gp: gap From Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 209. # gp: gap location: 2-74. origin: Spontaneous. discoverer: Bridges, 12a10. references: Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 208 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 212 (fig.), 226. phenotype: Vein L4 weak or has section missing beyond posterior crossvein. Overlaps wild type when homozygous; semidominant as heterozygote. RK3. # Gpdh: (-Glycerol phosphate dehydrogenase location: 2-17.8 [located with respect to cl (16.5) and Sp (22.0) (Grell)]; 2-20.5 [based on 422 recombinants between dp (13.0) and b (48.5)(O'Brien and MacIntyre, 1972)]. synonym: Gdh (Grell, 1967); (Gpdh-1 (O'Brien and MacIntyre, 1968); Gpd (Research Triangle Park Group, 1978, DIS 53: 117). references: Grell, 1967, Science 158: 1319-20. O'Brien and MacIntyre, 1968, DIS 43: 60. Niesel, Pan, Bewley, Armstrong, and Li, 1982, J. Biol. Chem. 257: 979-83. Skuse and Sullivan, 1985, EMBO J. 4: 2275-80. Wright, Shaffer and Bewley, 1985, J. Biol. Chem. 260: 5863- 66. Cook, Shaffer, MacIntyre, Wright and Bewley, 1985, Genetics 110: s13. Cook, Shaffer, Bewley, MacIntyre and Wright, 1986, J. Biol. Chem. 261: 11751-55. Cook, Bewley and Shaffer, 1988, J. Biol. Chem. 263: 10858-64. Kalm, Weaver, DeMarco, MacIntyre, and Sullivan, 1989, Proc. Nat. Acad. Sci. USA 86: 5020-24. phenotype: The structural gene for ( glycerol-3-phosphate dehy- drogenase (NAD+) [( GPDH (EC 1.1.1.8)], a homodimer with subunit molecular weight 31700 (Collier, Sullivan, and MacIn- tyre, 1976, Biochim. Biophys. Acta 429: 316-23). Purifica- tion and structural analysis of enzyme by Niesel, Bewley, Miller, Armstrong, and Lee (1980, J. Biol. Chem. 255: 4073- 80). Three isozymes designated GPDH-1, GPDH-2, and GPDH-3 in order of decreasing rate of migration toward the anode (Wright and Shaw, 1968, Biochem. Genet. 3: 343-53). The three forms respond alike to electrophoretic alleles, null alleles, and dosage of Gpdh+ (Bewley, Rawls, and Lucchesi, 1974, J. Insect. Physiol. 20: 153-75); all three are products of the same structural gene for developmental profile (see Bewley, 1981, Dev. Genet. 113-29). GPDH-1 first appears in late pupae and is present in high concentration in the adult thorax where it functions to provide energy for flight muscles; GPDH-2 also appears in late pupae and is present in low concentration throughout the fly; GPDH-3 is present throughout the life cycle; it is concentrated in the larval fat body (Rechsteiner, 1970, J. Insect. Physiol. 16: 1179-92) and the adult abdomen (Wright and Shaw); GPDH-1 and GPDH-3 present in equal amounts in adult head. Product of paternally inherited allele first appears at 22 hr, just before hatching of larva (Wright and Shaw). GPDH-1 is stable at 50 but decays at 57; GPDH-3 is labile at 50 (Bewley et al.). Studies by Bewley and Luccesi indicate the presence of a heat-labile RNase-resistant factor in crude larval extracts able to convert GPDH-1 into GPDH-2 and GPDH-3 but not vice versa; GPDH-3 lacks three C-terminal amino acids present on GPDH-1 (Niesel, Bewley, Miller, Armstrong, and Lee, 1980, J. Biol. Chem. 255: 4073-80). Homozygotes for null alleles are fertile, show reduced viabil- ity, and are unable to sustain flight (O'Brien and MacIntyre, 1972, Genetics 71: 127-38); ultrastructural integrity of flight muscle sarcosomes degenerates prematurely [O'Brien and Shimada, 1974, J. Cell Biol. 63: 864-82 (fig.)]. Homozygous stocks maintained for 25 generations regain the ability to fly despite continued absence of GPDH activity (O'Brien and Shi- mada). alleles: Natural populations are polymorphic for electro- phoretic variants as well as for regulatory elements that determine enzyme level; induced electromorphs have also been recovered. These variants are tabulated first. allele synonym origin mobility ________________________________________________ GpdhA Gpdh2, GpdhF, GpdhR Fast GpdhB Gpdh4, GpdhS Slow GpdhC (Gpdh-1CC EMS(GpdhB) Slower GpdhD GpdhH ( GpdhL ( GpdhP EMS(GpdhB) GpdhUF spont Faster ( GpdhH and GpdhL determine high versus low rates of accumula- tion of GPDH-3 in both larvae and adults (Bewley, Dev. Genet. 2: 113-192). Bewley attributes this polymorphism to a separate regulatory gene, Gdt-3, but we prefer to desig- nate the alternatives as alleles of Gpdh based on Bewley's finding that their effect is cis acting and his inability to separate them from Gpdh genetically. GpdhH has been found in association with both GpdhA (GpdhHA) and GpdhB (GpdhHB), whereas GpdhL has been found only with GpdhA (GpdhLA). The physical properties of the enzymes produced under the con- trol of these two regulatory elements are identical (Shaffer and Bewley, 1983, J. Biol. Chem. 258: 10027-33). Control postulated at the level of transcription (Wilkins, Shaffer, and Bewley, 1982, Dev. Genet. 