# g: garnet location: 1-44.4. discoverer: Bridges, 15b19. synonym: salmon. references: Bridges, 1916, Genetics 1: 151. phenotype: Eye color brownish, darkening with age; both pteri- dine and ommochrome pigments variably reduced in different alleles, giving rise to such descriptions as deep purplish ruby, pinkish, brownish, yellowish ruby, orange, etc. Nolte (1959, Heredity 13: 233-41) measured both pigments spectros- copically for g alleles (g1,g2,g3,g4) and detected subtle differences. Hexter (1963, Proc. Nat. Acad. Sci. USA 50: 372-79) claims g1,g2,g3, and g4 indistinguishable pheno- typically but g53d to be orange eyed and easily separable. Earlier authors claims g2 lighter than g1. Pigmentation of Malpighian tubules also reduced (Brehme and Demerec, 1942, Growth 6: 351-56). Eye color (g2) autonomous in transplants into wild type host (Beadle and Ephrussi, 1936, Genetics 21: 225-47). alleles: allele origin discoverer ref ( phenotype | ______________________________________________________________________ g1 spont Bridges, 15b19 1-5 g2 spont Bridges, 18c28 5, 13 partially dominant in car homozygotes (Schultz) g2rv g3 spont Bridges, 22d22 5, 13 g4 / X ray Glass, 1929 5, 6 g17B ` X ray 5, 20 male sterile g26-10 X ray Sobels, 57j 5, 19 g26-15 SMS Sobels, 57j 5, 19 *g26-41 SMS Sobels, 57j 5, 19 weak allele *g28-10 SMS Sobels, 1957 5, 19 g28-40 SMS Sobels, 1957 5, 19 *g29h spont E. Wallace, 29h 4 *g30d spont Bridges, 30d 4 *g32d spont Emerson, 32d 4 *g33j spont Bridges, 33j 4 *g33l spont Ives, 33e 4 *g34e spont Duncan 34e 4 *g37c spont Mossige, 37c 4 g37f spont Eeken, 37f 4 *g37k spont Mather, 37k 4 *g38b spont Bridges, 38b 4 g42a X ray Green, 42a16 4 g49h 32p King, 49h 11 females have 60% normal viability g50e 2, 3 g53d spont Hexter, 53d 9, 10 orange eye *g55k spont Williams, 55k 15 g64b - X ray Ives, 64b11 g68d EMS Maddern, 68el 8 g70k spont Schwink, 70k10 18 g79i spont Najera 16 *g271-2 X ray Demerec, 1933 5 male lethal, cell lethal *g271-6 X ray Demerec, 34a 5 male lethal, cell lethal *g271-9 X ray Hoover, 35h 5 male lethal *g271-10 X ray Hoover, 35h 5 male lethal *ge spont Gottschewski, 34g17 7 gEMS gF spont Waddle, 1974 gim g-l gS1 spont Schalet 3 gS2 spont Schalet 17 gS3 spont Schalet 17 gtuh1 spont Kuhn 12 gtuh2 spont Kuhn 12 reduced viability, fertility gw X ray Muller 2, 3, 14 subliminal allele gX n X ray Muller 14 female fertility reduced ( 1 = Bridges, 1916, Genetics 1: 151; 2 = Chovnick, 1958, Proc. Nat. Acad. Sci. USA 44: 333-37; 3 = Chovnick, 1961, Genetics 46: 493-507; 4 = CP552; 5 = CP627; 6 = Glass, 1935, DIS 2: 7; 7 = Gottschewski, 1935, DIS 4: 8,15; 8 = Hayman and Maddern, 1969, DIS 44: 50; 9 = Hexter, 1958, Proc. Nat. Acad. Sci. USA 44: 768-71; 10 = Hexter, 1963, Proc. Nat. Acad. Sci. USA 50: 372-79; 11 = King, 1950, DIS 24: 58; 12 = Kuhn, 1972, DIS 49: 38; 13 = Morgan, Bridges, and Sturtevant, 1925, Bibliogr. Genet. 2: 226 (fig.); 14 = Muller, 1946, DIS 20: 67; 15 = Muller, 1956, DIS 30: 30; 16 = Najera, 1985, DIS 61: 215; 17 = Schalet, 1986, Mutat. Res. 163: 115-44; 18 = Schwinck and Schwinck, 1972, DIS 49: 39; 19 = Sobels, 1958, DIS 32: 84; 20 = Valencia, 1966, DIS 41: 58. | Lists only special phenotypic attributes not mentioned for most alleles. / Induced in In(1)dl-49. ` Associated with In(1)12B14-15;19F superimposed on In(1)scSILSC8R+dl-49. - See DIS 60: 230. Associated with In(1) with breakpoints between dy and f. n Associated with In(1)12;19-20. cytology: Placed in 12B6-7 (Lefevre, 1976, Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, p59. other information: Alleles separable by conversion; g53d to the left of g2. G: Gull From Mohr, 1929, Z. Indukt. Abstamm. Vererbungsl. 50: 113-200. # G: Gull location: 2-12.0. origin: Spontaneous. discoverer: Mohr, 19k23. references: 1923, Studia Mendeliana (Brunae), pp. 266-87 (fig.). 1927, Proc. Intern. Congr. Genet., 5th., Vol. 2: 1136. 1929, Z. Indukt. Abstamm. Vererbungsl. 50: 113-200 (fig.). phenotype: Wings large, held out from sides at 45-90 angle, curved downward, and somewhat pointed. Vein L1 thickened; crossveins closer together, sometimes broken. Thoracic and vertical bristles duplicated in majority of flies. G/ft has exaggerated ft phenotype. Partially inhibited by ds/+ and much inhibited by ds/ds. Homozygous lethal. RK2. cytology: Placed in 24D3-8 based on its inclusion in Df(2L)M = Df(2L)24D3-4;25A2-3 but not in Df(2L)dp-h28 = Df(2L)24D7- 8;24F7-25A1 (Szidonya and Reuter, 1988, Genet. Res. 51: 197- 208). other information: Causes local shortening of map by about 1.1 units. Is a deficiency for or an allele of ft. # Grv: Gull-reverted origin: Spontaneous derivative of G. discoverer: Bridges, 1930. phenotype: Does not show G phenotype. Allelic to ft but does not exaggerate ft. Lethal in combination with G. RK2. # G protein: see G( and G| # g2: see Tkr # g-l: see sno # g, Inh: see gX # G(: G protein ( subunit G proteins belong to a family of membrane-associated guanine nucleotide-binding proteins that couple specific receptors for extracellular signals to specific intracellular effectors, thus regulating the activity of these effectors. When not interacting with the receptor, G proteins are usually in the form of a heterotrimer made up of (, |, and / subunits, with the ( subunit bound to GDP. Upon activation by the receptor, the ( subunit exchanges GDP for GTP, dissociates from the |-/ subunits, and interacts with the effector. Afterwards GTP is hydrolyzed, and the heterotrimer of (, |, and / subunits is formed again. In Drosophila melanogaster, three genes coding for different ( subunits have been identified. gene location ( subunit encoded ref ( cytology ______________________________________________________________ G ( 47A | 2-{60} Go1,Go2 1, 5-7 47A G ( 60A 2-{106} Gs 2, 6 60A G ( 65A / 3-{20} Gi 3, 4, 6 65A ( 1 = DeSousa, Hoveland, Yarfitz, and Hurley, 1989, J. Biol. Chem. 264: 18544-51; 2 = Provost, Somers, and Hurley, 1988, J. Biol. Chem. 263: 12070-76; 3 = Quan, Wolfgang, and Forte, 1990, Nat. Acad. Sci. USA 86: 4321-25; 4 = Quan and Forte, 1990, Mol. Cell Biol. 10: 910-17; 5 = Thambi, Quan, Wolfgang, Spiegel, and Forte, 1989, J. Biol. Chem. 264: 18552-60; 6 = Wolfgang, Quan, and Forte, 1990, unpub- lished; 7 = Yoon, Shortridge, Bloomquist, Schneuwly, Perdew, and Pak, 1989, J. Biol. Chem. 264: 18536-43. | Synonym: dgo (Yoon et al., 1989). / Synonym: DG(1 (Provost et al., 1989). # G(47A: G protein ( subunit at 47A phenotype: Encodes a G protein ( subunit that is expressed mainly in the nervous system (DeSousa et al., 1989; Thambi