# To: see Sod # Told: see Fs(2)Sz11 # Toll: see Tl # tolloid: see tld # tom: see ix2 # Tomaj: see Fs(3)Sz22 # tomboy: see ix2 #*ton: tonochaetae location: 1-60.1. origin: Induced by 1:4-dimethanesulfonoxybut-2-yne (CB. 2058). discoverer: Fahmy, 1951. references: 1958, DIS 32: 76. phenotype: Bristles short and thin. Eyes large, have deranged facets. Wings short, have incised inner margins and abnormal venation. Variable expression of eye and wing effects. Eclo- sion slightly delayed. Male infertile; viability about 50% wild type. Female sterile. RK2. other information: One allele induced by CB. 1506. # Tonuz: see Fs(3)Sz23 # tonomacrochaetae: see tmc # top: see Egfr # Top2: Topoisomerase 2 location: 2- {53} (very close to Sd). references: Hsieh and Brutlag, 1980, Cell 21: 115-25. Sander and Hsieh, 1983, J. Biol. Chem. 258: 8421-28. Shelton, Osheroff, and Brutlag, 1983, J. Biol. Chem. 258: 9530-35. Sander, Nolan, and Hsieh, 1984, Proc. Nat. Acad. Sci. USA 81: 6938-42. Berrios, Osheroff, and Fisher, 1985, Proc. Nat. Acad. Sci. USA 82: 4142-46. Udvardy, Schedl, Sander, and Hsieh, 1985, Cell 40: 933-41. Wang, 1985, Ann. Rev. Biochem. 54: 665-97. Heller, Shelton, Dietrich, Elgin, and Brutlag, 1986, J. Biol. Chem. 261: 8063-69. Nolan, Lee, Wyckoff, and Hsieh, 1986, Proc. Nat. Acad. Sci. USA 83: 3664-68. Hsieh, Lee, Nolan, and Wyckoff, 1987, NCI Monographs 4: 7-10. Wyckoff, Natalie, Nolan, Lee, and Hsieh, 1988, J. Mol. Biol. 205: 1-13. phenotype: Top2 is an essential gene that encodes the large subunit of type II DNA topoisomerase, an enzyme believed to play an important role in the condensation, decondensation, and segregation of chromosomes. The enzyme is a major com- ponent of the nuclear matrix of Drosophila cells (Berrios et al., 1985) and is distributed along polytene chromosomes paralleling the distribution of the DNA (Heller et al., 1986). It is believed to act by passing a DNA segment through a tran- sient double-stranded break in another segment. Major cleavage sites for type II topisomerase have been found in nontranscribed spacer segments and in the 5' and 3' ends of Hsp70 and the histone genes (Udvardy et al., 1985). When prepared from embryos, the purified enzyme is made up of a major polypeptide encoded by Top2 of 166,000 daltons, with binding sites for both DNA and ATP, and, in addition, smaller polypeptides of 30,000-40,000 and 132,000-145,000 daltons (Sander and Hsieh, 1983; Shelton et al., 1983; Heller et al., 1986). Protein kinase activity is associated with Drosophila topoisomerase II (Sander et al., 1984; Ackerman, Glover, and Osheroff, 1985, Proc. Nat. Acad. Sci. USA 82: 3164-68). cytology: Located at 37D2-6 (Nolan et al., 1986; Hsieh et al., 1987) or at 36E1-2 (Philip, Heller, and Brutlag) by in situ hybridization to the salivary chromosomes. It is a single-copy gene. molecular biology: Top2 has been cloned and the DNA sequenced (Nolan et al., 1986; Hsieh et al., 1987; Wyckoff et al., 1988). The gene is 5.1 kb in length, as would be expected for a gene encoding topoisomerase II (MW about 170,000) and is divided into five exons of approximately 230, 600, 400, 3100, and 700 nucleotides (Nolan et al., 1986) and four introns of 933, 57, 66, and 81 nucleotides (Wyckoff et al., 1988). The direction of transcription is thought to be from centromere toward telomere (Hsieh). The predicted protein is 1447 amino acids in length with a molecular weight of 164,424. Droso- phila topoisomerase II shows significant sequence identity with the type II topoisomerases of B. subtilis, E. coli, bac- teriophage T4, and two yeasts. The overall sequence identity between Drosophila and yeast is about 46% (Wyckoff and Hsieh, 1988, Nat. Acad. Sci. USA 85: 6272-76). cDNA sequences encoding Drosophila topoisomerase II, when under the tran- scriptional control of a yeast promoter, were able to comple- ment the lethality of temperature-sensitive or null yeast mutants (provided the Drosophila genes were continually expressed by growth of yeast cells in galactose media) (Wyck- off and Hsieh, 1988). # tor: torso location: 2- {57}. references: Schupbach and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 302-17. Nusslein-Volhard, Frohnhofer, and Lehmann, 1987, Science 238: 1675-81. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. Klingler, Erdelyi, Szabad, and Nusslein-Volhard, 1988, Nature (London) 335: 295-77. Casanova and Struhl, 1989, Genes Dev. 3: 2025-38. Schupbach and Wieschaus, 1989, Genetics 121: 101-17. Sprenger, Stevens and Nusslein-Volhard, 1989, Nature (London) 338: 478-83. Strecker, Halsell, Fisher, and Lipschitz, 1989, Science 243: 1062-66. phenotype: Maternal-effect lethal; embryos from homozygous mothers show alterations in the anterior-posterior pattern. Hypoactivity (loss-of-function) mutant embryos lack anterior- most head structures (labrum, dorsal bridges) as well as structures posterior to the seventh abdominal segment. Hyperactivity (gain of function) mutant embryos, on the other hand, show segment defects in the middle of the embryos, but may have enlarged terminal structures (Klingler et al., 1988; Strecker et al., 1989). A large number of revertants have been obtained from dominant or semi-dominant hypermorphic alleles. During cellularization at the blastoderm stage, hypoactivity mutant embryos show a "pole hole" phenotype. A funnel of yolk-free cytoplasm with a small number of nuclei (between 10 and 20) is formed at the posterior pole, extending from the egg periphery to the inner yolk mass. At gastrulation the cephalic furrow is shifted toward the anterior and the germ- band extends all the way to the posterior end. Analysis of germline clones indicates that the torso mutant is germline autonomous (Schupbach and Wieschaus, 1986, Dev. Biol. 113: 443-48). alleles: Unless indicated otherwise, alleles are assumed to be recessive. rv in superscript = revertant. allele origin discoverer synonym comments ________________________________________________________________ tor1 EMS Wieschaus, torWK Nusslein-Volhard tor2 EMS Schupbach, torHH Wieschaus tor3 EMS Schupbach, torHM Wieschaus tor4 EMS Schupbach, torPM Wieschaus tor5 EMS Schupbach, torQA Wieschaus tor6 EMS Schupbach, torQK2 5 kb insertion Wieschaus tor7 EMS Schupbach, torQ4 Wieschaus tor8 EMS Schupbach, torQL Wieschaus tor9 EMS Schupbach, torRI Wieschaus tor10 EMS Mohler torJM tor11D EMS Schupbach splcRL3, semidominant; torsplc, heat-sensitive torRL3 tor12D EMS Klingler torY9 semidominant tor13D EMS Szabad tor4021 dominant tor14 HD Schupbach torTC17 2.9 kb insertion torrv1 EMS Klingler torre1 torrv2 EMS Klingler torre2 torrv3 EMS Klingler torAL1 torrv4 EMS Klingler torAL2 torrv5 EMS Klingler torAL3 torrv6 EMS Klingler torAL4 torrv7 EMS Klingler torAL5 torrv8 EMS Klingler torAL6 torrv9 EMS Klingler torAL7 torrv10 EMS Klingler torAL8 torrv11 EMS Klingler torAL9 torrv12 EMS Klingler torAL10 torrv13 EMS Klingler torAL11 torrv14 EMS Klingler torAL12 torrv15 EMS Klingler torAL13 torrv16 EMS Klingler torAL14 torrv17 EMS Klingler torAL15 torrv18 EMS Klingler torAL16 torrv19 EMS Klingler torAL17 torrv20 EMS Klingler torAL18 torrv21 EMS Klingler torAY1 torrv22 EMS Klingler torAY2 torrv23 EMS Klingler torAY3 torrv24 EMS Klingler torAY4 torrv25 EMS Klingler torAY5 torrv26 EMS Klingler torAY6 torrv27 EMS Klingler torAY7 torrv28 EMS Klingler torAY8 torrv29 EMS Klingler torAY9 torrv30 EMS Klingler torAY10 torrv31 EMS Klingler torAY11 torrv32 EMS Klingler torAY12 torrv33 EMS Klingler torAY13 torrv34 EMS Klingler torAY14 torrv35 EMS Klingler torAY15 torrv36 EMS Klingler torAY16 torrv37 