3: 129-42). cytology: Placed in 25F5 by deficiency analysis (Kotarski, Pickert and MacIntyre, 1983, Genetics 105: 371-86) and in 26A (distal) by in situ hybridization to the salivaries (Cook et al., 1986). molecular biology: Genomic and cDNA clones of the gene have been isolated (Cook et al., 1985, 1986, 1988), and the genomic and predicted amino acid sequences determined (Cook et al., 1988; Kalm et al., 1989). The transcript of Gpdh+ is about 4.9 kb in length and is composed of eight exons interrupted by seven introns. There is a tandem duplication of a portion of the coding region. The duplication is truncated at the 5 end and is polymorphic in natural populations [Koga, Kusakabe, Tajima, Harada, Bewley and Mukai, 1988, Proc. Japan Acad. 64 (B): 9-12]. The DNA sequence data predict three transcripts, each differing in the 3 untranslated region (Cook et al., 1988). Poly(A) site selection may occur in exon 6, exon 7, or exon 8, producing mRNAs of different size ranges from alter- nate splicing pathways and producing three different isozymes (GPDH-1, GPDH-2, GPDH-3) differing in the amino acid sequences at their COOH-terminal ends although encoded by the same structural gene (Skuse and Sullivan, 1985; Cook et al., 1988). Each transcript and each isozyme is tissue-specific in its expression. The amino acid sequence at the COOH terminal end of GPDH-3 is Asn-His-Glu-His-Met-COOH; the sequence of GPDH-1 is extended by the three amino acid sequence Glu-Asn-Leu-COOH. Xenopus laevis oocytes injected with poly(A)+ RNA from Droso- phila melanogaster direct synthesis of two immunologically- related proteins, a 32-kd protein from Gpdh+ and a 34-kd pro- tein from a CRM-null Gpdh mutant (Wright et al., 1985). other information: A series of Gpdh-Gpo double mutants were constructed by Davis and MacIntyre (1988, Genetics 120: 755- 66); four of these mutants were found to be viable and flight- less; two others were allele-dependent synthetic lethals. A trans acting regulatory element tightly linked to the Gpdh locus has been isolated in a natural population of Drosophila melanogaster in Tasmania (Gibson, Wilks, Cao and Freeth, 1986, Experientia 42: 191-92). Flies homozygous for second chromo- somes carrying the element (designated H31) have half the GPDH activity of normal homozygotes. There are a number of spontaneous and induced amorphic and hypomorphic alleles. These are tabulated also. _________________________________________________________________________________________________________________________ allele synonym origin ref ( enzymatic phenotype Physiological Phenotype _________________________________________________________________________________________________________________________ allele treatment %wildtype relative flight | | | | %CRM | activity / mobility `| | viability ability _________________________________________________________________________________________________________________________ Gpdhn0 GpdhB0-0 GpdhB EMS 1, 3, 4 16, 31 0 >GpdhB .20 - Gpdhn1-4 GpdhB0-1-4 GpdhB EMS 1, 3, 4 >5 1 >GpdhB .20 - Gpdhn1-5 GpdhB0-1-5 GpdhB EMS 3 26.1 GpdhA GpdhnNC2 GpdhnNC718 spont 2 + GpdhnNC3 GpdhnNC738 spont 2, 4 64 - =GpdhA GpdhnNC4 GpdhnNC967 spont 2, 4 32 + =GpdhA GpdhnNC5 GpdhnNC1009 spont 2, 3, 4 0 6.0 =GpdhA GpdhnNC5 GpdhnNC1023 spont 2, 3, 4 42 6.0 =GpdhA GpdhnNC7 GpdhnNC1405 spont 2, 3, 4 22 7.5 =GpdhA GpdhnR1 Gpdhn/ 20066 GpdhA / ray 6 GpdhnR2 Gpdhn/ 50066 SM1, GpdhA / ray 1, 6 0.8 10 - GpdhnR3 Gpdhn/ 50075 GpdhA / ray 6 GpdhnR4 Gpdhn/ 50078 GpdhA / ray 6 0 GpdhnR5 Gpdhn/ 70018 SM1, GpdhA / ray 1, 4, 6 14 0 =GpdhA GpdhnGL1 GpdhB EMS 3 ++ 4.4 GpdhB 1.30 + GpdhnS8 GpdhB EMS 3 ++ 0.0 =GpdhB 0.81 + GpdhnS10 GpdhB EMS 3 ++ 74.8 GpdhB 0.76 + ( 1 = Bewley, DeZurile, and Pagelson, 1980, Mol. Gen. Genet. 178: 301-308; 2 = Burkhart, Montgomery, Langley, and Voelker, 1984, Genetics 107: 295-306; 3 = Kotarski, Pick- ert, Leonard, LaRosa, and MacIntyre, 1983, Genetics 105: 387-407; 4 = Lee, Niesel, and Bewley, 1980, Biochem. Genet. 18: 1003-18; 5 = Mukai and Cockerham, 1977, Proc. Nat. Acad. Sci. USA 74: 2514-17; 6 = Racine, Langley, and Voelker, 1980, Environ. Mutagen. 2: 167-77. | Cross reacting material measured by a) rocket immunoelectro- phoresis (numberical values), b) immunoprecipitation (++) or c) radioimmune assay (+). / Activity measured in some studies (numerical values); merely noted in others (+ or -). ` Mobility measurable directly in mutants with residual enzyme activity and indirectly in nulls that form an active hetero- dimer. + = heterodimer formed but mobility not noted. - = no active heterodimer. - GpdhJH253 and GpdhJH254 probably independent recoveries of same mutant. # Gpo: (-Glycerophosphate oxidase location: 2-75.5. references: O'Brien and MacIntyre, 1972, Biochem Genet. 7: 141-61. O'Brien and Gethmann, 1973, Genetics 75: 155-67. Davis and MacIntyre, 1988, Genetics 120: 755-66. phenotype: The structural gene for sn-glycerol-3-phosphate oxi- doreductose [(GPO (EC 1.1.99.5)], a 100,000 dalton protein localized on the inner mitochondrial membrane. alleles: Gpo mutants were induced by ethyl methanesulfonate; a hypomorphic allele Gpon318 and an almost null mutant Gpon322 were recovered (Davis and MacIntyre, 1988), both viable but flightless. cytology: Localized to 52C9-D3 by deficiency analysis (Davis and MacIntyre) since included in Df(2R)WMG = Df(2R)52A4-B1;- 52D7-E1 but in neither Df(2R)XTE18 = Df(2R)51E3-4;52C9-D1 nor Df(2R)KL9 = Df(2R)52D3;52D7-9. other information: A series of Gpdh-Gpo mutants were con- structed (Davis and MacIntyre, 1988); four of these mutants were viable but flightless; two others were allele-dependent synthetic lethals. # Gpt: Glutamate pyruvate transaminase location: 1-42.6. references: Leigh Brown and Voelker, 1980, Biochem. Genet. 18: 303-09. phenotype: Structural gene for glutamate-pyruvate transaminase [GPT (EC 2.6.1.2)]. Molecular weight is 87,000 daltons, and similar to the enzyme from other sources, it is most likely dimeric in structure (Leigh Brown, 1980, DIS 55: 82-84). Homozygotes exhibit three bands of activity on starch gels, which could represent different degrees of binding of a pyri- doxal phosphate ligand to the enzyme. alleles: Three alleles designated Gtp2, Gtp4, and Gtp6 in order of increasing electrophoretic mobility in starch gel. cytology: Placed in region 11F1 through 12A2 based on its inclusion in Df(1)C246 = Df(1)11D;12A1-2 but not Df(1)N12 = Df(1)11D1-2;11F1-2. #*gr: gracile location: 1-36.4. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1959, DIS 37: 86. phenotype: Small fly with narrow abdomen. Wings frequently held atypically, either upward or downward. Very inviable, many dying less than 24 hr after eclosion; males sterile. RK3. # gr: see grt # gra: see grn # gra: gravel location: 1-28.5. origin: Spontaneous. references: Thompson, 1973, DIS 50: 59 (fig.). phenotype: Eye texture rough owing to irregularly arranged and roughened facets. Suppresses ve, making veins L2, L3, and usually L4 complete; in ve+ flies produces extra vein segments in the marginal, distal, and second and third posterior cells. # gracile: see gr # grain: see grn # grandchildless: see gs grandchildless on chromosome 2 of Mariol: see gs(2)M # gravel: see gra #*gre: green body color location: 1- (not located). origin: Spontaneous. discoverer: Bridges, 13e. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 73. phenotype: Body color tinged greenish black with marked trident pattern. Overlaps wild type. RK3. other information: Possibly an allele of ptg. # grg: giant ring gland location: 1-17.0. origin: Induced by triaziquone. synonym: l(1)grg. references: Klose, 1980, Wilhelm Roux's Arch. Dev. Biol. 189: 57-67. phenotype: Recessive lethal; third larval instar protracted. Ring gland enlarged, and neurosecretory cells of brain abnor- mal. Ecdysteroid levels low; not correctable by exogenous hor- mone. # grk: gurken location: 2-30. origin: Induced by ethyl methanesulfonate. references: Schupbach, 1987, Cell 49: 699-707. phenotype: Maternal-effect lethal. Wild-type allele required for normal dorsoventral pattern in the egg. In mutants, the ventral regions of the chorion and the embryo are expanded at the expense of the dorsal regions. The pattern of the chorion is altered, a second micropyle and a small patch of operculum-like material often forming at the posterior pole in extremely mutant eggs; fewer cells contribute to the dorsal appendage, which is usually shifted posteriorly, but more fol- licle cells contribute to the main body of the chorion. In the embryo the major increase in cell mass occurs in the meso- derm as an invagination on the ventral side during early gas- trulation. Analysis of mosaic females in which germ cells and sister nurse cells are of different genotype indicate that grk mutations act only in the germ line. alleles:: allele synonym phenotype of eggs and embryos ________________________________________________ grk1 grkDC intermediate and strong grk2 grkHG weak and intermediate grk3 grkHK intermediate and strong grk4 grkHL intermediate and strong grk5 grkQI mostly intermediate, but can vary from weak to strong grk6 grkWG mostly intermediate but can vary from weak to strong cytology: Placed in 29C. # grn: grain location: 3-47. origin: Induced by ethyl methanesulfonate. synonym: gra. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). phenotype: Homozygous lethal; filzkorper or embryo not elongated; head skeleton defective. alleles: Two. # gro: see E(spl)2 # grooved: see gv # grooveless: see gvl # grotle: see grt # groucho: see E(spl)2 # grounded: see gnd # grt: grotle location: 1-64 [Recombination tests by Roberts and Hewitt place grt 15.3 cM to the right of f; however, it is to the left of ot at 1-65.7, since it is not covered by y+Ymal106 which does cover ot (Schalet, 1972, DIS 49: 36)]. origin: Spontaneous. synonym: gr (preoccupied). references: Roberts and Hewitt, 1969, DIS 44: 49. phenotype: Homozygotes and heterozygotes have wing abnormali- ties with variable expression. Extreme expression, wings with fluid-filled sac covering 75% of wing area, leaving wings crumpled when sac bursts; weak expression, small blisters and incised margins of posterior cells on wings. Penetrance com- plete. cytology: Distal to region 19 based on failure of y+Ymal106 to cover grt (Scalet, 1972, DIS 49: 36; Schalet and Lefevre, 1973, Chromosoma 44: 183-202). # gs: see gv # gs: grandchildless location: 1-21 (less than 1cM to the right of ct). origin: Induced by ethyl methanesulfonate. references: Thierry-Mieg, Masson, and Gans, 1972, C.R. Hebd. Seances. Acad. Sci. Ser. D 175: 2751-54. Thierry-Mieg, 1976, J. Microsc. Biol. Cell 25: 1-6. phenotype: Homozygous females normal in appearance. When oogenesis in such females proceeds at 28.5 80-85% of the eggs cease development before the blastoderm stage. Most embryos reaching gastrulation continue development normally except for the frequent absence of pole cells; 11-15% of surviving adult progeny have agametic gonads; if the maternal females are also homozygous for an X-linked modifier, mod, the incidence of agametic survivors increases to 60-65%. Oogenesis at 10 leads to 62% hatch and 6-10% agametic, which is decreased to <3% in the presence of homozygous mod. Outcome not influenced by genotype of father. The temperature-sensitive period for sur- vival of zygotes produced by mod gs females is monophasic extending from stages 9 to 14 of oocyte development, whereas that for agametic gonads is diphasic with one sensitive period at stages 6-7 and the other more severe period from stages 10-14; stages 7-9 temperature insensitive. The histology