et al., 1989) and shows homology to mammalian Go(. Low levels of this G protein are found in the embryo until completion of germband shortening; then high levels begin to be expressed in the neuropil (Wolfgang, et al., 1990). molecular biology: The gene has been cloned using rat, bovine, and human cDNA as probes. Genomic, cDNA and putative amino acid sequences have been obtained (DeSousa et al., 1989; Thambi et al., 1989; Yoon et al., 1989). Three transcripts have been identified, a 3.8-4.2 kb transcript expressed at high levels in heads and bodies of adults, a 5.3-6 kb tran- script expressed at high levels in the heads only, and a 3.4- 3.5 kb transcript found in bodies (Thambi et al., 1989; Yoon et al., 1989). Transcripts are also found in embryos, larvae, and pupae. The mRNA occurs abundantly in the cell bodies of neurons in the cortex of the brain and the thoracic ganglia; a low level of mRNA is found in nurse cells and oocytes (De Sousa et al., 1989). Two classes of cDNA that differ in DNA sequences in the 5 -noncoding region and the 5 -most part of the coding region are generated by the splicing together of seven exons. The first exon in the splice differs in length and location in the two classes; the last six exons are ident- ical in both classes (Yoon et al., 1989). This alternative splicing results in the encoding of two proteins 354 amino acids long that differ in seven amino acids in the amino ter- minal region (De Sousa et al., 1989; Thambi et al., 1989; Yoon et al., 1989). Transcripts corresponding to both classes of cDNA are found in the central nervous system (De Sousa et al., 1989). Membrane preparations from Drosophila melanogaster heads contain high levels of a pertussin toxin (PTX) substrate with 82% sequence identity to vertebrate G proteins that are modified similarly by PTX (De Sousa et al., 1989, Thambi et al, 1989). # G(60A: G protein ( subunit at 60A phentotype: Encodes a stimulatory G protein ( subunit with high homology to mammalian Gs( that is responsible for the coupling of extracellular receptors to adenylate cyclase and an increase in the second messenger cAMP (Quan et al., 1989). The protein is expressed at low levels until completion of germband shortening; then high levels begin to be expressed in the neuropil (Wolfgang et al., 1990). molecular biology: The gene has been cloned from head DNA using bovine cDNA as a probe. The genomic, cDNA and putative amino acid sequences determined (Quan et al., 1989; Quan and Forte, 1990). The gene is 4.5 kb long. Transcripts are most abun- dant in the central nervous system; mRNAs were also isolated (using PCR) from whole flies and bodies (Quan and Forte, 1990). There are 9 exons separated by 8 introns, the introns showing a size variation of 56 bp to 1.4 kb. Alternate splic- ing at the 3 end of intron 7 produces transcripts that encode a long or short G protein ( subunit. The cDNAs differ by the inclusion or deletion of nine nucleotides at the exon 7-8 junction. The long or short protein products differ by inclu- sion or deletion of three amino acids and the substitution of a Ser in the long protein and for a Gly in the short protein (Quan and Forte, 1990). The apparent molecular weights of these two forms are 51,000 and 48,000 daltons. # G(65A: G protein ( subunit at 65A phenotype: Encodes a G protein ( subunit displaying sequence homology to mammalian Gi( that inhibits adenylate cyclase activity. The G protein is uniformly distributed in oocytes, becomes restricted to the posterior pole of the embryo during early cleavage and is lost during the blastoderm stage (Wolf- gang et al., 1990). molecular biology: The gene has been cloned using bovine transducin ( subunit cDNA as a probe; the genomic, cDNA, and putative amino acid sequences were determined. There are five exons separated by four introns. A major 2.3 kb transcript and a minor 1.7 kb transcript have been identified. These tran- scripts, first isolated in very young embryos, are most abun- dant in the embryonic and pupal stages. The gene encodes a G protein ( subunit with amino acid sequences showing 77-78% identity to the sequences in bovine inhibitory G proteins; an isoleucine in the Drosophila protein, however, has been sub- stituted for a cysteine in the vertebrate proteins (Provost et al., 1989). # Gad: Glutamic acid decarboxylase (J.C. Hall) location: 3-{15}. origin: From molecular cloning, based on cross-hybridization with feline GAD-encoding gene. references: Jackson, Newby, and Kulkarni, 1990, J. Neurochem. 54: 1068-78. phenotype: The structural gene for glutamic acid decarboxylase. Gad probes detect putative GAD-encoding 3.1-kb mRNA, from 4-8 h of embryogenesis to adulthood; a 2.6-kb RNA was also found, in embryos and pupae only; in situ hybridization detects the RNA(s) in widely, but not uniformly, distributed CNS cortical regions (of adult heads and larvae), with no detectable sig- nals in non-neural tissues. cytology: Gad cDNA probe hybridized to 64A3-5; adults heterozy- gous for Df(3L)HR277 [= Df(3L)63B12;64B12] and a normal third chromosome display a. 30-45% reduction in GAD levels. molecular biology: Sequence of cross-hybridizing cDNA clones predicts a 510-amino-acid protein with overall sequence iden- tity to feline coding material of ca. 50% (after alignment of Drosophila sequence with residues 81-585 of cat GAD); in vitro translation of Drosophila cDNA leads to ca. 57-kd protein (would correspond to a 510-residue polypeptide); this was immunoprecipitable and Western-blotable with anti-rat-GAD, though the latter experiments also found a 76-kd band. other information: Gad cDNA probe did not cross hybridize with Ddc clone, though the sequences of these two genes indicate a region of sequence similarity in their coding regions (corresponding to pyridoxal-phosphate-binding region). # Gal: |-Galactosidase location: 2-{20}. references: Kotarski, Pickert, and MacIntyre, 1983, Genetics 105: 387-407. Knipple and MacIntyre, 1984, Mol. Gen. Genet. 