EMS Klingler torAY17 torrv38 EMS Klingler torAY18 torrv39 EMS Klingler torAY19 torrv40 EMS Klingler torAY20 torrv41 EMS Klingler torAY21 torrv42 EMS Klingler torAY22 torrv43 EMS Klingler torAY23 torrv44 EMS Klingler torAY24 torrv45 EMS Klingler torAY25 torrv46 EMS Klingler torAY26 torrv47 EMS Klingler torAY27 torrv48 EMS Klingler torAY28 torrv49 EMS Klingler torAY29 torrv50 EMS Klingler torAY30 torrv51 EMS Klingler torAY31 torrv52 EMS Klingler torAY32 torrv53 EMS Klingler torAY33 torrv54 EMS Klingler torAY34 torrv55 EMS Klingler torAY35 torrv56 EMS Klingler torAY36 torrv57 EMS Klingler torAY37 torrv58 EMS Klingler torAY38 torrv59 EMS Klingler torAY39 torrv60 EMS Klingler torAY40 torrv61 EMS Klingler torAY41 torrv62 EMS Klingler torrx2 torrv63 EMS Klingler torrx8 torrv64 EMS Klingler torrx9 torrv65 ( EMS Klingler torYRE16 torrv66 | EMS Klingler torXR1 9.5 kb deletion torrv67 / EMS Klingler torXY83 0.5 kb insertion ( Revertant of tor12D (Klingler et al., 1988). | Revertant of tor11D (Sprenger et al., 1989). / Revertant of tor12D (Sprenger et al., 1989). cytology: Placed in 43C5-E7 by deficiency mapping (Schupbach and Wieschaus, 1989) and 43E by in situ hybridization (Casanova and Struhl, 1989; Sprenger et al, 1989). molecular biology: Gene cloned from DNA isolated by P-element transposon tagging from tor14 (=torTC17), an allele carrying a P insert (Sprenger et al., 1989). Two clones hybridized to tor+ salivary chromosomes at 43E5-11. 35 other tor mutants were analyzed and three of them (as well as tor14) showed res- triction map alterations in the cloned region. Rescue of the tor1 mutant was accomplished by germ-line transformation with P elements using a 12 kb EcoRI fragment carrying tor+ (Sprenger et al., 1989). A transcript of 3.6 kb was demonstrated by Northern blot analysis in tor+ mRNA (transcript not shown in torrv66 mRNA). This transcript was also demonstrated by in situ hybridization of tor+ mRNA to tissue sections of wild-type ovaries; a high level of evenly-distributed transcript was found in nurse cells and oocytes as well as in 0-4 hour-old embryos. The transcript level was much reduced in older embryos, but some could be detected throughout development. A high level of transcript expression was found in adult females, but not in males. The genomic and cDNA's of torso have been sequenced (Sprenger et al., 1989) and the amino acid sequence of the protein predicted. The 3.6 kb transcript includes at least 13 introns, their lengths varying from 54 to 152 kb. The cDNA sequence includes a single open reading frame of 2,936 bp, 2,768 bp of which encode a putative protein of 923 amino acids. Although the amino-terminal half of the torso protein shows no significant identity to any published sequences, the rest of the protein shows significant amino-acid identity to growth-factor receptor tyrosine kinases of other organisms and includes an intermediate hydrophobic region of 22 bp that resembles in structure the transmembrane domain of the recep- tor protein kinases (Sprenger et al., 1989). The tor protein is associated with the surface membrane in early embryos and is distributed everywhere along the cell surface (Casanova and Struhl, 1989), although its activity is localized at both poles. Different levels of active tor protein are able to specify distinct parts of the terminal pattern. other information: A single dose of tll1 from a tor11D/tor11D mother can partially rescue the tor11D mutant effect in the embryo (loss of abdominal segments); complete rescue may occur when the embryo is homozygous for tll1, receiving the gene from both parents (Strecker et al., 1989). Injection of tor+ cytoplasm from early cleavage embryos can partially rescue tor loss-of-function mutants. ftz expression is reduced or lost in strong gain-of-function mutants (Klinger et al., 1988; Strecker et al., 1989). phl mutations have been found to be epistatic over tor gain-of-function alleles (Nusslein-Volhard et al.). # torp: torpid (J.C. Hall) location: 1-15.5. origin: Induced by ethyl methanesulfonate. references: Singh and Siddidqi, 1981, Mol. Gen. Genet. 181: 400-02. phenotype: Adults reversibly paralyzed at 35 or higher. Time of onset of paralysis increases as temperature is lowered (down to 35); recovery period on return to room temperature is directly proportional to length of high-temperature paralysis time. Flies seem normal after development at 29 or below; larvae unaffected behaviorally at temperatures up to 39. After anterior nerve stimulation, responses of flight muscles are blocked in all-or-none fashion at about 35. Mosaic exper- iments suggest that heat-induced paralysis of individual legs is due to neural defects, possibly in thoracic ganglia. # torpedo: see Egfr # torpid: see torp # torso: see tor # torsolike: see tsl # tov: tiny ovaries location: 3- (unmapped). origin: Induced by ethyl methanesulfonate. discoverer: Nusslein-Volhard. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. phenotype: Female sterile; no eggs laid; ovaries rudimentary; may be agametic. alleles: allele synonym ___________________ tov1 tov012 tov2 tov155 tov3 tov267 tov4 tov345 tov5 tov404 # Tp1: Temporal protein 1 location: 2- {54}. synonym: T1. references: Fruscoloni, Al-Atia, and Jacobs-Lorena, 1983, Proc. Nat. Acad. Sci. USA 80: 3359-63. phenotype: Present during oogenesis and later embryogenesis, gene codes for small, acidic protein (TI). cytology: Located in 39C-D by in situ hybridization. molecular biology: mRNAs (prepared from egg chambers or embryos) translated in a cell-free system; found to be associ- ated with polysomes in eggs and 18 hr embryos, but not in early embryos. Cloned probe with cDNA complementary to Tp1 mRNA hybridized to salivaries. # Tpi: Triosephosphate isomerase location: 3-101.3 (between Acph-1 and bv). references: Voelker, Langley, Leigh-Brown, and Ohnishi, 1978, DIS 53: 200. Voelker, Ohnishi, and Langley, 1979, Biochem. Genet. 17: 769-83. Voelker, Langley, Leigh-Brown, Ohnishi, Dickson, Montgomery, and Smith, 1980, Proc. Nat. Acad. Sci. USA 77: 1091-95. phenotype: Structural gene for the glycolytic enzyme triosphos- phate isomerase [TPI (EC5.3.1.1)] found in muscle. Heterozy- gote contains the parental isozymes plus a hybrid isozyme. alleles: Two electrophoretic alleles, Tpi4, the most common and slower allele, and Tpi6, the fast allele (Voelker et al., 1979). cytology: Located in 99B-E since included in the duplication segregant of Tp(3;Y)L127 = Tp(3;Y)99B;99E. # Tpl: Triplo-lethal location: 3-47.4 (Roehrdanz and Lucchesi, 1980); to the left of Ki [no ri-Tpl crossovers among 59 ri Ki recombinants (Dorer and Christensen)]. origin: Segmental aneuploidy, using the Y-autosome transloca- tions T(Y;3)L132 and T(Y;3)A109 (Lindsley et al., 1972). references: Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero, 1972, Genetics 71: 157-84. Denell, 1974, DIS 51: 124. 1976, Genetics 84: 193-210. Keppy and Denell, 1979, Genetics 91: 421-41. Lucchesi and Roehrdanz, 1979, Genetics 91: s71. Roehrdanz and Lucchesi, 1979, Genetics 91: s105. 1980, Genetics 95: 355-66. 