# t: tan (J.C. Hall) location: 1-27.5. references: McEwen, 1918, J. Exp. Zool. 25: 49-106. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 237. Demerec, Kaufman, Fano, Sutton, and Sansome, 1942, Year Book- Carnegie Inst. Washington 41: 191. Benzer, 1967, Proc. Nat. Acad. Sci. USA 58: 1112-19. Pak, Grossfield, and White, 1969, Nature (London) 222: 351- 54. Hotta and Benzer, 1969, Nature (London) 222: 354-56. Heisenberg, 1971, J. Exp. Biol. 55: 85-100. Konopka, 1972, Nature (London) 239: 281-82. Heisenberg and Gotz, 1975, J. Comp. Physiol. 98: 217-41. Heisenberg and Buchner, 1977, J. Comp. Physiol. 117: 127-62. Wright, 1987, Adv. Genet. 24: 127-222. phenotype: Body color varies from light tan to almost wild- type. Easiest to identify by light tan antennae; male easier than female. Larval mouthparts in mutant alleles, t1, t2, and t3 lighter than normal at basal prongs; classifiable with dif- ficulty in larvae (Brehme, 1941, Proc. Nat. Acad. Sci. USA 27: 254-61). Neurological defect first observed in t1 by McEwen (1918), who reported that the mutant flies behaved as if they were nonphotactic in his test apparatus (tube with light at one end); Benzer (1967) and Pak et al., (1969), using a similar but more elaborate apparatus and EMS-induced tan alleles, reached the same conclusion. In a Y-maze test for phototaxis, however, tan mutants are sensitive to light (Hadler, 1984, Biol. Bull. 126: 264-73). In the electrore- tinogram (ERG) tracing obtained when one electrode is inserted in the first optic ganglion (lamina) below the ommatidia, the on- and off-transients of tan flies are reduced or missing, but the other ERG components are present, indicating that the mutant is not blind although it appears behaviorly blind in some tests. Mosaic studies (Hotta and Benzer, 1970, Proc. Nat. Acad. Sci. USA 67: 1156-63) indicate that the ERG pheno- type of tan is cell autonomous. The optomotor responses of mutants to horizontal and vertical movements are abnormal in that light intensity thresholds for responses are raised, the extent depending on the allele (Heisenberg, 1971, DIS 46: 68; Heisenberg and Gotz, 1975; Heisenberg and Buchner, 1977). No walking optomotor responses are detected, but there can be positive responses in flying optomotor tests if the rotating vertical stripes are relatively wide. The enzyme tyrosinase, which converts tyrosine to 3,4- dihydroxyphenylalanine (DOPA), is formed in tan adults (Horowitz). Dopamine, an important component of catecholamine metabolism (involved in both melanization of cuticle and syn- thesis of neurotransmitters), has been found in reduced amounts (about 60% of the wild-type concentration) in t1 and t5 (Konopka, 1972). The dopamine was detected only in late pupae that show some pigmentation and in adult flies. One of the enzymes involved in the formation of dopamine, |- alanyldopamine hydrolase (BAH), shows no activity in t/t and t/Y mutants and reduced activity in t/+ heterozygotes as com- pared to wild-type (Black, Pentz, and Wright). This dosage effect implicates tan as the structural gene for BAH (Wright, 1987). The mutant tan is defective in courtship behaviors, the males showing aberrant visually-mediated responses to moving female flies (Cook, 1980, Biol. Cybernet. 37: 41-51; Tomp- kins, Gross, Hall, Gailey, and Siegel, 1982, Behav. Genet. 12: 295-307). alleles: No complementation for body color or phototaxis between t1 and t5, t6, t8, t9, and t0. Deficiencies listed in rearrangement section. allele origin discoverer synonym ref ( comments _________________________________________________________________________ t1 spont Bridges, 14g16 2, 6-15 nonphototactic; dopamine < t+; ERG abnormal t2 spont Bridges, 19d5 3, 13 darker than t1 t3 spont Bridges, 31e11 3 lighter than t1; tan spot on abdomen t4 spont Bridges, 33c14 weak t in color t5 Konopka dopamine < t+; ERG abnormal t6 EMS Homyk, t101 8 flight abnormal; | Sheppard ERG abnormal t7 EMS Heisenberg opm8 5 weak optomotor response; ERG abnormal t8 EMS Heisenberg opm24 7 ERG abnormal t9 EMS Benzer PC13 14 ERG abnormal t10 EMS Pak x-7 1, 4, nonphototactic; 14, 15 ERG abnormal ( 1 = Alawi and Pak, 1971, Science 172: 1055-57; 2 = Benzer, 1967, Proc. Nat. Acad. Sci. USA 58: 1112-19; 3 = Brehme, 1941, Proc. Nat. Acad. Sci. USA 27: 254-61; 4 = Grossfield and Pak, 1971, DIS 47: 59; 5 = Heisenberg, 1971, DIS 46: 68; 6 = Heisenberg, 1971, J. Exp. Biol. 55: 85-100; 7 = Heisenberg and Buchner, 1977, J. Comp. Phys. 117: 127- 62; 8 = Homyk, 1977, Genetics 87: 105-28; 9 = Hotta and Benzer, 1969, Nature (London) 222: 354-56; 10 = Hotta and Benzer, 1970, Proc. Nat. Acad. Sci. USA 67: 1156-63; 11 = Konopka, 1972, Nature (London) 239: 281-82; 12 = McEwen, 1918, J. Exp. Zool. 25: 49-106; 13 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 237; 14 = Pak, 1975, Handbook of Genetics (King, ed.). Plenum Press, New York and London, Vol. 3, pp. 703-33; 15 = Pak, Grossfield, and White, 1969, Nature (London) 222: 351-54. | Legs not retracted in flight (Homyk and Sheppard, 1977, Genetics 87: 95-104). cytology: Placed in region 8C2-D1 (Demerec et al., 1942) on the basis of its inclusion in Df(1)t282-1 = Df(1)8C2-3;8C14-D1. other information: t suppresses jump response of stnts (Kelly, 1983, Cell Molec. Neurobiol. 