198: 75-83. Fargnol, Hyde, and Sofer, 1985, Genetics 110: s7. phenotype: Inferred to be the gene that codes for the enzyme | galactosidase [B-GAL (EC 3.2.1.23)] because of response of the enzyme level to gene dosage. A null strain (Galn9) does not survive on medium containing lactose (Fargnol et al., 1985), but the Bethylie wild-type strain shows more than 95% survival on lactose medium. Induction in cell culture by hormone stu- died by Best-Bellpomme, Courgen, and Rambach (1978, Proc. Nat Acad. Sci. USA 75: 6102-06). alleles: Galn1 and Galn2 (Knipple and MacIntyre, 1984), Galn9 (Fargnol et al., 1985). cytology: Placed in 26A8 since located between autosomal break- points of T(Y;2)H69 = T(Y;2)26A7-8 and T(Y;2)D211 = T(Y;2)26B3-5 and uncovered by Df(2L)GpdhA = Df(2L)26D7- E1;26A8-9 but not by Df(2L)cl7 = Df(2L)26D7-E1;26A7-8 (Knipple and MacIntyre, 1984). # gap: see gp # Gapdh1: Glyceraldehyde dehydrogenase 1 location: 2-{57}. references: Tso, Sun, Wu, 1985, J. Biol. Chem. 260: 8820-28. phenotype: One of two genes (Gapdh1 and Gapdh2) that code for the enzyme glyceraldehyde-3-phosphate dehydrogenase [G3PD (EC.1.2.12)]. These genes are expressed in almost all cells, especially those that undergo a high rate of glycolysis. cytology: Glyceraldehyde 1 has been located at 43E-F by in situ hybridization to the salivaries. molecular biology: Gapdh1 has been cloned and its nucleotide and deduced amino acid sequences determined. Gapdh1 and Gapdh2 show a striking degree of identity in their coding regions but are entirely different in their 5 and 3 flanking regions. Since, for the enzymes encoded by these genes, there are only eight amino acid residue differences in a total of 332 resi- dues, Tso et al. suggest that the two genes have arisen by duplication and translocation events. The transcription ini- tiation site and the polyadenylation site of Gapdh1 have been determined; the gene is transcribed from left to right and its transcript is present in adult flies. In its -30 bp region, Gapdh1 resembles many RNA polymerase II transcribed promotors in the lack of a sequence homologous to the TATA box. No introns are found in its coding region. # Gapdh2: Glyceraldehyde dehydrogenase 2 location: 1-{54}. references: Tso, Sun, Wu, 1985, J. Biol. Chem. 260: 8820-28. Sun, Lis, and Wu, 1988 , Genes Dev. 2: 743-53. phenotype: Another gene that codes for the enzyme glyceraldehyde-3-phosphate dehydrogenase (see Gapdh1). The level of expression of Gapdh2 has been found to be regulated developmentally (Sun et al., 1988). cytology: Glyceraldehyde 2 has been located at 13F by in situ hybridization to the salivaries. molecular biology: Gapdh2 has been cloned and its nucleotide and deduced amino acid sequences determined. As in Gapdh1, the transcription initiation site and the polyadenylation sites of Gapdh2 have been determinded. The promoter region of Gapdh2 (unlike that of Gapdh1) contains a consensus TATA box sequence as well as a CAAT box sequence (Tso et al., 1985). There is an intron located in the 5 noncoding region, but no other inter- vening sequences. There are two distinct regulatory regions, URS1 and URS2, in the first 145 bp of the 5 flanking region of Gapdh2. URS1 acts throughout development to activate tran- scription; URS2 acts along with URS1 to activate transcription in larval and adult stages, but represses transcription in Schneider cells and perhaps some embryonic stages (Sun et al., 1988). # garnet: see g # Gart: see ade3 # gastrulation defective: see gd # gat: gate (J.C. Hall) location: 2-60. origin: Induced by ethyl methanesulfonate. references: Jackson, 1983, J. Neurogenet. 1: 3-15. phenotype: Eclosion of flies is poorly synchronized in light- dark cycle; eclosion becomes arrhythmic in constant darkness; fluctuations of male's courtship song interpulse intervals define a sloppy rhythm or are arrhythmic (Jackson and Kyriacou). other information: Allelic to psi-2, based on aberrant short- term rhythms of courtship song in gat/psi-2 males (Kyriacou). # G|13F: G protein | subunit at 13F location: 1-{51}. references: Yarfitz, Provost and Hurley, 1988, Proc. Nat. Acad. Sci. USA 85: 7134-38. phenotype: This gene encodes one isoform of the G protein | subunit in Drosophila melanogaster. After the G protein ( has interacted with the effector, the |-/ subunits reassociate with the ( subunit and bring the ( subunit to its specific receptor. cytology: Located at 13F by in situ hybridization to the salivaries. molecular biology: Gene cloned using bovine transducin | subunit cDNA as a probe, and the genomic, cDNA and the puta- tive amino acid sequences determined. There is an open read- ing frame (ORF) of 1023 bases which codes for a predicted pro- tein of 340 amino acids showing more than 80% identity to the corresponding mammalian proteins. The Drosophila protein is unique at 15% of the amino acid positions. Transcripts of 5.2, 4.2, 3.3, 3.0 and 1.9 kb are expressed from mid-embryo through adult stages, the highest level of expression being in late embryos and pupae. Expression is low in larvae and can hardly be detected in adults. Early embryos also show tran- scripts of 3.1, 2.5 and 2.0 kb. In adult flies there is more mRNA in the heads than in the bodies. Restriction mapping and DNA sequencing indicate the absence of introns in the presump- tive coding region of the gene; however, at least two introns are present in the 5 noncoding region and there is evidence for alternative splicing in this region. # gcd: giant cell defect (J.C. Hall) location: 1-48. origin: Induced by ethyl methanesulfonate. discoverer: Heisenberg. phenotype: Cellular cortex of central brain shows one giant cell body lateral to base of each calyx (bulges located rela- tively dorsally and at posterior edge of cortex); penetrance of this phenotype approximately 85%. # gd: gastrulation defective location: 1-36.78. origin: Induced by ethyl methanesulfonate. synonym: fs(1)A573, fs(1)M18. references: Gans, Audit, and Masson, 1975, Genetics 81: 683- 704. Anderson and Nusslein-Volhard, 1984a, Nature (London) 311: 223-27. 1984b, Pattern Formation (Malacinski and Bryant, eds.). Mac- millan, New York. pp. 269-89. Konrad and Mahowald, 1984, Molecular Aspects of Early Develop- ment (Malacinski and Klein, eds.). Plenum, New York. pp. 167-88. Anderson, Bokla, and Nusslein-Volhard, 1985, Cell 42: 791-98. phenotype: Maternal-effect lethal; embryos produced by homozy- gous females exhibit hyperplasia of dorsal cuticular elements and aplasia of ventral elements; phenotye of strong alleles, e.g. gd7, indistinguishable from that of dl. Weaker alleles display some ventral elements. Gastrula exhibits excessive furrowing both dorsally and ventrally [Zalokar, Audit, and Erk, 1975, Dev. Biol. 47: 419-32 (fig.)]