1981, Dev. Genet. (Amsterdam) 2: 147-58. Kennison and Russell, 1987, Genetics 116: 75-86. Dorer and Christensen, 1989, Genetics 122: 397-401. phenotype: Unique dosage-sensitive locus at 83D-E; lethal when present in either one (Tpl/Df) or three doses (Tpl/Dp) in an otherwise diploid individual. These individuals do not sur- vive to the adult stage, but a few larvae with three doses of 83D-E develop to the third instar. The surviving larvae are also hyperploid for the X chromosome (as in 3X;2A metafe- males); they can be produced in genotypes duplicated for 7C and 7D-E (Roehrdanz and Lucchesi, 1979, 1981). Flies with a deficiency for 83D-E in one 3 and a duplication for the region in the other (two doses in all) are viable (Denell, 1976). Crosses of these Df/Dp flies to wild-type (Tpl-normal) mates fail to produce viable adults (Keppy and Denell, 1979). When wild-type flies or flies bearing a duplication and a defi- ciency for 83D-E (i.e., viable Df/Dp stocks) are treated with EMS or /-rays (Keppy and Denell, 1979; Roehrdanz and Lucchesi, 1980), new deficiencies and mutations that are viable over Tpl duplications but lethal over Tpl deficiencies and Tpl-normal chromosomes are produced. No function in measuring the X/A ratio has been observed in Tpl; it does not interact with the sex-determining genes Sxl and da (Christiansen and Lucchesi, 1988, DIS 67: 15). alleles: Cytologically normal reversions to the wild-type Tpl phenotype at 83D-E were obtained by mutagen-treatment of Df Tpl/Dp Tpl flies. Complementation tests confirm the allelism of these mutants; they are viable over Tpl-duplicated and Tpl-normal chromosomes, but lethal over Tpl deficiencies; they are homozygous lethal. Tpl deficiencies (viable over Tpl duplications; lethal over Tpl-deficient and Tpl-normal chromo- somes) are described in the section on chromosome rearrange- ments. Tpl reversions are listed in the following table: revertant origin synonym ref ( ____________________________________ Tplrv1 EMS 10d77-6 2 Tplrv2 HCHO 18i77 2 Tplrv3 | EMS tpl10 1, 3 Tplrv4 | EMS tpl17 1, 3 Tplrv5 | EMS tpl38 1, 3 ( 1 = Dorer and Christensen, 1989, Genetics 122: 397-401; 2 = Keppy and Denell, 1979, Genetics 91: 421-41; 3 = Roehrdanz and Lucchesi, 1980, Genetics 95: 355-66. | Causes an increase in recombination between flanking markers of 6.5-10.5 times, while recombination in other adjacent regions is not changed. cytology: Located in 83D5-E1 since included in Df(3R)Tpl4 = Df(3R)83D4-5;83E1-2 and Df(3R)Tpl7 = Df(3R)83D4-5;83E1-2 (Keppy and Denell, 1979). # Tpn: Troponin location: 2- {67}. discoverer: French and Pardue. phenotype: Structural gene for troponin-C. cytology: Placed in 49D3-50A3 based on the deletion of the cloned sequence in Df(2R)vg = Df(2R)49D3-4;49F15-50A2-3. # tpw: see stotpw #*tr261: triangle 261 location: 3- (not located). origin: Spontaneous. discoverer: Spencer. references: 1934, DIS 1: 35. 1935, Am. Naturalist 69: 222-38. phenotype: Small extra crossvein between marginal vein and L2, near their juncture. Variable; overlaps wild type. RK3. # tra: transformer (M. McKeown and J.M. Belote) location: 3-45 (between st and cp). origin: Spontaneous. references: Sturtevant, 1945, Genetics 30: 297-99. Brown and King, 1961, Genetics 46: 143- 56. Marsh and Wieschaus, 1978, Nature 272: 249-51. Belote, McKeown, Andrew, Scott, Wolfner, and Baker, 1985, Cold Spring Harbor Symp. 50: 605-14. Butler, Pirrotta, Irminger-Finger, and Nothinger, 1986, EMBO J. 5: 3607-3613. McKeown, Belote, and Baker, 1987, Cell 48: 489-499. McKeown, Belote, and Boggs, 1988, Cell 53: 887-95. Belote, McKeown, Boggs, Ohkawa, and Sosnowski, 1989, Dev. Genet. 10: 143-54. phenotype: XX flies homozygous for tra transformed into sterile males with fully developed sex combs, male-colored abdomen, male abdominal tergites and plates, external and internal male genitalia. Mate readily with females. Testes rudimentary, without sperm, and with ovarian nurse-cell-like cells [Brown and King, 1961]. Testes reduced in size, but of normal color and shape. Transformed female slightly larger than normal male, developmental rate about that of female. X/X/Y; tra/tra also sterile. tra not required in male since X/Y, tra/tra flies are normal males. X/X/X and X/X/Y, tra/tra/tra like diploid, i.e. male in phenotype, but with larger wing cells as expected of triploids. Normal testis anlagen transplanted into tra female becomes attached to duct apparatus and pro- duces sperm. Not needed for female germ cell development since X/X, tra/tra pole cells transplanted into a wild-type female embryo give rise to progeny of both sexes [Marsh and Wieschaus, 1978]. Cell autonomous in mitotic clones [Baker and Ridge, 1980, Genetics 94: 383-423]. alleles: allele origin discoverer synonym __________________________________________ tra1 ( spont Sturtevant tra tra2 | spont Carpenter traAC tra3 / EMS Roost traZ4 tra4 | EMS Hoffmann traV1 tra5 | EMS Hoffmann traV2 tra6 ( HD Jacquenoud traZ5 ( tra1 and tra6 result from ~1 kb deletions which remove most or all of the tra locus. | tra2, tra4 and tra5 are not detectably rearranged. / tra3 contains an insertion of ~200 bases. cytology: Placed in salivary chromosome region 73A8-9 as a result of its exclusion from Df(3L)st-E5 and Df(3L)st-7P and its inclusion in Df(3L)st-E52 and Df(3L)st-g24 [Belote et al., 1985; Butler et al., 1986; McKeown et al., 1987]. molecular biology: tra has been cloned [Belote et al., 1985; Butler et al., 1986; McKeown et al., 1987] and shown to lie approximately 85 kb to the right of st, at position +85 in the map of McKeown et al. or position -1 in the map of Butler et al. The immediately adjacent gene on the distal side is l(3)73Ah [Boggs, Gregor, Idriss, Belote, and McKeown, 1987, Cell 50: 739-747]. The gene immediately to the proximal side has not been identified mutationally. Nucleotide sequences have been obtained for the genomic region around tra, for the non-sex-specific cDNA, and for the female-specific cDNA; the sequence of the putative female-specific tra protein has been inferred (Boggs et al, 1987). The tra transcription unit is just over 1050 nucleotides long. Transcription is from proxi- mal to distal. There are two size classes of tra RNA. One is 0.9 kb and is female-specific and the other is 1.1 kb and is present in both sexes. Both of these overlap the 3' end of l(3)73Ah by about 70 bases. These two classes of RNA differ as a result of the use of an alternative splice acceptor for the first intervening sequence. The 0.9 kb RNA has a single long open reading frame and is capable of supplying essentially all tra+ function while the 1.1 kb RNA has no long open reading frame and is dispensable in both males and females [Boggs et al., 1987; McKeown et al., 1988]. Sex-specific splicing, but not transcription, is dependent upon Sxl+. There is no requirement for tra+, tra2+ or dsx+ for transcription or sex- specific splicing of tra [McKeown et al., 1988; Nagoshi, McKeown, Burtis, Belote, and Baker, 1988, Cell 53: 229-36]. Expression of the 0.9 kb RNA causes XY flies to develop as somatic females. This transformation is independent of Sxl+ and dependent upon tra2+, dsx+ and ix+ [McKeown et al., 1988]. Molecular studies of dsx show that lack of tra+ expression results in dsx being expressed in its male mode [Nagoshi et al., 1988], while gain of tra+ expression results in dsx being expressed in its female mode [McKeown et al., 1988]. This sug- gests that, in a formal genetic sense, the regulatory hierar- chy controlling sex is organized in the following order: X:A ratio > Sxl > tra > tra2 > dsx _ ix > terminal differentiation (Belote et al., 1989). # traD: see dsxD # tra2: transformer 2 location: 2-70, between Bl and L (Watanabe, 1975). references: Watanabe, 1975, Jpn. J. Genet. 50: 269-71. Fujihara, Kawabe, and Oishi, 1978, J. Hered. 6: 229-36. Baker and Ridge, 1980, Genetics 94: 383-423. Belote and Baker, 1981, Genetics 97: s9. Ota, Fukunaga, Kawabe, and Oishi, 1981, Genetics 99: 429-41. Baker and Belote, 1983, Annu. Rev. Genet. 