of agametic gonads of both males and females resemble those pro- duced by ultra-violet irradiation of embryonic pole cells (Lauge, Sauphanov, and Randrianandrianina, 1977, C.R. Hebd. Seances Aca. Sci. Ser. D 284: 1187-89). # gs(1)N26 location: 1-33.8. origin: Induced by ethyl methanesulfonate. references: Niki and Okada, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 1-10 (fig.). Niki, 1984, Dev. Biol. 103: 182-89 (fig.). phenotype: Fecundity and fertility of homozygous females low; mortality of sons higher than that of daughters. Fraction of surviving progeny agametic depends on temperature of oogenesis; 93% agametic at 25, 56% agametic at 18. In eggs produced at 25 migration of nuclei to posterior pole abnormal; almost no pole cells produced in half the embryos. Polar granules present in posterior egg cytoplasm, defects in failure of nuclear migration. # gs(1)N41 location: 1-39.6. origin: Induced by ethyl methanesulfonate. synonym: gs(1)N441. references: Nikki and Okada, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 1-10 (fig.). phenotype: Fecundity and fertility of homozygous females nor- mal. 71% and 19% agametic progeny when females raised at 25 and 18, respectively. Peripheral migration of nuclei at blas- toderm formation normal; pole cell formation inhibited. Tem- perature sensitive period extends from stages 9-13 of oocyte development. # gs(2)M: grandchildless on chromosome 2 of Mariol location: 2- (between S and Sp). origin: Induced by ICR-170. references: Mariol, 1981, Mol. Gen. Genet. 181: 505-11. phenotype: At 28.5, homozygous females lay normal numbers of eggs but about 20% fail to hatch and about 40% die just after hatching; these mostly lack pole cells. A fraction of the surviving embryos are also devoid of pole cells and develop into adults with agametic gonads. Abnormalities most frequent in 8-12-day-old females. Paternal genotype without influence. At 16, 75% of eggs hatch and develop into normal fertile adults. Last four days of oogenesis at 28.5 temperature insensitive. Incidence of agametic progeny increases with successive generations of homozygosity of mothers from one to four, constant thereafter; one generation of heterozygosity returns level to ground state. # gsb: gooseberry location: 2-107.6. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard and Wieschaus, 1980, Nature (Lon- don) 287: 795-801 (fig.). Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.). Bopp, Burri, Baumgartner, Frigerio and Noll, 1986, Cell 47: 1033-40. Baumgartner, Bopp, Burri and Noll, 1987, Genes Dev. 1: 1247- 67. Cote, Preiss, Haller, Schuh, Kienlin, Seifert, and Jackle, 1987, EMBO J. 6: 2793-801. Perrimon and Mahowald, 1987, Dev. Biol. 119: 587-600. phenotype: Homozygous lethal; embryos show segment-polarity defects. The posterior portion of each segment is deleted and the anterior portion duplicated in mirror image fashion; the ventral segments are almost entirely covered with denticles, the posterior fraction of which point anteriorly. Segment boundaries persist normally and segments maintain their indi- viduality. The mutants show alterations in the identity of neurons, both underneath and outside the modified ectoderm (Patel, Schafer, Goodman, and Holmgren, 1989, Genes Dev. 3: 890-904); posterior commissures are almost totally absent. alleles: No point mutations were obtained in embryonic lethal screens by Nusslein-Volhard et al., 1984, or Cote et al., 1987. cytology: Placed in 60E9-F1 (Nusslein-Volhard et al., 1984) since uncovered by Df(2R)gsb = Df(2R)60E9-10;60F1-2. molecular biology: Wild-type gsb function provided by two closely-linked duplicated genes, the proximal gsb-p (=BSH4) and the distal gsb-d ((=BSH9) (Bopp et al., 1986; Baumgartner et al., 1987; Cote et al., 1987). These gsb genes were mapped by microdissection and microcloning of bands in the 60E9-60F1 region followed by chromosome walking from the proximal break- point of Df(2R)SB1 to the distal breakpoint of Df(2R)gsb. The gsb-p transcript is made up of five exons and is transcribed in the opposite direction from the two-exon gsb-d transcript. The almost complete DNA sequence and corresponding amino acid sequence of the putative protein has been obtained for the two gsb genes (Baumgartner et al., 1987). The longest open read- ing frame of gsb-p would encode a protein of 452 amino acids; the longest ORF of gsb-d would encode a protein of 427 amino acids. # GsI: Glutamine synthetase I location: 2-{0}. references: Scalenghe and Ritossa, 1976, Atti Accad. Naz. Lin- cei. Cl. Sci. Fis. Nat. Rend. 13: 439-538. Caizzi and Ritossa, 1983, Biochem. Genet. 21: 267-85. Caggese, Caizzi, Bozetti, Barsanti, and Ritossa, 1988, Biochem. Genet. 