. Polarity of the egg shell unaffected. Temperature-sensitive period of temperature-sensitive alleles begins several hours prior to ovoposition and persists until 1.5 h after fertilization. Five of eight mutants classed as weak on the basis of filzkorper development; these five tend to be more dorsalized in posterior than in anterior parts of the embryo, as the setal bands become progressively narrowed posteriorly. gd7/gd7; Toll/+ females produce lateralized embryos; most ven- tral and dorsal pattern elements missing; lateral cephalic furrow seen both dorsally and ventrally, and ventral setae formed at all dorsal-ventral positions. alleles: allele synonym discoverer ref ( _____________________________________________ gd1 fs(1)A573 Audit 2, 7 gd2 fs(1)M1811-1524 Mohler 4, 5 gd3 fs(1)M1812-4955 Mohler 4, 5 gd4 fs(1)M1813-935 Mohler 4, 5 gd5 fs(1)M1813-1697 Mohler 5 gd6 | fs(1)M1813-1853 Mohler 4, 5 gd7 / fs(1)M1814-743 Mohler 1, 5 gd8 fs(1)190.5 1, 6 ( 1 = Anderson and Nusslein-Volhard, 1984, Pattern Formation (Malacinski and Bryant, eds.). Macmillan, New York, pp. 269-89; 2 = Gans, Audit, and Masson, 1975, Genetics 81: 683-704; 3 = Konrad and Mahowald, 1984, Molecular Aspects of Development (Malacinski and Klein, eds.). Plenum, New York, pp. 167-88; 4 = Mohler, 1977, Genetics 85: 259- 72; 5 = Mohler and Carrol, 1984, DIS 60: 236-41; 6 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26; 7 = Zalokar, Audit, and Erk, 1975, Dev. Biol. 47: 419-32 (fig.). | gd6 complements gd3 and partially complements gd2. / Pattern of ftz protein stripes in homozygous females identi- cal to that of other maternal dorsalizing mutants (Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32). cytology: Placed in 11A1-7, since uncovered by Df(1)KA10 = Df(1)11A1;11A7-8 (Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26). #*Gd: Gulloid location: 3-78. origin: Spontaneous in Dp(2;3)P. discoverer: Bridges, 22g26. phenotype: Gd/+ wings shorter, blunter, slightly more spread, and have crossveins closer together than wild type. Homozy- gous lethal. RK3A. cytology: Inseparable from Dp(2;3)P = Dp(2;3)58E3-F2;60D14- E2;96B5-C1. # Gdh: Glutamate dehydrogenase location: 3-81.7 (between hh and tx). references: Caggese, dePinto, and Ferrandino, 1982, Biochem. Genet. 20: 449-60. Novak and Piechowska, 1986, DIS 63: 102-04, 104-07. phenotype: Structural gene for NAD- dependent glutamate dehy- drogenase [GDH (EC1.4.1.4)], which comprises six 57,000 dalton subunits. Enzyme activity inducible by addition of glutamate to medium. Nearly all larval activity can be isolated with the mitochondria. alleles: GdhF and GdhS identified; heterozygote produces broad band on cellulose acetate gel. # Gdh: see Gpdh # gdl: gonadal location: 3-{42}. references: Schultz and Butler, 1989, Genes Dev. 3: 232-42. Schultz, Schlomchik, Cherbas, and Cherbas, 1989, Dev. Biol. 131: 515-23. phenotype: Member of cluster of overlapping genes; gdl is prox- imally overlapped by Eip28/29 and distally by Z600. The func- tion of the gdl gene in the germ lines of both males and females is unknown at present (Schultz and Butler, 1989). cytology: Located in 71C3-D4 (Schultz and Butler, 1989). molecular biology: Gene cloned and partially sequenced. gdl is expressed in either of two modes (male or female). There are four transcripts, both due to different transcription initia- tion sites and multiple polyadylation sites at their 3 ends. gdlM transcripts are first detectable during late larval development, appear at higher levels in pupae, and occur abun- dantly in the testes of adults, being 1200 and 1500 nucleo- tides long; gdlF transcripts are found in adult ovaries, early embryos and Kc cells, are 1000 and 1300 nucleotides long. and have the same terminal exons as gdlM transcripts. A common ORF occurs in all four transcripts. None of these transcripts are found in male or female animals lacking a germ line. In each mode, the longer transcript is the result of a polyadenylation site within the 5 exon of Eip28/29. The two genes Eip28/29 and gdl do not share coding DNA. Transformation experiments indicate that gdl can be expressed outside its normal overlap- ping gene environment. # Gdt-3: see GpdhH and GpdhL #*ge: genitalless location: 1-0.1. origin: Induced by methyl methanesulfonate (CB. 1540). discoverer: Fahmy, 1955. references: 1958, DIS 32: 70. phenotype: External male genitalia absent or grossly deformed. Bristles fine; wings often small and deformed. Tergites abnormal; abdomen frequently contains melanotic tumors. Males viable but sterile. RK3. # Gerec: see Fs(3)Sz9 # gespleten: see gv # gfA: giant fiber A (J.C. Hall; R.A. Wyman) location: 1- 62 (between f and the centromere). origin: Induced by ethyl methanesulfonate. references: Thomas, 1980, Neurosci. Abstr. 6: 742. Thomas and Wyman, 1984, J. Neurosci. 4: 530-38. phenotype: Adults have an aberrant startle response; they do not jump when presented with a lights-off stimulus. The dorso-longitudinal indirect flight muscles (DLMs) are abnor- mally driven by the giant fiber pathway neurons (see entry for ben). DLMs are driven at long and variable latencies after brain stimulation. Morphology of the giant fiber and its response to stimulation is normal. The motor neuron of the tergotrochanteral (jump) muscle is driven normally by the giant fiber. The physiological defect in gfA is probably located at the synapses between the peripherally synapsing interneuron (PSI) and the DLM motor neurons in the thoracic ganglion. gfA complements pas. alleles: allele discoverer synonym _____________________________ gfA1 Thomas nj-54 gfA2 Thomas nj-75 gfA3 Tanouye 4-22-09 gfA4 Baird nj-507 gfA5 Baird nj-520 gfA6 Baird nj-522 cytology: Located between 18A5 to 18D1-2, based on uncovering by Df(1)JA27 = Df(1)18A5;18D1-2. other information: gfA1/Df(1)JA27 is said to be indistinguish- able from gfA1/gfA1 (Thomas and Wyman, 1984). Physiological effects of gfA1 and gfA2 are ostensibly the same. # gg: goggle location: 1-23.1 (no crossovers with oc among 4300 flies). phenotype: Eyes protruding and bulging, placed far back on a narrow head. Facets very large in rough areas. Wings smaller with fringed marginal hairs; dusky; pebbly appearance caused by large cells. Bristles coarse and irregular; hairs sparse and irregular, especially on abdomen. Body small in late counts. Viability reduced. Females usually sterile; males usually fertile. RK3. alleles: allele origin discoverer ref ( comments | _____________________________________________________________________ *gg1 spont Nichols-Skoog, 34e14 2 20% viability gg2 spont Waletsky, 37e 1, 2 postorbital bristles sparse; no oocytes at 19, few at 25, no ovoposition gg3 spont R.F. Grell, 53d 2, 3 both sexes fertile gg4 spont Mohler, 54j28 2, 5 weak allele-pebbly wings diagnostic gg5 / X ray Lefevre 4 gg6 ` X ray Lefevre 4 gglS1 spont Schalet reduced viability gglS2 spont Schalet reduced viability ( 1 = Beatty, 1949, Proc. R. Soc. Edinburg Sect. B: Biol. 63: 249-70; 2 = CP627; 3 = Grell, 1953, DIS 27: 59; 4 = Lefevre, 1981, Genetics 99: 461-80; 5 = Mohler, 1956, DIS 30: 78. | Special phenotypic features differing from description of nominate allele. / Synonym: l(1)C210. Cytology: Tp(3;1)7F9;76B;80B. ` Synonym: l(1)N83. Cytology: In(1)7F9-8A1;9A4. cytology: Placed in 7F10 by Lefevre (1981, Genetics 99: 461- 80) on the basis of two rearranged gg alleles [In(1)N83 = In(1)7F1;9A4 and Tp(3;1)C210 = Tp(3;1)7F1;76B;80]. # ggy: groggy (J.C. Hall) location: 3-between cu and sr (based on mapping of physiologi- cal defects). origin: Induced by ethyl methanesulfonate. references: Timpe, Moats, Jan, and Jan, 1987, Neurosci. Abstr. 