17: 345-83. Belote and Baker, 1983, Dev. Biol. 95: 512-17. Belote, Handler, Wolfner, Livak, and Baker, 1985, Cell 40: 339-48. Butler, Pirrota, Irminger-Finger, and Nothiger, 1986, EMBO. J. 5: 3607-13. Belote and Baker, 1987, Proc. Nat. Acad. Sci. USA 84: 8026- 30. Amrein, Gorman, and Nothiger, 1988, Cell 55: 1025-35. Goralski, Edstrom, and Baker, 1989, Cell 56: 1011-18. Mattox, Palmer, and Baker, 1990, Genes Dev. 4: 789-805. phenotype: One role of tra2+ (like tra+) is to regulate sex determination by directing dsx+ in such a way that female pri- modia are expressed and male primodia repressed in chromosomal females. In addition, tra2+ serves as a regulator of sper- miogenesis and copulation; as a result, functional sperm are produced by chromosomal males and transmitted to the females. Null or amorphic tra2 mutations, however, transform chromo- somal females into flies that are phenotypically male in regard to external cuticular morphology, pigment pattern, internal genital ducts, and mating behavior. Their gonads are much reduced and lack sperm and they are not affected by mle (Fujihara et al., 1978). tra2 mutations in chromosomal males produce normal looking adult males showing normal sexual behavior, but the sperm are amotile (Watanabe, 1975; Belote and Baker, 1981). Some tra2 mutants are temperature- sensitive; homozygotes become phenotypic males when reared at 29, but phenotypic females when reared at 16 (Belote and Baker, 1983). When X/X;tra2ts2 homozygotes are shifted to the female-specifying temperature during or before the third instar, no development of the male accessory glands occurs (Chapman and Wolfner, 1988, Dev. Biol. 126: 195-202). In X/X;tra2ts2 homozygotes reared throughout development at the permissive temperature of 16, yolk polypeptide synthesis occurs as in X/X;tra2ts2/+ controls; in X/X;tra2ts2 homozy- gotes raised and kept at 29, however, no synthesis of yolk polypeptides can be detected (Belote et al., 1985). Tempera- ture shift experiments with this temperature-sensitive allele show that tra2+ function must be present in the adult for the initiation and maintenance of yolk polypeptide synthesis. This control over YP on the part of tra2+ was shown to be at the level of transcription (Kraus, Lee, Lis, and Wolfner, 1988, Mol. Cell Biol. 8: 4756-64). tra2ts homozygous females do not always maintain male courtship behavior at 29, but transformed females hemizygous for tra2 [tra2ts1/Df(2R)trix] court in a reliably male fashion (Belote and Baker, 1987). Temperature-shift experiments indicate that the TSP for induc- tion of male courtship starts in the last half of the pupal period and ends before the end of pupation. alleles: allele origin ref ( comments _______________________________________________________________ tra2 spont 2-4, 8, 10, 11 null | tra2ad 6 strong allele tra2B EMS 3 amorphic / tra2OTF spont 3, 8-10 leaky ` tra2P HD 1 tra2P/tra2P females sterile, males fertile - tra2Pd1 HD 1 tra2Pd1/tra2Pd1 females male-like intersexes, males normal and fertile tra2Pd2 HD 1 tra2Pd2/tra2Pd2 lethal n tra2ts1 EMS 2-4, 7 temperature-sensitive tra2ts2 EMS 2, 3, 5 temperature-sensitive ( 1 = Amrein, Gorman, and Nothiger, 1988, Cell 55: 1025-35; 2 = Belote and Baker, 1982, Proc. Nat. Acad. Sci. USA 79: 1568-72; 3 = Belote and Baker, 1983, Dev. Biol. 95: 512-17; 4 = Belote and Baker, 1987, Proc. Nat. Acad. Sci. USA 84: 8026-30; 5 = Belote, Handler, Wolfner, Livak, and Baker, 1985, Cell 40: 339-48; 6 = Dotti and Nothiger, unpublished; 7 = Epper and Bryant, 1983, Dev. Biol. 100: 294-307; 8 = Fujihara, Kawabe, and Oishi, 1978, J. Hered. 69: 229-36; 9 = Oishi and Ota, 1982, DIS 58: 121; 10 = Ota, Fukunaga, Kawabe, and Oishi, 1981, Genetics 99: 429-41; 11 = Watanabe, 1975, Jpn. J. Genet. 50: 269- 71. | No yolk-protein precursors in males or females (Ota et al., 1981). / tra2B/tra2B identical to tra2B/tra2 or to tra2B/Df(2R)L4 (Baker and Ridge, 1980, Genetics 94: 383-423). ` Ovaries rudimentary (Fujihara et al., 1978). - Mutant can be reverted to wild type or a more extreme mutant. In homozygous females, tergite 6 partially pig- mented, vaginal bristles long, sex combs not malelike. tra2P/tra2 females intersexes. tra2Pd1/tra2 females pseudomales, tra2Pd1/tra2 males normal and fertile. n tra2Pd2/tra2 females pseudomales. cytology: Located in 51B4-6 since gene deleted by Df(2R)trix = Df(2R)51A1-2;51B6 but not by Df(2R)L48 = Df(2R)51A1;51B4 (Goralski et al., 1989). molecular biology: DNA from the 51B region was cloned from wild-type and tra2P flies by microdissection-microcloning and chromosome walking (Amrein et al., 1988; Goralski et al., 1989; Mattox et al., 1990); mutants, rearrangements, and a P- element insertion were located on the molecular map of the region. Nucleotide sequences of the entire genomic DNA and of ten cDNAs have been obtained and the amino acid sequences of the corresponding proteins predicted (Amrein et al., 1988; Goralski et al., 1989; Mattox et al., 1990). A DNA fragment of 3.9 or 4.5 kb from the tra2 region was able to rescue (by P-element transformation) homozygous tra2 flies, both in regard to sex determination and male fertility (Amrein et al., 1988; Goralski et al., 1989). Alternative splicing of tra2 mRNA creates at least four overlapping transcript structures, each of which encodes one of four different polypeptides. Different combinations of ribonucleoprotein consensus sequences (RNP-CS) and arginine-serine rich regions are included in each polypeptide. The mature mRNAs are described in the following table: mRNA location in fly exons polypeptide size ______________________________________________________ type A soma of males 1,2,4-7 264 amino acids and females type B ovary( 1-7 226 amino acids type C| testis 3-7 179 amino acids type D/ testis 3-7 136 amino acids type E` ( Some type B mRNA has been found in somatic tissues (males and females). | Intron of 232 nucleotides included in the mRNA. / Found in low abundance. ` Not characterized.. tra2 proteins show similarities to certain known RNA-binding proteins. A tra2 -lacZ fusion protein has been localized by antibody stains to the nuclei of salivary gland and fat body cells in Drosophila melanogaster (Mattox et al., 1990). Molec- ular studies show that the mutants tra2OTF, tra2P, and tra2Pd1, which are not null alleles, carry insertions of about 1.7 kb and presumably map in the 5' flanking region of the gene; cytological and molecular studies indicate that the mutant tra2Pd2 is associated with an inversion and is accom- panied by a deletion (Amrein et al., 1988). The tra2 product regulates the splicing pattern of the primary transcript of the "downstream" gene dsx in females [Baker, 1989, Nature (London) 340: 521-524; Goralski et al., 1990; Mattox et al., 1990]. tra2 activity in somatic tissues is believed to be regulated by means of a post-translational sex-specific interaction with the protein product of the tra gene (Mattox et al., 1990). # tracheae broken: see tbr # trachealess: see trh # Tramtrack: see Ttk # Transcription factor: see Trf # transformer: see tra # transformer 2: see tra2 # transient receptor potential: see trp # translucent: see trl # trapped: see ted # trb: thread bristle location: 1-36.3. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1955. references: 1959, DIS 33: 93. phenotype: Bristles short and very thin. Hairs small and sparse. Wings more rounded at tips, margins often incised; veins slightly thickened. Trident pattern slightly darker than wild type. Male viable and fertile; female sterile. RK2. other information: One allele induced by CB. 3026. # trc: tricorner location: 3-46 (to left of Pc at 47.1). references: Ferrus, 1976, Ph.D. Thesis, Univ. Autonoma de Madrid. Struhl, 1981, Nature 293: 36-41. Gubb and Garcia-Bellido, 1982, J. Embryol. Exp. Morph. 