26: 571-84. phenotype: Structural gene for glutamine synthetase I [GS (EC 6.3.1.2)] in Drosophila melanogaster. The enzyme catalyzes the formation of glutamate and ammonia by cleaving ATP into ADP and phosphate (Caggese et al., 1988). The GSI protein was purified from Drosophila larvae (Scalenghe and Ritossa, 1976; Caggese and Ritossa, 1983); it is a multimer of two subunits (MW 43,000 and 64,000) (Caggese and Ritossa, 1983); the 43,000 dalton protein is usually the more abundant. The molecular weight for the complete enzyme is apparently 380,000. A fast electrophoretic variant (GsIf), an intermediate and common electrophoretic variant (GsIc), and a slow electrophoretic variant ((GsIs) have been found. Hybrids between variants show a strongly stained intermediate band (Caggese et al., 1988). The GSI protein but not the GSII protein is found in the epidermis of Drosophila (Scalenghe and Ritossa, 1976). alleles: allele origin synonym comments __________________________________________________________ GsI1 EMS l(2)C7 null derivative of GsIs GsI2 EMS l(2)C8 hypomorphic derivative of GsIs GsI3 EMS l(2)M9 null derivative of GsIc GsI4 ENU l(2)R26 null derivative of GsIc GsI5 ENU l(2)R34 null derivative of GsIc GsIc nature common allele in nature GsIf nature rare fast allele GsIs nature rare slow allele cytology: Located in 21B3-6 since between proximal breakpoints of Df(2L)PM1 = Df(2L)21A1;21B3-5 and Df(2L)PMG = Df(2L)21A1- 2;21B4-6. molecular biology: GsI and GsII show partial DNA identity with each other and with the DNA from the hamster (De Pinto, Cag- gese, Prezioso, and Ritossa, 1987, Biochem. Genet. 25: 821- 36). other information: Mutations in GsI do not affect the GSII enzyme (Caggese et al., 1988). # GsII: Glutamine synthetase II location: 1-{34}. references: Scalenghe and Ritossa, 1976, Atti Accad. Naz. Lin- cei. Cl. Sci. Fis. Nat. Rend. 13: 439-538. Caggese, Caizzi, Grieco, Bozzetti, and Ritossa, 1986, Mol. Gen. Genet. 204 : 208-13. De Pinto, Caggese, Prezioso, and Ritossa, 1987, Biochem. Genet. 25: 821-36. phenotype: Structural gene for glutamine synthetase II. Com- pletely separable from glutamine synthetase I by DEAE chroma- tography. The GSII protein was purified from adult Drosophila (Scalenghe and Ritossa, 1976) and was isolated by sequence identity with the hamster gene (De Pinto et al., 1987). The enzyme is a multimer of a single subunit (MW 42,000). The complete enzyme has an approximate molecular weight of 360,000 and differs from the GSI enzyme in both subunit molecular weight and in isoelectric point. 90% of glutamine synthetase activity is due to GSII, which is the most abundant adult form. cytology: Located in 10B8-11 by in situ hybridization. Varia- tion in the dose of a chromosomal segment from 9F3 to 10C1-2 results in proportional variation in the amount of the GSII enzyme without influencing the amount of GSI (Caggese et al., 1986). molecular biology: Shows partial DNA identity with GsI and with the hamster gene (De Pinto et al., 1987). gt: giant Left: wild type female. Right: giant female. From Bridges and Gabritschevsky, 1928, Z. Indukt. Abstamm. Vererbungsl. 46: 231-47. # gt: giant location: 1-0.9 (0.04 cM to the left of tko). origin: Spontaneous. discoverer: Gabritschevsky, 25i2. references: Bridges and Gabritschevsky, 1928, Z. Indukt. Abstamm. Vererbungsl. 49: 231-47 (fig.). Gabritschevsky and Bridges, 1928, Z. Indukt. Abstamm. Verer- bungsl. 49: 248-84. Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. Narachi and Boyd, 1985, Mol. Gen. Genet. 199: 500-06. Petschek, Perrimon and Mahowald, 1987, Dev. Biol. 19: 175-89. Mohler, Eldon and Pirrotta, 1989, EMBO J. 8: 1539-48. phenotype: Larval development 4 days longer than normal result- ing in giant larvae, pupae, and imagos. Adult weight 1.7 times normal; increased size caused by increase in cell size and not cell number [Simpson and Morata, 1980, Develop- ment and Neurobiology of Drosophila (Siddiqi, Babu, Hall and Hall, eds.). Plenum Press, New York and London, pp. 129-40]. Pupariation delayed owing to delayed increase in ecdysteroid titers; level reached at pupariation lower than normal; pupal interval of normal length (Schwartz, Imberski, and Kelly, 1984, Dev. Biol. 103: 85-95). Not all genetically giant flies show the giant character, the rest have normal size; distribution sharply bimodal. Percentage giant greatest in well-fed cultures, also raised by modifying action of bb11. Penetrance of viable alleles enhanced in heterozygotes with lethal alleles and deficiencies; viability decreased (Kaufman, 1972, Genetics 71: s28-29). Abnormalities in DNA metabolism found in homo- or heteroallelic third instar gt females (Nara- chi and Boyd, 1985). Salivary gland chromosomes of double thickness in some cells (Bridges, 1935, J. Heredity 26: 60- 64). Feulgen staining shows extra round of DNA synthesis; polytene chromosome can be analyzed in gt/Df larvae (Kaufman, 1972, Genetics 71: s28-29). Embryos carrying lethal giant mutations have defects in the anterior and the posterior domains (Petschek et al., 1987; Mohler et al., 1989). Poste- rior compartment of the labial segment deleted from blasto- derm; cell death at germ-band elongation deletes anterior com- partments of abdominal segments 5-7. Posterior-compartment structures of A5-7 in the peripheral nervous system fuse in mature embryos (Petschek and Mahowald). Hemizygotes for lethal alleles, gt13z and gtX11, fail to hatch (Kaufman, 1973, Genetics 74: s133); denticle belts of the fifth through the seventh abdominal segments partially or completely absent; internally corresponding neuromeres absent; eight abdominal neuromeres disconnected from remainder. Head does not com- plete involution, shows characteristic "buttonhead" phenotype with ventral skeleton extruded from the anterior end of the larva (Mohler et al., 1989), pharynx and pharyngeal chitinized sclerites shorter, and brain lobes somewhat smaller than nor- mal; extensive cell death in epidermal and neural components of embryo (Honisch and Campos-Ortega, 1982, DIS 58: 76-77). Effect cell autonomous in mosaic embryos. (Gergen and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 49-62). Germline clones viable (Garcia-Bellido and Robbins, 1983, Genetics 103: 235-47). gt stocks (homo- or