13: 578. phenotype: Found as heat-sensitive adult paralytic; in physio- logical experiments on larvae, recordings from neuromuscular junctions show spontaneous depolarizations at room tempera- ture, which probably result from anomalous spontaneous firing of motor neurons (e.g., kainic acid, which blocks evoked junc- tional potentials, also blocks the spontaneous ones); patch- clamp experiments reveal no abnormalities of potassium- dependent-A or delayed-rectifying currents. # gho: ghost location: 2-68. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.) phenotype: Homozygous lethal; embryonic cuticle undifferen- tiated. alleles: Three. # giant: see gt # Giant: see Gt # giant cell defect: see gcd # giant fiber A: see gfA # giant nuclei: see gnu # giant ring gland: see grg # giantoid: see gtd # gl: glass location: 3-63.1. references: Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 188 (fig.). Morgan, Bridges and Sturtevant, 1925, Bibliog. Genet. 2: 214. Pak, Grossfield and White, 1969, Nature (London) 222: 351-54. Moses, Ellis and Rubin, 1989, Nature (London) 340: 531-36. phenotype: Null mutations of glass remove photoreceptor cells in all of the three organs in which they occur. The mutants have compound eyes that are reduced in size and elliptical or diamond shaped; the texture is glassy from fused facets and irregular surface. Ocelli are flattened and lack pigment; there is no ocellar neuropil (Moses et al., 1989). In larvae, the visual Bolwig organs are absent in gl2, but present in gl3. Neither mutant expresses chaoptin (Moses et al., 1989). Color of compound eyes and Malpighian-tubules variably reduced depending on allele. In the presence of the dimorphic sex- linked modifier, msd(gl)d, males have more pigment than females, whereas males have the same eye color as females when they carry the monomorphic allele msd(gl)m [Birchler, 1984, Genet. Res. 44: 125-32]. dsx homozygotes of either X consti- tution but especially XX produce more pigment than dsx+ (Smith and Lucchesi, 1969, Genetics 61: 607-18); however msd(gl) was not controlled by Smith and Lucchesi. Pigmentation increases with increased developmental temperature. At high or very low levels of pigment production the sexual dimorphism disappears. Weak alleles have small smooth eyes and normal pigment levels in both sexes. Mild alleles have eyes reduced to two-thirds normal size and approximately 20% normal eye-pigment levels and male levels approximately 2X female levels. Moderate alleles reduce eye size to half normal and pigment to about 5% normal levels with male levels approximately 3X those of females. Strong alleles have eye area less than half normal, and eyes are virtually colorless in both sexes (Smith and Lucchesi). The optic lamina is virtually nonexistent and the medulla is very small and disorganized in gl1; the lamina and medulla are both small and disorganized in gl2 and gl3 [Mey- erowitz and Kankel, 1978, Dev. Biol. 62: 112-42 (fig.)]. Mosaic studies using gl3 show that the gl genotype of the eye, rather than that of the optic lobe, determines the axon array of the optic lobe (Meyerowitz and Kankel, 1978). Structures of individual neurons studied by S.H. Garen and Kankel (1983, Dev. Biol. 96: 445-56). Retinula cells of the mutant are irregular and rhabdomeres are lacking; the electroretinogram shows no response to light (Pak, Grossfield and White, 1969). gl flies are nonphototactic and males exhibit depressed court- ship activity [Merrell and Underhill, 1956, Genetics 41: 469-85; Hall, Tomkins, Kyriacou, Siegal, Von Schilcher and Greenspan, 1980, Developmental Neurobiology of Drosophila (Siddiqi, Babu Hall and Hall, eds.). Plenum Press, New York, pp. 425-56]. Wing beat frequency increased (Williams and Reed, 1944, Am. Nat. 78: 214-23). alleles: allele origin discoverer ref ( strength _______________________________________________________________ gl1 spont Muller, 18b 2, 4, 5, 11 moderate 12, 15 gl2 spont R.L. King, 1927 4, 5, 11, 13 mild 15 gl3 spont Stern 4-6, 11, 13 weak 15 *gl4 spont Villee, 40d 4, 5, 16, 17 moderate *gl38l spont Steinberg, 38l13 4 *gl40h spont Ives, 40h 4, 5, 9 weak *gl41e spont Oliver, 41e1 5, 14 weak *gl51k spont Edmondson, 51k 5, 7 moderate gl54g spont Hexter, 54g 5, 8 strong gl60j 15 gl62d spont Tano, 62d 3 weak *gl63a spont Ashburner, 63a14 1, 15 mild gl63d | / ray Ives, 63d29 10 weak gl63f spont Ashburner, 63f6 1, 15 mild glB2 EMS Moses 13 glB16 / EMS Moses 13 glBX2 X ray Moses 13 glBX5 X ray Moses 13 glBX6 ` X ray Moses 13 glBX7 / X ray Moses 13 glBX9 X ray Moses 13 glWG1 / ray Moses 13 glWG2 / ray Moses 13 glWG3 / ray Moses 13 ( 1 = Ashburner and Hudson, 1966, DIS 41: 60; 2 = Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. 327: 118 (fig.); 3 = Burdick, 1963, DIS 37: 47; 4 = CP552; 5 = CP627; 6 = Csik, 1929, Biol. Zentralbl. 49: 419-21; 7 = Edmondson, 1952, DIS 26: 60; 8 = Hexter, 1956, DIS 30: 72; 9 = Ives, 1941, DIS 14: 39; 10 = Ives, 1965, DIS 40: 35; 11 = Meyerowitz and Kankel, 1978, Dev. Biol. 62: 112-42 (fig.); 12 = Morgan, Bridges and Sturtevant, 1925, Bibliogr. Genet. 2: 214 (fig.), 226; 13 = Moses, Ellis, and Rubin, 1989, Nature (London) 340: 531-36; 14 = Oliver, 1942, DIS 16: 53; 15 = Smith and Lucchesi, 1969, Genetics 61: 607- 18; 16 = Villee, 1941, DIS 14: 40; 17 = Villee, 1942, Univ. Calif. Publ. Zool. 49: 137; | Associated with T(2;3)gl63d = T(2;3)47B;91A (Robinson and Curtis, 1972, Can. J. Cytol. Genet. 