68: 37-57. Vinson and Adler, 1987a, DIS 66: 150. 1987b, Nature (London) 329: 549-51. phenotype: Mutant wing and notum have rosettes of three or more short trichomes instead of single long hairs as in wild type. Useful as cell marker. Mutant cell autonomous in mitotic cells in a wild-type background, but not in a Minute back- ground (Vinson and Adler, 1987a). # trd: tridenticle location: 2-. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1983, DIS 59: 158-60. phenotype: Larval denticles thickset and forked. Some alleles viable. #*tre: triangle eye location: 1-20.2. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1959, DIS 33: 93. phenotype: Eyes triangular with apex pointing forward. Fly large. Wings broad, blunt tipped, and slightly divergent. Male viable and fertile; female sterile. RK3. # Tre: Trehalose sensitivity (J.C. Hall) location: 1-13.6 (linked to cx). origin: Spontaneous (naturally occurring variants). references: Tanimura, Isono, Takimura, and Shimada, 1982, J. Comp. Physiol. 147: 433-37. Tanimura, Isono, and Yamamoto, 1988, Genetics 119: 399-406. phenotype: Locus determining differences in sensitivity to the taste of the disaccharide trehalose in behaviorly-based (fluid intake) tests (no differences in sensitivity to glucose, fruc- tose, or sucrose). The Tre+ allele results in high trehalose sensitivity, the Tre allele in low trehalose sensitivity. Females with half the normal dose of a given Tre+ allele are half as sensitive to trehalose, but flies (male or female) with twice the normal dose of Tre+ show only a slight increase in sensitivity as compared to normal flies. Tre is thought to be a structural gene for the trehalose specific receptor in D. melanogaster (Tanimura et al., 1988). alleles: Two alleles, Tre+ and Tre, are found in wild-type strains. cytology: Placed by Tanimura et al., 1988, between 5A10 and 5B1-3 by analyzing the sensitivity to trehalose in segmentally aneuploid flies carrying deficiencies or duplications from T(1;Y) translocations with breaks in the 5A-C region. # trefoil: see tf # Treh: Trehalase location: 2-92.9. references: Oliver, Huber, and Williamson, 1978, Biochem. Genet. 16: 927-40. Oliver and Williamson, 1978, Can. J. Genet. Cytol. 20: 452. Laurie-Ahlberg, Wilton, Curtsinger, and Emigh, 1982, Genetics 102: 191-206. phenotype: Structural gene for trehalase [TRE (EC 3.2.1.28)], a hydrolase that splits the sugar trehalose into two glucose molecules. Polyacrylamide gel electrophoresis and isoelectric focusing indicates the presence of one molecular form of the enzyme in flight muscles, hemolymph, and abdomens of adult flies. No mutant alleles obtained. cytology: Placed in 55B-55E on the basis of dosage sensitivity determined by examination of the duplication- and deletion- bearing aneuploids. # Trehalose sensitivity: see Tre # Trf54F: Described as Ntf # Trf100D: Described as Ttk # trh: trachealess location: 3:-1. origin: Induced by ethyl methanesulfonate. references: Jurgens, Kluding, Nusslein-Volhard, and Wieschaus, 1983, DIS 59: 157-58. Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. phenotype: Embryonic lethal. Tracheae are absent and filzkorper not elongated. alleles: Two alleles, trh1 and trh2, isolated as trh5D and trh7J. cytology: Placed in 61E-F since covered by YP3D segregant of T(Y;3)A144 = T(Y;3)Xhy+;61F and by Dp(3;Y)G130 = Dp(3;Y)61E;66F. # tri: trident location: 2-55. origin: Spontaneous. synonym: Probably tri32k, tri33d27, and b-133g18 are the same. discoverer: Plough, 32k. references: Plough and Ives, 1934, DIS 1: 34. 1935, Genetics 20: 42-69. phenotype: Dark trident or streak on thorax. Scutellum and sternopleural plates also dark. Thorax often contains bub- bles. Variable; overlaps wild type but also semidominant. RK3. # triangle 261: see tr261 # triangle eye: see tre # tricorner: see trc # trident: see tri # tridenticle: see trd # trimmed: see fr2 # Triosephosphate isomerase: see Tpi # Triplo-lethal: see Tpl # trithorax: see trx # trk: trunk (T. Schupbach) location: 2-36. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 302-17. Nusslein-Volhard, Frohnhofer, and Lehmann, 1987, Science 238: 1675-81. Schupbach and Wieschaus, 1989, Genetics 121: 101-17. phenotype: Maternal-effect lethal; embryos from homozygous mothers lack anterior-most head structures and structures pos- terior to the seventh abdominal segment. At gastrulation cephalic furrow is shifted toward anterior and the germband extends all the way to the posterior end. During cellulariza- tion at the blastoderm stage a funnel of yolk free cytoplasm containing a small number of nuclei (between 10 and 30) forms at the posterior pole of the embryos extending from the egg periphery to the inner yolk mass. Analysis of germline clones indicates that the mutation is germline autonomous (Schupbach and Wieschaus, 1986, Dev. Biol. 113: 443-48). alleles: allele synonym ___________________ trk1 trkRA trk2 trkHD trk3 trkHH trk4 trkPI trk5 trkPK trk6 trkRI cytology: Located at 31A-C (Nusslein-Volhard et al., 1987). #*trl: translucent location: 2-45 or -65 (10 units from Bl). origin: Spontaneous. discoverer: Bridges, 20b17. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 238. phenotype: Eye color translucent ruby, like p. RK2. # trm: see fr2 # tRNA: see under RNA # Tropomyosin: see Tm1, Tm2 # Troponin: see Tpn # trp: transient receptor potential (J.C. Hall) location: 3-97 (Manning, unpublished); 3-106 (Hardy, Orevi, and Merriam, unpublished); 3-100 (inferred from cytology). synonym: Cosens-Manning mutant (=trpCM). references: Cosens and Manning, 1969, Nature (London) 224: 285-87. Cosens, 1971, J. Insect. Physiol. 17: 285-302. Cosens and Perry, 1972, J. Insect. Physiol. 18: 1773-86. Minke, Wu, and Pak, 1975, Nature (London) 285: 84-87. Minke, 1977, Biophys. Struct. Mech. 34: 59-63. Hu, Reichert, and Stark, 1978, J. Comp. Physiol. 126: 15-24. Reichert and Bicker, 1979, J. Comp. Physiol. 133: 283-90. Minke and Armon, 1980, Photobiol. 32: 553-62. Lo and Pak, 1981, J. Gen. Physiol. 77: 155-75. Swanson and Cosens, 1981, J. Insect Physiol. 27: 215-23. Levy, Ganguly, Ganguly, and Manning, 1982, Dev. Biol. 94: 451-64. Minke, 1982, J. Gen. Physiol. 79: 361-85. Chen and Stark, 1983, J. Insect Physiol. 29: 133-40. Minke, 1983, J. Comp. Physiol. 151: 283-86. Montell, Jones, Hafen, and Rubin, 1985, Science 230: 1040-43. Wong, Hokanson, and Chang, 1985, Invest. Opthal. and Vis. Sci. 26: 243-46. Wong, Yuh, Schaefer, Roop, and Ally, 1987, Somat. Cell and Molec. Genet. 13: 661-69. Montell and Rubin, 1989, Neuron 2: 1313-23. Suss, Barash, Stavenga, Stieve, Selinger, and Minke, 1989, J. Gen. Physiol. 