heteroallelic) show an increase in the frequency of spontaneous mutations, including deletions of y and w loci (Green, 1982, Proc. Nat. Acad. Sci. USA 79: 5367-69); these stocks also synthesize DNA of a reduced molecular weight and show many single-strand and double-strand breaks, suggesting abnormalities in DNA metabol- ism (Narachi and Boyd, 1985). RK3. alleles: In addition to those tabulated, Wieschaus, Nusslein- Volhard, and Jurgens (1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307) report eight embryonic lethal alleles, of which four are weak; these exhibit defects in head and in fifth through seventh abdominal segments. acquisition alleles origin discoverer number ref ( viability _____________________________________________________________________________ gt1 | spont Gabritschevsky, 25i2 1, 3, 9 viable-low penetrance gt13z NNG / Kaufman 5, 6 lethal gt30 P 9 gt123 4 sub vital gtE6 EMS Kaufman 5, 6 viable-low penetrance gtl1 190 2 lethal gtl2 ` 1685 2, 9 lethal gtl3 1710 2 lethal gtl4 1859 2 lethal gtl5 1903 2 lethal gtl6 1907 2 lethal gtl7 2413 2 lethal gtl8 2684 2 lethal gtl9 2868 2 lethal gtl10 4798 2 lethal gtl11 6749 2 lethal gtl12 7331 2 lethal gtl13 8868 2 lethal gtM102 MMS 7 lethal gtQ292 EMS Shen gtX11 X ray Falk 6, 8, 9 lethal gtXH 9 lethal gtYA82 9 lethal ( 1 = Bridges and Gabritschevsky, 1928, Z. Indukt. Abstamm. Vererbungsl. 49: 231-47 (fig.); 2 = Duttagupta, Das, and Dutta, 1984, DIS 60: 90-91; 3 = Gabritschevsky and Bridges, 1928, Z. Indukt. Abstamm. Vererbungsl. 49: 248-84; 4 = Garcia-Bellido and Robbins, 1983, Genetics 103: 235-47; 5 = Judd, Shen, and Kaufman, 1972, Genetics 71: 139-56; 6 = Kaufman, 1972, Genetics 71: s28-29; 7 = Liu and Lim, 1975, Genetics 79: 601-11; 8 = Mohler, Eldon and Pirrotta, 1989, EMBO J. 8: 1539-48; 9 = Petschek, Perrimon and Mahowald, 1987, Dev. Biol. 19: 175-89. | Associated with two inserts of DNA into the gt locus, one near +17 and the other near +32 on the molecular map (Mohler et al., 1989). / N-methyl-N1-nitro-N-nitrosoguanidine. ` Tp(1;1)l2 = Tp(1;1)3A2;8D;10B1; weak lethal allele induced by irradiation (Mohler et al., 1989). cytology: Placed in 3A2 by Judd, Shen, and Kaufman, 1972, Genetics 71: 139-56; and Lefevre, 1981, Genetics 99: 461-80; later placed in 3A1 by Mohler et al.,1989. molecular biology: Rearrangement breakpoints associated with gt were positioned on the genomic clone map of Mariani, Pirrotta, and Manet (1985, EMBO J. 4: 2045-52). Mohler et al., 1989, report confirmation of the cloning of gt by partial rescue with P-elements. The region from +18 to +21 on the molecular map is practically identical to a 1.9 kb RNA expressed in 2- to 4-hour embryos but barely detectable in 4- to 6-hour embryos; this region is included in the DNA fragment used in the complete rescue of the abdominal segmentation defects of the giant mutant gtX11 (Mohler et al., 1989). Sequencing of the cDNA of gt suggests that the gene encodes a novel protein that shows identity to opa but not to other pattern-forming genes (Eldon and Pirrotta, 1989). other information: Used by Bridges (1935) in the construction of salivary chromosome maps. Preliminary evidence of interal- lelic complementation with respect to phenotype and viability presented by Duttagupta, Das, and Dutta (1984, DIS 60: 90- 91). #*Gt2: Giant in chromosome 2 location: 2- (not located). origin: Spontaneous. discoverer: Bridges, 14i28. phenotype: Heterozygote normal but, in presence of homozygous gt3, gives giant, male-sterile flies. Homozygous lethal. RK3. #*gt3: giant in chromosome 3 location: 3-64. origin: Spontaneous. discoverer: Bridges, 14i28. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 120 (fig.). phenotype: Body size much larger than normal. Late hatching. Entirely sterile in male. Giant character produced only in flies homozygous for gt-3 and heterozygous for Gt-2. RK3. # gt4 location: 2-24.0. origin: Spontaneous. discoverer: Bridges, 30b14. phenotype: Giant flies hatch very late. Viability variable but around 15% wild type. RK3. # Gtd: Glucose-tasting-defective (J.C. Hall) location: 1-(v-f, closer to v). origin: Induced by ethyl methanesulfonate. references: Rodrigues, Sathe, Pinto, Balakrishnan, and Siddiqi, 1991, Mol. Gen. Genet. 226: 265-766. phenotype: Isolated after feeding-preference enrichment, against positive glucose response, of descendents of mutagen- ized flies. Subsequent detailed testing revealed enhanced attraction to NaCl in feeding-preference test, NaCl tolerance in ingestion test, relative indifference to sucrose, and higher than normal threshold for quinine avoidance; all of these phenotypes semi-dominant. Gustatory responses of larvae normal. No alteration in electrophysiologically measured response of peripheral (labellar) neurons to NaCl; causes lethality of males hemizygous for the mutation who also carry duplication for normal allele. cytology: Maps to 10E1 or 11A7, based on inclusion in Df(1)KA6 = Df(1)10E1-2;11A7-8 but not in Df(1)m259-4 = Df(1)10C2- 3;10E1-2 or Df(1)m30 = Df(1)10E2;11A6-7; in fact, females car- rying either of the latter two deficiencies in heterozygous combination with Gtd are near-normal in sucrose and quinine responses (i.e., closer to wild type than Gtd/+); yet, Gtd over either Df(1)v-L2 = Df(1)9F13;10A1 or Df(1)N105 = Df(1)10F7;11D1 leads to Gtd/+-like responses; Gtd/y+Yv+#3 (9F4;10E3-4) males die as second-instar larvae, whereas the y+Yv+ duplication (9F4;10A1) does not effect such synthetic lethality; the X factor responsible for the lethality (in con- junction with the larger duplication) was inseparable from Gtd locus. other information: Fails to complement nearby gustD mutations with respect to (recessive-type) quinine tolerance; when heterozygous with gustC, which is closely linked, flies show reduced response to sucrose that is more severe than in tests of either homozygous or hemizygous type; complements gustB in behavioral assays (re homozygous-type responses); three rever- tants of Gtd/y+Yv+#3 lethal interaction also reverted with respect to sucrose-indifference phenotype. #*gtd: giantoid location: 1-0.5. origin: Spontaneous. discoverer: Bridges, 21c12. references: Bridges and Gabritschevsky, 1928, Z. Indukt. Abstamm. Vererbungsl. 