14: 129-37). / Lethal allele. ` Associated with In(3R)glBX6 (Moses et al., 1989). cytology: Located in 91A1-2 since all the DNA in the central restriction map of a wild-type gl genomic clone lies within this polytene band; also In(3R)glBX6 and T(2;3)gl63d appear to have breakpoints within this region (Moses et al., 1989). molecular biology: The glass gene was cloned by chromosome walking and the limits of the gl2gene determined by P-element mediated germline transformation (Moses et al., 1989). The probe from one of the transforming fragments (9,954 bp) hybri- dized to a 3.0 kb poly(A)+ RNA in the heads of adult flies. All of the viable alleles tested affect only this transcript, believed to be that of glass, which is first detected in the early third larval instar, and remains to the adult stage in which it is head-specific. There are five exons and four introns. The 9,954 bp fragment has been sequenced and the predicted sequence of a protein of 604 amino acids determined. The protein encoded by the gl transforming fragment includes five zinc-finger repeats similar to those of the Kr protein but some sequences (Ser-Gln-Ser) have not been found in other zinc-finger proteins. Another fragment was obtained that extends further toward the centromere end of the chromosome and does not rescue glass gene function. The mutant glWG1 deletes about 600 bp near the centromere end of the gl transforming fragment; gl1, gl2, T(2;3)gl63d, and In(3R)glBX6 show breaks within the next region. The weak allele gl3 inserts about 2.5 kb and the allele gl60j inserts more than 30 kb into the third region, and glBX3 removes about 4.5 kb from the distal end of the transforming fragment. All of these alleles are viable. The lethal alleles glB16 and glBX7 occupy the DNA distal to glass at 91A1-2 as well as the distal part of the gl transforming fragment, deleting about 20 and 18.5 kb respectively. # Gl: Glued location: 3-41.4 [0.9 unit from Ly (Mossige, 1935, DIS 4: 59; 1938, Hereditas 24: 110-16)]. references: Plough and Ives, 1934, DIS 1: 31-4. Plough, 1934, DIS 2: 34-5. Plough and Ives, 1935, Genetics 20: 42-69 (fig.). Harte and Kankel, 1982, Genetics 101: 477-501 (fig.) Swaroop, Paco-Larson and Garen, 1985, Proc. Nat. Acad. Sci. USA 82: 1751-55. Swaroop, Sun, Paco-Larson and Garen, 1986, Mol. Cell Biol. 6: 833-41. Swaroop, Swaroop and Garen, 1987, Proc. Nat. Acad. Sci. USA 84: 6501-05. phenotype: Eyes rough, smaller, and oblong; facets rounded; surface smooth and shiny like gl. Pattern, as indicated by staining with monoclonal antibodies, abnormal in the posterior eye disk (Renfrenz and Benzer, 1989, Dev. Biol. 136: 411-29). Architecture of the optic ganglia severely deranged; attribut- able to the mutant genotype of the overlying eye tissue (Mey- erowitz and Kankel, 1978, Dev. Biol. 62: 112-42). Structures of individual neurons studied by S.H. Garen and Kankel (1983, Dev. Biol. 96: 445-56). Somatic-crossover studies and temperature-shift experiments with Glrv50, a temperature- sensitive allele, suggest that Gl+ gene product is required in mid third instar; abnormal retinula fiber projections first observed in late third instar [Harte and Kankel, 1983, Dev. Biol. 99: 88-102 (fig.)]. No electro-retinogram [Grossfield, 1975, Handbook of Genetics (R.C. King, ed.). Plenum Press, New York and London, Vol. 3, p. 690]. Bristles generally shor- tened slightly and straighter than normal. Viability and fer- tility of heterozygote good. With respect to severity of expression Df(3L)Gl2/+ = wild type; Gl/+/+/+ = very weak Glued; Gl/+/+ = weak Glued; Gl/+ = Glued; Gl/Gl/+ = few extreme Glued survivors, Gl/Df(3L)Gl-=Gl/Gl = lethal (Harte and Kankel). RK1. alleles: In addition to Gl1, which occurred spontaneously among the progeny of heat treated flies (Ives, 31f5), both Harte and Kankel (1982) and Garen, Miller, and Paco-Larson (1984, Genet- ics 107: 645-55) induced a number of new mutations and rear- rangements at the locus; these fall into two general classes: (1) new lethal alleles in which the dominant pheno- type is weak or absent, and (2) revertants of Gl1 induced by either ionizing radiation, ethyl methanesulfonate, or hybrid dysgenesis. 17 ethyl-methanesulfonate-induced lethal mutants are lethal in combination with either Gl1 or Df(3L)Gl2 and appear to be point mutations, since they complement lethals in flanking loci. The time of death varies. allele synonym ref ( Gll/Df(3L)Gl2 lethal period _______________________________________________________________ Gl1 3 embryo/early first instar Gll1 Gl1-3 1, 2 embryo/early first instar, cell lethal in eye or cuticle Gll2 Gl7-1 1, 2 embryo/early first instar Gll3 | ` Gl7-6 1, 2 early to mid pupa at 18, late third instar/early pupa at 29 Gll4 Gl5-5 1, 2 embryo/early first instar Gll5 Gl7E 1, 2 embryo/early first instar Gll6 Gl15C 1, 2 embryo/early first instar Gll7 1 embryo/early first instar Gll8 1 embryo/early first instar Gll9 1 embryo Gll10 1 embryo Gll11 1 early pupa Gll12 1 late embryo/early first instar Gll13 1 late embryo/early first instar Gll14 1 early pupa Gll15 1 late embryo/early first instar Gll16 1 late embryo/early first instar Gll17 1 late embryo/early first instar Glll8 Gl5J 2 embryo/early first instar Glll9 Gl5K 2 embryo/early first instar Gll20 Gl29-1 2 embryo/early first instar Gll21 Gl32-2 2 embryo/early first instar Gll22 / Gl34-3 2 mid to late pupa at 18, early to mid pupa at 29 ( 1 = Garen, Miller, and Paco-Larson, 1984, Genetics 107: 645-55; 2 = Harte and Kankel, 1982, Genetics 101: 477-501; 3 = Plough and Ives, 1934, DIS 1: 31-4. | Surviving homozygotes produced at both 18 and 29; homozygous stock can be established at 18 but not 29; in crosses to wild type, homozygous males fertile at both temperatures and eggs maturing at 18 but not at 29 able to produce progeny (Harte and Kankel, 1982). / Gl22 complements or partially complements other lethal alleles of Gl; Gl22/Gl1 lethal at 29; eyes extreme Glued, bristles reduced and wings small and outheld at 18; enhances phenotype of Gll18 and Gll6. *Gll21 also complemented. ` Gll20/Gll3 rarely survive as feeble adults. Approximately one-fourth (22/96) revertants of Gl induced by X or / irradiation fail to complement one or more flanking lethals and are therefore presumed to be deficiencies; those induced by ethyl methanesulfonate and hybrid dysgenesis on the other hand complement all flanking lethals. Phenotypic rever- tants induced by ionizing radiation and ethyl methanesulfonate remain lethal in heterozygous combination with either Gl or Df(3L)Gl2 and with each other; revertants tested in combina- tion with Df(3L)Gl2 die during the first larval instar. The majority of hybrid-dysgenesis-induced revertants (67/78) are viable in heterozygous combination with Df(1)Gl2 and most Gll