94: 465-91. Wong, Schaefer, Roop, LaMendola, Johnson-Seaton, and Shao, 1989, Neuron 3: 81-94. phenotype: Mutation believed to affect an intermediate step in phototransduction, the wild-type gene apparently encoding a protein involved in an intermediate step between photorecep- tion and opening of the light-sensitive ion channels (Minke, 1977, 1982; Minke and Armon, 1980; Montell and Rubin, 1989; Suss et al., 1989). Although the mutants behave normally in dim light, they behave as though blind in bright light and there is an abnormally slow dark recovery (Cosens and Manning, 1969; Cosens, 1971). The light-evoked response of the pho- toreceptors, as shown in the ERG, decays to baseline during an intense, prolonged stimulus, but not during a dim or brief stimulus (Cosens and Manning, 1969; Minke et al., 1975); each quantum bump, however, seems intrinsically normal in shape and amplitude (Suss et al., 1989); fluoride ions, which lead to excitation and adaptation of wild-type photoreceptors in the dark when superfused onto an eye slice, did neither to mutant cells. A hydrolysis-resistant analogue of GTP, which excites wild-type photoreceptors and results in noisy depolarizations, reduced the mutant's light response. The visual pigment in R1-6 photoreceptors is normal in young trp flies, but its concentration decreases with age (Minke, 1982). The rhabdomeres degenerate with age and there is accu- mulation of glycogen granules (Cosens and Perry, 1972). Ulti- mately, photoreceptor cell bodies also degenerate (Isono, unpublished). Raising the mutant flies in complete darkness prevents the degenerative changes from appearing but has no effect on the electrophysiological phenotype (Isono and Pak, unpublished). Initially, the light-evoked migration of pig- ment granules occurs in a normal manner (i.e., toward the rhabdomeres) in trp mutants, but the granules move away after only five seconds of sustained light (Lo and Pak, 1981). The trp mutation (unlike norpA) does not block degeneration caused by rdgB (Chen and Stark, 1983, J. Insect Physiol. 29: 133- 40); in a rdgB;trp genetic background, R1-6 photoreceptors are eliminated and the R7,8 photoreceptors that remain show the trp phenotype. trp is expressed in the photoreceptors of the ocelli as well as in those of the compound eyes (Hu et al., 1978; Montell et al., 1985). trp mutants seem to exhibit normal visually-mediated learn- ing under the high light-intensity conditions that largely eliminate photoreceptor potentials (Reichert and Bicker, 1979). alleles: Mutant alleles are listed in the following table: allele origin discoverer synonym comments ______________________________________________________________ trp1 spont Cosens, Manning trpCM temperature- sensitive ( trp2 EMS Pak trpP301 trp3 EMS Pak trpP302 trp4 EMS Pak trpP303 trp5 EMS Pak trpP304 trp6 EMS Pak trpP310 trp7 EMS Pak trpP313 temperature- sensitive | trp8 EMS Pak trpP338 trp9 EMS Pak trpP343 trp10 EMS Hardy, Orevi, Merriam trpUS4699 ( Rearing at 19 (instead of 25) slows the rate of the decay- to-baseline of the photoreceptor potential and leads to fas- ter initial dark recovery than occurs under non-permissive conditions. Rearing at 25, followed by shift of adults to 19, leads to more nearly normal behavior in bright light within four to six days (Minke, 1983). | Permissive temperature for normal ERG phenotype <25; res- trictive temperature _29. Temperature-sensitive period lim- ited to last 72 hours of pupal life (Wong et al., 1989). cytology: Located in 99C5-6 by in situ hybridization and break- point analysis (Montell et al., 1985; Wong et al., 1987, 1989). trp is covered by Dp(3;Y)L127 = Dp(3;Y)99B5-6;99F3-4 and Dp(3;1)52 [a duplication produced by translocation onto the X chromosome of a piece of the third chromosome (98F14- 99A12;100F), followed by deletion of 99A9-10;99C5-6 (Frisardi and MacIntyre, 1984, Mol. Gen. Genet. 197: 403-13)], but is not covered by Dp(3;1)78 = Dp(3;1)XP;99C5-7;100F (Pye, unpub- lished) and Dp(3;1)165P = Dp(3;1)XP;99B2-4;99C5-6 (Frisardi and MacIntyre, 1984; Wong et al., 1989). molecular biology: Cloned by isolation of DNA fragments hybri- dizing preferentially to head rather than body mRNA (Levy et al., 1982; Montell et al., 1985) and by genetic analysis and chromosomal walking (Wong et al., 1987, 1989). cDNA and puta- tive protein of trp sequenced (Montell and Rubin, 1989; Wong et al., 1989); total length of the 13 exons is 1645 bp (Wong et al., 1989). In germline transformation experiments (Mon- tell et al., 1985), a 7.1 kb genomic fragment rescued the ERG defects of trp1. Montell et al. (1985) identified a 4.1 kb transcript which appeared during the pupal stage and was localized to the retinula cells of the compound eyes and the ocelli. This transcript encodes a 143 kd integral membrane protein of 1275 amino acids with eight putative transmembrane domains; it is not similar in sequence to any previously analyzed protein (Montell and Rubin, 1989) and is concentrated in the rhabdomeres of the photoreceptor cells. Wong et al. (1987, 1989) identified a somewhat larger transcript (4.5 kb) that is believed to be "eye specific" by virtue of its absence from the mutant eyeless. This transcript also encodes an unique protein of 142 kd that seems to be associated with the photoreceptor membrane. Mutants trp1, trp2, and especially trp9 (according to Montell and Rubin, 1989) show reduced amounts of the 4.1 kb transcript and completely lack the trp protein. The mutant trp3 (according to Wong et al., 1989) also shows a reduction in transcript level, but they find that trp1 and trp7 show close to normal levels; trp protein is lacking in head extracts in all three mutants. Transformed trp flies show normal protein levels. other information: The same kinds of results from applying fluoride ions or the GPT analogue to the trp mutant in Droso- phila (see "phenotype") were observed in experiments on the nss mutant in the blowfly Lucilia. # Truncate 51b: see dpo1M # trunk: see trk # trw: see aptrw # trx: trithorax location: 3-54.2. references: Garcia-Bellido, 1977, Amer. Zool. 17: 613-29. Ingham and Whittle, 1980, Mol. Gen. Genet. 179: 607-14. Capdevila and Garcia-Bellido, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 339-50. Ingham, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 365-69. Duncan and Lewis, 1982, Developmental Order: Its Origin and Regulation (S. Subtelny, ed.). Alan R. Liss, Inc., New York, pp. 533-54). Ingham, 1983, Nature 306: 591-93. 1985a, Cold Spring Harbor Symp. Quant. Biol. 50: 201-08. 1985b, J. Embryol. Exp. Morph. 89: 349-65. Sato and Denell, 1987, Genetics 116: 389-98. Mozer and Dawid, 1989, Proc. Nat. Acad, Sci. USA 86: 3738-42. Shearn, 1989, Genetics 121: 517-25. phenotype: The presence of trx+ is required throughout embryonic and larval development for the appropriate differen- tiation in the adult of segments in the head, thorax, and abdomen (Ingham and Whittle, 1980; Ingham, 1981), the primary effect being in the thoracic segments. Mutants show transformations of the first and the third thoracic segments to the second thoracic segment as well as transformations in the abdomen (Mozer and Dawid, 1989). The gene seems to be involved in the positive regulation of the BXC and the ANTC (Duncan and Lewis, 1982). The viable mutant combinations trx1/trx1 and trxD/+ show variable segmental transformations in adults, as do heterozygous deficiencies [Df(3R)red-P52/+, for example]. The frequency of homeotic transformations in adults and, to some extent, in larvae of such genotypes varies inversely with the dosage of the BXC (Duncan and Lewis, 1982; Sato and Denell, 1987). A similar dosage effect has been pro- posed for the ANTC (Sato and Denell, 1987). When the mutant allele or deficiency is maternal in origin, the frequency of transformations is higher in adults (but not in larvae). The alleles trx2, trx3, and trxD are larval or pupal lethals as homozygotes, trans-heterozygotes, or deficiency heterozygotes, and may show weak homeotic transformations in larvae or in homozygous clones in adults (Capdevila and Garcia-Bellido, 1981; Ingham, 1981, 1983, 1985b). alleles: Alleles that show a recessive or dominant homeotic phenotype and fail to complement each other have been identi- fied. All