46: 232 (fig.). phenotype: Body size larger, especially head. Late hatching. Viability erratic, about 50% wild type. Separation difficult in females, easier in males. RK3. # gua1: guanosine requiring location: 1-31. origin: Induced by ethyl methanesulfonate. synonymn: gua1-1ts. references: Falk and Nash, 1974, Genetics 76: 755-56. phenotype: A temperature-sensitive guanosine auxotroph. Hemiz- ygous viability on guanosine-free medium reduced at 25; virtu- ally lethal at 29 although completely supplementable at that temperature. Normal allele thought to function in the conver- sion of inosinic acid to guanilic acid. cytology: Placed in 9D1-E1 by deficiency analysis; temperature sensitive on minimal medium in combination with Df(1)ras-v = Df(1)9D1-2;10A2-3, but not Df(1)v64f = Df(1)9E7-8;10A2-3 or Dp(1;2)v63i = Dp(1;2)9D4-E1;10A11-B1;56A (Johnson, Woloshyn, and Nash, 1979, Mol. Gen. Genet. 174: 287-92). This small region carries in addition pur1, ras, and lethals, which fail to complement the other three loci (Nash, Woloshyn, and Janca, 1979, Genetics 92: s87). # gua2: see bur # guanosine requiring: see gua1 Guanosine triphosphate cyclohydrolase: see Pu # Gull: see G # Gulloid: see Gd # gumper: see fliF # gurken: see grk # gus: gustatory (J. C. Hall) A series of ethyl-methanesulfonate-induced taste mutants selected by Tompkins et al., 1979. All mutants were crudely mapped and complementation tests performed between those map- ping to the same interval. references: Tompkins, Cardoza, White, and Sanders, 1979, Proc. Nat. Acad. Sci. USA 76: 884-86. mutant location alleles ______________________________________________________ gusA 1- (v - f) gusAQ1, gusAQ2, gusAQ3, gusAQ4 gusC 1- (cv - v) gusCN10 gusD 1- (v - f) gusDN9, gusDN12 gusE 1- (v - f) gusEN1 # gusA phenotype: Attracted to quinine (C20H24N2O2), unlike wild type, which is repelled; normal aversion to sodium chloride (NaCl). One allele, gusAQ1, leads to cold-sensitive phenotype, in that larvae or adults, raised at 22, show the aberrant attraction to quinine, but when raised at higher temperatures, these animals show normal behavior; the temperature-sensitive period of gusAQ1 is during embryogenesis (Tompkins, 1979, Dev. Biol. 73: 174-77). other information: Not allelic to gusD or gusE. # gusB: see gustC # gusC phenotype: Attracted to sodium chloride (NaCl), unlike wild type, which is repelled; normal aversion to quinine (C20H24N2O2). # gusD phenotype: Attracted to quinine (C20H24N2O2) and to sodium chloride (NaCl), unlike wild type, which is repelled by both. other information: Not allelic to gusA or gusE. # gusE phenotype: Attracted to quinine (C20H24N2O2) and to sodium chloride (NaCl), unlike wild type, which is repelled by both; larval chemosensory behavior normal; is cold-sensitive, such that exposure of third larval instar to 22 (but not higher temperatures) results in aberrantly responding adults (Tomp- kins, 1979, Dev. Biol. 73: 174-77). other information: Not allelic to gusA or gusD. # gusF: see gustB # gust: gustatory defective (J.C. Hall) Another series of ethyl-methanesulfonate-induced taste mutants that affect the fly's responses to attractants and repellents. All mutants were crudely mapped and complementa- tion tests performed between those mappings to the same inter- val. Complementation tests with gus mutants were also per- formed. Sodium chloride (NaCl) elicits responses from two sensory neurons (L1 and L2) in each taste sensillum; another sensory neuron (S) involved in response to sugars (Siddiqi, Joshi, Arora, and Rodrigues, 1989, Genome 31: 646-51). A fourth neuron is inhibited by sodium chloride (NaCl) and sugars (Arora et al., 1987). mutant location synonym ref ( alleles _______________________________________________________________ gustA 1-45 gustx1, gustx2 3, 4 gustAx1, gustAx4 gustB 1-38 gustx5, gusF 1, 3-5 gustBx5, gustBx7, gustBFN5, gustBFN32 gustC 1- (v - f) gusB, gustx2 3-5 gustCx2, gustCB04, gustCB05 gustD 1- (v - f) gustx3, gustx6 3, 4 gustDx3, gustDx6 gustE | 1- 4 gustEv86 gustF 4 gustM 3- {71} 2 GustR 3- (ru - h) 4 GustS 4 ( 1 = Arora, Rodrigues, Joshi, Shanbhag, and Siddiqi, 1987, Nature (London) 330: 62-63; 2 = Morea, 1985, Experientia 41: 1381-84; 3 = Rodrigues and Siddiqi, 1978, Proc. Indian Acad. Sci. 87B: 147-60; 4 = Siddiqi, Joshi, Arora, and Rodrigues, 1989, Genome 31: 646-51; 5 = Siddiqi and Rodri- gues, 1980, Development and Neurobiology of Drosophila (Sid- diqi, Babu, Hall, and Hall.). Plenum Press, New York, pp. 347-59. | Cytological location between 6C11 and 6E4-5 (Siddiqi et al., 1989). # gustA phenotype: Insensitive to pyranose sugars (C7H12O6), but shows normal response to fructose (C6H12O6) and normal aversion to quinine (C20H24N2O2) and sodium chloride (NaCl). Receptor defective mutant (Siddiqui et al., 1989). One type of sense hairs on the labellum shows reduced physiological responses to pyranoses (Rodrigues and Siddiqi, 1981, Mol. Gen. Genet. 