- dorf, and Davis, 1987, Nature 329: 721-24). A probe from the region of exon 6 identifies polyadenylated RNA's of 9.5, 7.4, 7.2, 7.0, 5.4, and 4.2 kb in RNA from adults flies; exons 1 and 2 share homology with the 9.5 kb mRNA and at least one of about 7.2 kb. The 5.4 kb species found in all developmental stages; the 9.6-, 7.4-, 7.2-, and 7.0-kb species found in late embryos and beyond; the 4.5-kb species found in early embryos and adults but not elsewhere (Davis and Davidson, 1986, Mol. Cell. Biol. 6: 1464-70). cDNA clones representing part of transcript contains an open reading frame that could define a 40,000 dalton polypeptide; the deduced amino acid sequence exhibits greater than 50% sequence identity with bovine Ca2+/calmodulin-dependent cyclic nucleotide phosphodiesterase; lesser and more restricted regions of homology seen with cAMP-dependent protein kinase and Aplysia californica egg- laying hormone precursor. Genomic clones reveal the presence of five introns in the sequence containing this open reading frame (Chen, Denome, and Davis, 1986, Proc. Nat. Acad. Sci. USA 83: 9313-17). other information: Df(1)N71h24/Df(1)dm75e19 females survive, even though they are completely deleted for some five bands, including 3D4; such females are defective in learning and are sterile. dncM11-induced sterility partly suppressed by rut (Livingstone et al., 1984), and this phenotype of the double mutant used to select two new purported rut alleles, one of which (rut2) also suppresses learning defects associated with dncM14 (Feany, 1990, Proc. Nat. Acad. Sci. USA 87: 2795-99).