alleles, whereas they are lethal in combination with Gl1, Gll9, and Gll10; 7/67 are viable in all the above combinations and 4/67 are inviable in all combinations. Available pheno- typic observations on Glrv/+ summarized in accompanying table. allele phenotype of Glrv/+ ______________________________ Glrv3 wild type Glrv9 wild type Glrv17 wild type Glrv18 wild type Glrv22 wild type Glrv24 female sterile Glrv26 weak Glued Glrv32 very weak Glued Glrv33 weak Glued Glrv34 wild type Glrv50 weak Glued Glrv70 weak Glued Glrv72 wild type Glrv73 wild type Glrv80 wild type Glrv86 wild type Glrv296 cytology: Placed in 70C2 on basis of in situ hybridization of cloned sequence (Garen et al., 1984). molecular biology: The Glued locus was cloned by P-element insertion in 70C2 as a chromosome marker (Swaroop et al., 1986). The dominant Gl allele differs from Gl+ in the pres- ence of the transposon roo near the 3 end of the transcribed region, resulting in the formation of a truncated 5.1 kb tran- script instead of the 6 kb transcript of Gl+ (Swaroop et al., 1985). The normal transcript has been found in about all of the tissues of Gl+ homozygotes. The complete cDNA sequence of Gl+ contains an open reading frame encoding 1319 amino acids (Swaroop et al., 1987). There are five exons, two of them in the 5 untranslated region. One of the introns interrupting the Glued ORF encodes at least two polyadenylated transcripts. The Glued polypeptide predicted from the sequence encoded by the ORF has extensive (-helical internal domains (Swaroop et al., 1987). Similar in sequence and structure to those of filamentous proteins of other species. # gl-l: see gl41e # Gla: Glazed location: 2- (rearrangement). references: Morgan, Bridges, and Schultz, 1936, Year Book - Carnegie Inst. Washington 35: 293. phenotype: Eye reduced to one-fourth normal area and narrowed to a point ventrally. Eye color generally diluted but with some black patches. Ommatidia coalesce into gleaming, smooth sheet. Malpighian tubes of larva somewhat lighter than wild type; difficult to classify (Brehme and Demerec, 1942, Growth 6: 351-56). Abdomen of heterozygous female fails to distend with eggs; fertility impaired (Craymer, 1980, DIS 55: 200). Homozygous lethal. RK2A. cytology: Associated with In(2LR)Gla = In(2LR)27D;51E, superim- posed on In(2L)t = In(2L)22D3-E1;34A8-9. # glass: see gl # glass-like: see gl41e # glassy mouth part: see glm # Glazed: see Gla # Gld: Glucose dehydrogenase location: 3-48 (based on 30 st-cu recombinants). synonym: Go: Glucose oxidase. references: Cavener, 1980, Biochem. Genet. 18: 927-37. Cavenar and MacIntyre, 1983, Proc. Nat. Acad. Sci. USA 80: 6268-88. Whetten, Organ, Krasney, Cox-Foster, and Cavener, 1988, Genet- ics 120: 475-84. phenotype: The structural gene for FAD glucose dehydrogenase [GLD (EC1.1.99.10)]. The formation of a hybrid band in GldF/GldS heterozygotes indicates a dimeric enzyme. Molecular weight given as 110,000 daltons. Gene expressed during pupal stages of both sexes; enzyme found in pupal stage 3-4 moulting fluid where it modifies puparium cuticle. Gld also expressed in the ejaculatory duct of males; genital disc transplantation experiments indicate that GLD expression in ejaculatory duct is autonomous (Cavener); enzyme transferred from males to females during copulation. Lethality of null alleles in the pupal stage observed; Gldn flies can be rescued by pre- eclosion excision of pupal operculum. alleles: Two naturally occurring electrophoretic alleles, GldF and GldS and five EMS-induced null alleles Gldn1 - Gldn5. allele origin discoverer synonym ref ( comments | _________________________________________________________ Gldn1 EMS Grigliatti l(3)4.11 1 viable / Gldn2 X ray Denell l(3)d5 1-3 T(2;3)84C8-D1; homozygous lethal Gldn3 EMS Cavener l(3)g9 1 lethal Gldn4 EMS Cavener l(3)g10 1, 3 lethal Gldn5 EMS Cavener l(3)g11 1 lethal GldF spont Cavener GoF 2 GldS spont Cavener GoS 2 ( 1 = Cavener and MacIntyre, 1983, Proc. Nat. Acad. Sci. USA 80: 6268-88; 2 = Cavener, Otteson and Kaufman, 1986, Genetics 114: 111-13; 3 = Lewis, Kaufman, Denell, and Tal- lerico, 1980, Genetics 95: 367-81. | Measured in Gldn/Df(3R)Antp17. / 1% wild-type enzyme activity in pupae and adult males. Gld2 through Gld5 lethal in all pairwise combinations except that Gld2 partially complements Gld4 and Gld5. cytology: Placed in 84D on the basis of its being in the region of overlap between Df(3R)A41 = Df(3R)84B1-2;84D1-2 and Df(3R)dsx29 = Df(3R)84D2-3;84F8-10 (Cavener, Otteson and Kauf- man, 1986, Genetics 114: 111-23). molecular biology: Structural gene cloned from EMBL-4 Oregon-R genomic library (Cavener, Corbett, Cox, and Whetten, 1986, EMBO J. 5: 2939-48). Clones identified by locating deficiency and translocation breakpoints delimiting Gld. A 2.8 kb poly(A) RNA transcript identified with temporal and spatial expression similar to that of Gld. Expression of Gld induced immediately before larval and pupal moults. The three 5 exons of the gene have been sequenced and the start sites for transcription and translation identified (Whetten et al., 1988). The first exon contains 335 nucleotides; the second exon contains the Gld translation start codon. The putative amino acid sequence at the amino terminus has three serine- alanine tandem repeats and numerous cysteine residues. The Gld lethal phenotype was rescued by P-element-mediated germ- line transformation (Whetten et al., 1988). # gleam: see gm #*gli: glide location: 1-38.0. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 70. phenotype: Wings held horizontally at right angles to body. Pigmentation of tergites frequently interrupted along mid- dorsal line; tergites occasionally show a nick in the poste- rior border. Males sterile; viability about 70% wild type. RK2. # glisten: see gn # glossy: see lz # glossy like: see sno # Glt: Glutactin location: 2-{30}. references: Fessler and Fessler, 1989, Annu. Rev. Cell Biol. 5: 309-39. phenotype: Encodes an acidic sulfated glycoprotein of basement membranes. cytology: Placed in 29D by in situ hybridization. molecular biology: Gene sequenced and found to code for a 1024-residue polypeptide that has a signal peptide, a major amino domain of 600 residues with the coding region inter- rupted by one intron, and an acidic carboxyl domain. Amino and carboxyl domains separated by 13 threonine residues; four O-sulfated tyrosines present. The protein preferentially binds Ca++ in the presence of excess Mg++. # Glu: |-Glucuronidase location: 3-{101}. references: Langley, S.D., Wilson, Gross, and Finnerty, 1983, J. Biol. Chem. 258: 7416-24. phenotype: May or may not be a structural gene for |-D- Glucuronidase (EC 3.2.1.31). The enzyme is a glycoprotein and exists in two chromatographically separable forms. Form I is membrane bound, has a pI of 8.0 - 8.5, and can be irreversably inactivated by either incubation at 55 for 20 min or by incu- bation at 37 in the presence of 6M urea; form II exists in both membrane-bound and free states, has a pI of 4.5, and is resistant to inactivation by the above treatments. The two are kinetically similar, having similar Km and Vmax and are precipitated by antibody raised against form II. alleles: GluH has high activity owing to the presence of both forms I and II; GluL has the same level of form II activity but lacks form I and exhibits low activity. Heteroallelic genotypes exhibit intermediate levels of form I activity. Observations suggests that GluH may be a duplication or GluL is an amorphic mutant in a duplicate gene. cytology: Placed in 98F-100F by gene dosage studies. # Glucose dehydrogenase: see Gld # Glucose oxidase: see Gld # |-Glucuronidase: see Glu # Glue proteins: see Sgs # Glued: see Gl # Glutactin: see Glt # Glutamate dehydrogenase: see Gdh # Glutamate oxaloacetic transaminase: see Got # Glutamine pyruvate transaminase: see Gpt # Glutamine synthetase: see Gs # Glyceraldehyde dehydrogenase: see Gapdh # (-Glycerol phosphate dehydrogenase: see Gpdh # (-Glycerophosphate oxidase: see Gpo Glycinamide ribotide transformylase: see ade3 # gly: see lzg # gm: gleam location: 3- (not located). origin: Spontaneous. discoverer: Bridges, 27c1. phenotype: Eyes small and rough; irregular hairs and facets cause glints. Body small. Viability about 10% wild type but variable. RK3. cytology: Associated with In(3L)P, according to Bridges (Mor- gan, Bridges, and Schultz, 1937, Year Book - Carnegie Inst. Washington 36: 301). # gmp: see fliF #*gn: glisten location: 3-67.3. origin: / ray induced. discoverer: Wallbrun, 61i6. references: Eyes rough but of normal size; facets and hairs irregular. RK2. # gnd: grounded (J.C. Hall) location: 1-58 (proximal to f). origin: Induced by ethyl methanesulfonate. synonym: Originally called 694, 623, 200 (Deak et al., 1980). references: Deak, Rahmi, Bellamy, Bienz, Blumer, Fenner, Golin, Ramp, Reinhardt, Dubendorfer, and Cotton, 1980, Development and Neurobiology of Drosphila (Siddiqi, Babu, Hall, and Hall, ed.). Plenum Press, New York, pp. 183-92. Deak, Bellamy, Bienz, Dubuis, Fenner, Gollin, Rahmi, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81. Homyk and Emerson, 1988, Genetics 119: 105-21. phenotype: Flight is defective; indirect flight muscles have relatively mild abnormalities of Z-bands and myofibrils; mosaic analysis suggests that thoracic nerves or muscles could be primary site of mutant defect. All alleles lead to reduced amount of at least two high molecular-weight proteins from indirect flight muscles. alleles: Three mutant alleles: gnd1, gnd2, gnd3. other information: Could be allelic to fltM, fltN, fltO, flrdR, or flrdQ. # gnu: giant nuclei location: 3-42.5. origin: Induced by ethyl methanesulfonate. references: Freeman, Nusslein-Volhard, and Glover, l986, Cell 46: 457-68. phenotype: Maternal-effect lethal. Embryos produced by homozy- gous or hemizygous females exhibit normal levels of DNA syn- thesis, but do not display normal nuclear division; a small number of giant nuclei formed. Cytoplasmic elements such as centrosomes, microtubules, and actin appear to attempt to fol- low the normal developmental program, demonstrating that con- trol of nuclear and cytoplasmic components of syncytial nuclear divisions can be uncoupled. cytology: Placed in 70D2 or 70E4-8 on the basis of its inclu- sion in Df(3L)fz-m21 = Df(3L)70D2-3;70E4-5 but not Df(3L)fz- d21 = Df(3L)70D3;70E3-8. # Go: see Gld # Go: Gold tip location: 2-64.3 (57.5 to 71.1; between cn and cg). origin: Spontaneous. discoverer: Sturtevant, 1948. references: 1948, DIS 22: 55. phenotype: Tips of many bristles and hairs pale and curved. Bristles often short (tips broken off ?). Wild-type bristles sometimes have pale tips, thus interfering with positive clas- sification. Lethal when homozygous. Expression best at low temperatures. RK2. # goggle: see gg # Gold tip: see Go # gonadal: see gdl # gooseberry: see gsb # Got1: Glutamate oxaloacetic transaminase location: 2-75 (between L and nwD). synonym: Designated Got2 by Band (1975) and also by Cavener and Clegg (1976). references: Band, 1975, Genetics 80: 761-71. Cavener and Clegg, 1976, J. Hered. 67: 313-14. Grell, 1976, Genetics 83: 753-64. Chase and Kankel, 1987, J. Neurobiol. 18: 15-41. phenotype: The structural gene for the more rapidly anodally migrating of two glutamate oxaloacetic transaminases [GOT1 (EC 2.6.1.1) = L -aspartate: 2-oxyglutarate aminotransferase] found in Drosophila. alleles: Two alleles described by Grell, Got1M, monomorphic in all stocks examined and Got1lo an ethyl methanesulfonate- induced allele with low activity; Got1lo homozygotes normal in viability and fertility. cytology: Located at 52D9-15. # Got2 location: 2-4.8 [based on 70 al-cl recombinants (Cavener and Clegg)]. references: Band, 1975, Genetics 80: 761-71. Cavener and Clegg, 1976, J. Hered. 67: 313-14. Grell, 1976, Genetics 83: 753-64. Chase and Kankel, 1987, J. Neurobiol. 18: 15-41. phenotype: The structural gene for the more slowly anodally migrating of the two glutamate oxalacetic transaminases. Enzyme is a dimer based on formation of a hybrid molecule. alleles: The most common allele is designated Got1 by Band, Got24 by Voelker and Langley (1978, DIS 53: 117), and Got2M by Grell; we establish Got21 as the designation. allele synonym ref ( anodal migration _________________________________________________ Got21 Got11 1, 2 Got21 Got26 6 Got27 6 >Got22 Got2J | 3 >Got21 Got2n4 Got2 / 40058 5 Got2nJ Got2nJH385 =Got21? Got2nNC Got2nNC1 4 =Got21 Got2nNC2 4 =Got21 Got2nNC3 4 ( 1 = Band, 1975, Genetics 80: 761-71; 2 = Cavener and Clegg, 1976, J. Hered. 67: 313-14; 3 = Grell, 1976, Genetics 83: 753-64; 4 = Langley, Voelker, Leigh Brown, Ohnishi, Dickson and Montgomery, 1981, Genetics 99: 151-56; 5 = Racine, Langley, and Voelker, 1980, Environ. Mutagen. 2: 167-77; 6 = Research Triangle Park, 1978, DIS 53: 117. | Induced by EMS in Got21. cytology: Placed in 22A7-B7 on the basis of its being distal to the 2L breakpoint of T(Y;2)H56 = T(Y;2)22B5-8 and its inclu- sion in Df(2L)S2 = Df(2L)21D1;22A6-B1. # gouty legs: see gy