81: 406-08); another type of sense hairs is insensitive to the normal inhibition by pyranose sugars. # gustB phenotype: Originally said to be "indifferent" to sodium chloride (NaCl), but now known to give positive responses (greater than wild type) to this salt in the feeding prefer- ence test which consist of behavioral (proboscis extension) and physiological (labellar recording) responses (Arora). Responds normally to sucrose (C12H22O11) and quinine (C20H24N2O2). In this mutant, the S neuron, usually involved in the sugar response, is excited by sodium chloride (NaCl) (Arora et al., 1987). Two forms of alpha-glucosidase activity (enriched in tarsal leg segments relative to other tissues in wild type) are lower than normal in two of the gustB alleles (unspecified) (Bhavsar, Rodrigues, and Siddiqi, 1983, J. Biosci. 5: 279-87). cytology: Placed in 10E1 since included in Df(1)m259-4 = Df(1)10C2-3;10E1-2 and Df(1)KA6 = Df(1)10E1;11A7-8 (Arora et al., 1987). other information: Allelic to gusF of Tompkins, Cardosa, White, and Sanders (1979, Proc. Nat. Acad. Sci. USA 76: 884-86). # gustC phenotype: Originally said to be "indifferent" to sodium chloride (NaCl), but now known to give responses (greater than wild type) to this salt in the feeding preference test (Arora). Indifferent to quinine (C20H24N2O2), and sucrose (C12H22O11). Also at least one allele (gustCx2) leads to lower amounts of two forms of alpha-glucosidase activity that are normally found in the legs [and are enriched in the tarsi of these appendages in wild type (Bhavsar et al., 1983)]. other information: Allelic to gusB (Tompkins et al., 1979). # gustD phenotype: Insensitive to quinine (C20H24N2O2), but shows nor- mal responses to sucrose (C12H22O11) or to sodium chloride (NaCl); both alleles are heat-sensitive, in that rearing at 28C leads to aberrant responses of adults, but development at low temperature leads to normal-behaving flies; levels of leg-specific alpha-glucosidases are normal or nearly so (Bhav- sar et al., 1983). other information: Not allelic to gusA, gusB, gusD, or gusE. # gustE phenotype: No attraction to sodium chloride (NaCl) in feeding tests (gustEv86); response to potassium chloride (KCl) is the same as in wild type. # gustF phenotype: Electrophysical sensitivity to both sodium chloride (NaCl) and potassium chloride (KCl) reduced; behavioral characteristics not tested by Siddiqui et al., (1989). # gustM phenotype: Insensitive to sodium chloride (NaCl) and quinine sulfate (C20H24N2O2) in proboscis extension responses (i.e. these substances fail to inhibit the sugar-induced reflex); further behavioral testing, however, reveals abnormally pro- longed drinking of salt solutions and attraction to quinine; sugar responses normal. cytology: The mutant is located at 93D and associated with In(3R)AFA (86C4-5;93D1-2); the behavioral abnormalities are uncovered by Df(3R)e-N12 (93B1-2;93D6-7), Df(3R)e-GC9 (93B11- 13;93D9-10), and Df(3R)e-D7 (93C3-6;93F5-8), implying that the righthand inversion breakpoint is responsible. # GustR phenotype: Attracted to sodium chloride (NaCl) but not potas- sium chloride (KCl); shows reduced attraction to all sugars. L1 neurons involved in sodium chloride (NaCl) response (Sid- diqi et al., 1989). # GustS phenotype: Attracted to sodium chloride (NaCl) but not potas- sium chloride (KCl); shows reduced attraction to all sugars. # gustatory: see gus # gustatory defective: see gust #*gv: grooved location: 3-37.3 (based on its position of 0.2cM to the left of eyg). origin: Spontaneous. discoverer: Ives, 43l28. references: 1946, DIS 20: 65. synonym: gs: gespleten. phenotype: A longitudinal medial groove in thorax; in extreme individuals, thorax nearly cleft. Eyes reduced, sometimes missing. Irregular and often extra alar bristles. Viability and fertility good. RK1. allele origin discoverer synonym ref ( ______________________________________________________________ *gv1 spont Ives, 43l28 2 gv2 spont Smelink-den-Hollander, 56l gs 3 gvP / ray gsP 1 gvU | / ray gsU 1 ( 1 = Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215-25; 2 = Ives, 1946, DIS 20: 65; 3 = Smelink-den- Hollander, 1957, DIS 31: 85. | Associated with In(3LR)gvu=In(3LR)69C1-2;81; homozygous lethal. cytology: Placed in 69C on the basis of its exclusion from Df(3L)vin7 = Df(3L)68C8-11;69B3-C1 and the gv phenotype of gv/In(3LR)gvu=In(3LR)69B5-C4;81 (Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215-25). # gvl: grooveless location: 4-0.2 [in diplo-4 triploids (Sturtevant, 1951, Proc. Nat. Acad. Sci. USA 37: 405-7)]. origin: Spontaneous. discoverer: Bridges, 33e10. references: 1935, Biol. Zh. (Moscow) 4: 401-20. phenotype: Short transverse groove between scutellum and thorax is nearly eliminated; no overlap with wild type. Black scars appear on scutellar groove at sides, in pleural region, and behind sternopleurals. Viable and fertile. RK1. # gy: gouty legs location: 4- 0.2. origin: Spontaneous. discoverer: Muller. references: 1965, DIS 40: 36. phenotype: Legs shortened and thickened, especially the meta- tarsi of the hind legs, which are often swollen. Usually classifiable; viability and fertility good. gy/eyD is gy. RK2. cytology: Tentatively placed at 102B10-E9 between Df(4)M4 = Df(4)101E-F;102E2-10 and tip (Hochman, 1971, Genetics 67: 235-52).