pairwise combinations of trxB14, trxB16 - trxB18, and trxE1 - trxE13 are inviable except for rare survivors of the genotypes trxE11/trxB16, trxE11/trxB17, and trxB16/trxB17. Deficiencies are listed in the rearrangement section under Df(3R)red. allele origin discoverer synonym ref ( comments _______________________________________________________________________________ trx1 spont Ingham 3-6 recessive; viable in (1980) homozygotes trx2 EMS Ingham 4, 5 recessive; lethal in (1981) homozygotes or with trx3 or trxD trx3 EMS Ingham 4, 5 recessive; lethal in (1981) homozygotes or with trx2 or trxD trxB14 / rays Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxB16 | HD Kennison 8 1.5 kb insertion into 3 kb fragment at DNA map site 29-32 trxB17 HD Kennison 8 1 kb insertion into distal part of 5.4 kb fragment at DNA map site 21-26.5 trxB18 | HD Kennison 8 2.5 kb insertion into 3 kb fragment at DNA map site 29-32 trxD / ` spont Lewis Rg-bx 1, 2, 3 dominant; lethal in (1968) l(3)bxv homozygotes or with trxL trx1, trx2, or trx3 trxE1 / rays Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE2 / rays Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE3 EMS Kennison, 7 dominant; suppresses Tamkun antenna to leg trans- formation in AntpNs; deletion of 100 bp at map site 16 trxE4 EMS Kennison trxE5 EMS Kennison trxE6 EMS Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE7 EMS Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE8 EMS Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE9 EMS Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE10 EMS Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE11 EMS Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE12 EMS Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxE13 / rays Kennison, 7 dominant; suppresses Tamkun extra sex combs in Pc4/+ trxP2 cloning Ingham 8 0.9 kb P-element insertion in 1.35 kb fragment at DNA map site 33-34.5 trxrib7 - HD Karpen trxP/rib7,ry+ 8 21 kb P-element insertion in 1.35 kb fragment at DNA map site 33-34.5 trxrv4 HD Ingham 4.5 doublet band lost; wild-type 9 kb band restored ( 1 = Capdevila and Garcia-Bellido, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 339-50; 2 = Garcia-Bellido, 1977, Am. Zool. 17: 613-29; 3 = Ingham, 1980, DIS 55: 63-64; 4 = Ingham, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 365-69; 5 = Ing- ham, 1985, J. Embryol. Exper. Morph. 89: 349-65; 6 = Ingham and Whittle, 1980, Mol. Gen. Genet. 179: 607-14; 7 = Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40; 8 = Moser and Dawid, 1989, Proc. Nat. Acad. Sci. USA 86: 3738-42. | Breakpoint in long intron (Moser and Dawid, 1989). / Slightly reduced pigmentation of fifth abdominal tergite in heterozygotes (Lewis, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 155-72). ` Cited by Capdevila and Garcia-Bellido, 1981. - Carries transposon P[rib7/ry+] with one Drosophila melano- gaster ribosomal transcription unit and ry+ marker at 88B (Karpen, Schaeffer, and Laird, 1988, Genes Dev. 2: 1745- 63); fails to complement trx (Moser and Dawid, 1989). cytology: Placed in 88A12-B5 since uncovered by Df(3R)red-P52 = Df(3R)88A12-B1;88B4-5. molecular biology: The gene was cloned by P-element transposon tagging. Five insertion mutants were located within a region of 10 kb; reversion of one of these mutations resulted in excision of the P-element insertion (Moser and Dawid, 1989). Two major mRNAs of 12 and 15 kb, transcribed in a distal to proximal direction, are present. The 12-kb mRNA is most abun- dant in embryos of 0-6 hours, but it also appears in larvae and pupae. The 15 kb mRNA is most abundant in larvae, in pupae eight to nine days after oviposition, and in male and female adults; it also appears in 3- to 6-hr embryos. A 10 kb transcript was seen (but rarely) in 1- to 3-hr embryos and also in adult females; it may be maternally derived. Early embryos show an uniform distribution of transcript, but later (14-15 hours after fertilization) the ventral nerve cord has a higher concentration than other parts (Moser and Dawid, 1989). other information: 22-52% of double heterozygotes involving a null allele of Ash-1 and the trx deficiency, Df(3R)red-P93, show partial transformations of halteres to wings and/or par- tial transformations of third (and sometimes first) legs to second legs, whereas in single heterozygotes no transforma- tions are shown (Shearn, 1989). Heterozygosis for null alleles of trx suppresses the extra sex combs phenotype of +/Df(3L)Pc-MK, and increases penetrance of the maternal-effect homeotic phenotype of fs(1)h. trx function seems to be neces- sary for optimal expression of Scr- (Sato, 1988, Roux's Arch. Dev. Biol. 197: 435-40). # trx1 phenotype: Flies homozygous for trx1 show a variety of partial homeotic transformations [ventral prothorax and metathorax to mesothorax and second to seventh abdominal segments to first abdominal segment (Ingham and Whittle, 1980)]. Penetrance of the transformation phenotype is stronger in hemizygotes than homozygotes and increases as the temperature is raised from 18 to 25C. At the higher temperature, the penetrance of the mutant offspring of trx1/trx1 females is almost 100%, while mutant offspring of trx1/+ females show only about 50% penetrance. The temperature-sensitive period occurs prior to hatching. Ingham (1980) noted the following abnormalities in extreme trx1 mutants: (1) Extra bristles between humerus and coxa and on the distal tibia of the first leg; (2) Similar changes on the third leg; (3) Loss or reduction of transverse bristle rows, and, in males, decrease in number of sex comb teeth on the first leg; (4) Replacement of halter disk deriva- tives by wing blade, notal, and scutellar structures; (5) Rotated genitalia and abnormal tergite pigmentation in male flies. 75% of heterozygotes with Df(3R)red or with the lethal allele trx3 are lethal, either as larvae or pupae (Ingham, 1981); the heterozygotes that survive show cuticular transfor- mations of the ventral prothorax and the metathorax, an extra mesonotum developing posterior to the normal one, and anteriorly-directed abdominal transformations (Ingham, 1985a). # trx2 phenotype: The recessive embryonic lethal trx2 fails to comple- ment trx1, trx3, or trxD, either for the transformation pheno- type or for lethality. Trans-heterozygotes of trx2 with another allele or with a deficiency for the locus show weak expression of the trx homeotic phenotype and about 40-50% pupal lethality. Since the lethal mutations are cell viable, trx2/trx3 clones have been induced by mitotic recombination in trx2/trx3;Dp(3;1)kar5l, trx+ flies (Ingham, 1981, 1985b). The clones produced showed transformations of the antenna, eye, head capsule, and proboscis, bristle abnormalities in the legs, vein and bristle abnormalities in the wings, and transformations of halter to wing tissue and of genital to thoracic tissue; mutant clones in abdominal segments one to seven were not found (Ingham, 1985b). # trx3 phenotype: Like trx2. About 75% of the trx1/trx3 trans- heterozygotes are lethals, larval and pupal (Ingham, 1981). # trxD phenotype: Adult trxD/+ flies are viable and characterized by their "bithorax variegated" phenotype (Lewis). These mutants show no prothoracic transformations, but do show patchy transformations of halter into wing and third leg into second leg (as in bx and pbx) and variable transformations of poste- rior abdominal segments into more anterior ones (Capdevila and Garcia-Bellido, 1981; Duncan and Lewis, 1982). In homozy- gotes, deficiency heterozygotes, or trans-heterozygotes over trx1, trx2, or trx3, the trxD allele is lethal or semilethal in larvae or pupae; in clones it is cell viable. Transformed trxD/trxD clones were found in the head region (but not in the thorax or abdomen) by Capdevila and Garcia-Bellido (1981), while transformed trx2/trxD clones were found in both head and thorax (but not in the abdomen) by Ingham (1985b). # Try: Trypsin locaton: 2- [60]. references: Davis, 1985, Genetics 110: s12. phenotype: Structural gene for enzyme trypsin. cytology: Placed in 47D-47F. #*ts: telescope location: 2-68. discoverer: Bridges, 15l27. references: Bridges and Morgan, 1919, Carnegie Inst. Wash. Publ. No. 278: 291 (fig.). phenotype: Abdominal segments somewhat drawn out. Wings droop- ing and divergent. Overlaps wild type. RK3. # ts398: see l(1)11Af # tsg: twisted gastrulation location: 1-36.8. origin: Induced by ethyl methanesulfonate. references: Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. Zusman and Wieschaus, 1985, Dev. Biol. 111: 359-71. Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52. phenotype: Gene expressed 1.5-3.5 hours after oviposition. Mutants are embryonic lethals and show abnormal gastrulation, with deep dorsal folds resulting in temporary blockage of germband extension. Later, dorsal folds released, but poste- rior midgut abnormal in position, dorsal cells very thick, and cephalic folds very deep (Zusman and Wieschaus, 1985). At the end of embryonic development, tsg cuticle shows head defects and condensed, retracted posterior spiracles. Ventral nervous system split posteriorly. No particular cell must be wild type for survival in tsg//+ mosaics, but wild-type cells on dorsal side are most effective in rescue (Zusman and Wieschaus, 1985). alleles: Four tsg alleles have been described. allele origin synonym ref ( _______________________________________ tsg1 EMS tsgB8 2, 3 tsg2 EMS tsgN9 2, 3 tsg3 EMS 2 tsg4 EMS tsgRF32 1 ( 1 = Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52; 2 = Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307; 3 = Zusman and Wieschaus, 1985, Dev. Biol. 111: 359-71. cytology: Placed in 11A1-8 since uncovered by Df(1)KA10 = Df(1)11A1;11A7-8 (Wieschaus et al., 1984); also placed in 11A2-3 (Perrimon et al., 1989). molecular biology: The region containing tsg has been cloned and the nucleotide sequence determined (Konrad and Marsh, 1989). A transcript has been found in early embryos. # tsl: torsolike location: 3-71. origin: Induced by ethyl methanesulfonate. references: Frohnhofer and Nusslein-Volhard. Nusslein-Volhard, Frohnhofer, and Lehmann, 1987, Science 238: 1675-81. phenotype: Maternal-effect lethal. Anterior- and posteriormost structures (labrum, dorsal bridge, telson, eighth and part of seventh abdominal segments) deleted in embryos produced by homozygous mothers. tsl pole cells transplanted into wild- type hosts produce normal progeny, whereas the reciprocal transplant produces tsl embryos. alleles: allele synonym comments ____________________________________________ tsl1 tsl035 tsl2 tsl135 temperature-sensitive tsl3 tsl146 tsl4 tsl691 tsl5 tsl174 tsl7 tslMK cytology: Placed in 93F6-14; uncovered by Df(3R)e-F4 = Df(3R)93C3-6;93F11-14, but not by Df(3R)e-D7 = Df(3R)93C3- 6;93F6-8. # tt: tilt location: 3-40.0. discoverer: Bridges, 15h29. references: Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 134 (fig.). Mossige, 1938, Hereditas 24: 115. phenotype: Wings spread, elevated, and warped in a compound curve. Vein L3 shows gap. Eye color may be slightly dilute. Developmentally, L3 originally complete but central section disappears during contraction period (Waddington, 1940, J. Genet. 41: 75-139). Synthetic lethal in presence of su(r) (Str|men, 1974, Hereditas 78: 157-68). RK2. tt: tilt From Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 135. # tta: tetanic location: 1-. references: Ferrus, Llamazares, de la Pompa, and Yuste, 1987, J. Neurogenet. 4: 125-26. phenotype: Viable, but shows tetanization under anaesthesia. Unable to learn. tta males with two doses of the Shaker gene complex are lethal. # Ttk: Tramtrack location: 3-{102}. references: Harrison and Travers, 1990, EMBO J. 9: 207-16. phenotype: Gene encodes a zinc-finger protein binding to a number of sites involved in the transcriptional control of fushi-tarazu in the Antennapedia complex. cytology: Located in 100D by in situ hybridization to the salivary chromosomes. molecular biology: Ttk clones from a Drosophila melanogaster embryonic cDNA library contain a protein associated with bind- ing site #16 in the ftz promoter region. At least three addi- tional Ttk binding sites are believed to be present in the ftz promoter [Harrison and Travers, 1988, Nucleic Acids Res. 16: 11403-16; Topol, Wiederrecht and Parker, 1987, Genetic Regulation of Development (Loomis, ed.). Alan R. Liss, New York, pp. 3-12]. Nucleotide and putative amino acid sequences were obtained from the Ttk cDNA (Harrison and Travers, 1990). The translated protein has a predicted molecular weight of 69 kd. Two zinc-finger DNA-binding motifs (Cys-Cys His-His class) occur within the 327 amino acids believed to make up the Ttk binding domains; the zinc fingers show significant homology to the consensus finger motif and to the fingers of the protein products of Kr and hb (Rosenberg, Schroder, Preiss, Kienlin, Cote, Riede, and Jackle, 1986, Nature 319: 336-39; Tautz, Lehmann, Schnurch, Schuh, Seifert, Kien- lin, Jones, and Jackle, 1987, Nature 327: 383-89). The Ttk protein also contains PEST sequences found in proteins with short half-lives, as well as a serine and alanine-rich region at the C terminus [as in the hb and inv gene products (Cole- man, Poole, Weir, Soeller, and Kornberg, 1987, Genes Dev. 1: 19-28]. Ttk RNA (probably maternal in origin) can be detected in embryos before stage 3; this RNA has almost disap- peared by the start of ftz expression in stage 4 and is com- pletely absent by the time the characteristic seven ftz stripes develop in the embryo. Ttk zygotic expression can be detected in stage 7 in the anterior mid-gut primordia and pole cells and later in the posterior mid-gut primordia. At stage 9, when ftz stripes are no longer present, Ttk RNA forms a pattern of about 14 stripes in the ectoderm and mesoderm of the extended germ-band. These stripes later fuse, forming a "tramtrack" pattern around the germ-band; at stage 13, the Ttk RNA is only found in the developing epidermis and gut. Larvae and adults show very weak expression of the zygotic tran- script. other information: Trf100D: Transcription factor in 100D is a more informative designation. #*ttr: tetrapter location: 3-51.3. discoverer: Tshetverikov, 25b. references: Astaurov, 1929, Wilhelm Roux's Arch. Entwick- lungsmech. Org. 115: 424-47. 1930, Z. Indukt. Abstamm. Vererbungsl. 55: 183-262. Timofeeff-Ressovsky, 1934, Z. Indukt. Abstamm. Vererbungsl. 67: 248 (fig.). Villee, 1942, Univ. Calif. (Berkeley) Publ. Zool. 49: 180-81. phenotype: Like bx. Halteres tend to become winglike. Most flies wild type but may have, in place of a haltere, an organ one-half the size of a normal wing with veins, bristles, and sense organs. RK3. # ttx: tetrodotoxin-sensitive (J.C. Hall) location: 3-45. origin: Spontaneous. discoverer: Kelly, L.M. Hall. references: Gitschier, Strichartz, and Hall, 1980, Biochim. Biophys. Acta 595: 291-303. phenotype: Adults and larvae highly sensitive to the sodium channel blocker tetrodotoxin (TTX) by feeding; mutant adults are especially sensitive. alleles: One mutant allele, ttx1, causing accentuated TTX sen- sitivity.