3: 143-49). # T2: see dpolv2 # T1: see Tp1 # T-cp1: T-complex 1 location: 3- {76}. origin: Molecular cloning. references: Ursic and Ganetzky, 1988, Gene 88: 267-74. phenotype: Codes for a cDNA from Drosophila melanogaster that shares 66% sequence identity with the mouse Tcp-1 gene encod- ing TCP1 (t-complex polypeptide 1). cytology: Placed in 94B1-2 by in situ hybridization to salivaries. molecular biology: Gene cloned and sequenced. The predicted protein is made up of 557 amino acids and is 72% identical to the mouse polypeptide. The yeast Saccharomyces cerevisiae also carries a genomic fragment that can be detected by the Drosophila T-cp1 cDNA. # ta: tapered (J.C. Hall) location: 2-56.6. origin: Ultraviolet induced. discoverer: Edmondson and Meyer, 49c. references: 1949, DIS 23: 61. Wood and Butterworth, 1972, DIS 49: 67-68. phenotype: Wings narrow and pointed, somewhat longer than nor- mal. Veins close together. Viability good. Female fertility low; male sterile. Males show abnormal courtship pattern, i.e. vague interest in circling and approaching female with no interest in touching. Periodic wing vibrations at 90 and pro- boscis movements occur, but females not receptive to mutant males. 20% of ta/ta males had non-motile spermatozoa. Fre- quently, accessory glands on one or both sides were atrophied; testes often atrophied or show club-like structures on the apical ends (Wood and Butterworth, 1972). RK2. # ta: see tar # Ta: Thickened arista location: 3- {47}. synonym: TaL: Thickened arista-Lethal (used by Cavener et al., 1986b, for Ta1). origin: / ray induced (Ta1). references: Kaufman, 1978, Genetics 90: 579-96. Kaufman, Lewis, and Wakimoto, 1980, Genetics 94: 115-33. Lewis, Kaufman, Denell, and Tallerico, 1980, Genetics 95: 367-81. Cavener, Corbett, Cox, and Whetten, 1986a, EMBO J. 5: 2939- 48. Cavener, Otteson, and Kaufman, 1986b, Genetics 114: 111-23. phenotype: Semidominant homeotic mutant that transforms aristal segments into tarsal segments. Both Ta1 and Ta2 are homozy- gous lethal; lethality of Ta2 may be due to its association with a Minute. The heteroallelic combination Ta1/Ta2 is viable and shows transformation of the whole arista and the fourth and fifth antennal segments into a segmented tarsus with a claw at the distal end; little or no transformation of the third antennal segment; males show extreme reduction in the number of sex-comb teeth on the first leg, as in Df(3R)Scr (Kaufman et al., 1980). Ta1/+ and Ta2/+ flies have a less extreme antennal phenotype without the reduction in the number of sex-comb teeth. alleles: Two mutant alleles have been identified: Ta1, associ- ated with T(2;3)Ta, and Ta2, which is cytologically normal. These alleles are partially complementing. Both are viable (but mutant) over Df(3R)Scr = Df(3R)84A1-2;84B1-2; Ta2 is also viable over Df(3R)Antp17 = Df(3R)84B1-2;84D11-12. cytology: Placed in 84C1-2 on the basis of molecular data for the breakpoint of T(2;3)Ta = T(2;3)51E1-2;84C1-2 which lies between the proximal breakpoint of Df(3R)dsx2M = Df(3R)84C1- 2;84E1-2 and the distal breakpoint of Df(3R)Scx2 = Df(3R)84A4-5;84C1-2. molecular biology: Distal (84C1-2) breakpoint of T(2;3)Ta located at about +34 kb [in the 15 kb overlap of Df(3R)Scx2 and Df(3R)dsx2M (Baker and Wolfner, 1988, Genes Dev. 2: 477- 89; 0 point = Hind III site in (Tub84B; "+" values to the right, "-" values to the left)]. # Tab: see BXC # Tac: see PinTac # tailless: see tll # tailup: see tup # tammo: see tmo # tan: see t # tapered: see ta # tar: tarry location: 1-27.3 (0.4 unit from lz, probably to the left). origin: Found among progeny of deuteron-irradiated male. discoverer: Hildreth, 51i. synonym: ta (preoccupied). references: 1953, DIS 27: 56. phenotype: Expression ranges from small black spots on distal end of femora or proximal end of tibiae to cases in which the tibiae, femora, and bases of coxae are encapsulated in a dark, brownish-black, glossy covering. Legs weak. Some overlap wild type. Viability reduced. RK2. other information: Possibly an allele of me (1-29.0). # Tarhos: see Fs(2)Sz9 # Tarnished: see bwV3 # tarry: see tar # tarsi irregular: see ti # tasteblind: see tbl #*taw: tawny location: 1-41.1. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1955. references: 1958, DIS 32: 75-76. phenotype: Head and thorax slightly dark; abdomen pale. Wings usually scooped or tips curved. Female tergites often narrow, serrated, or broken. Viability and fertility good. RK3. # taxi: see tx #*tb: tiny bristle location: 1-35.8. discoverer: Bridges, 16a4. references: 1919, J. Gen. Physiol. 1: 645-56. phenotype: All bristles short and fine; wings somewhat short. Female fertility low. RK2. # tb: see tbr # Tb: Tubby location: 3-90.6. synonym: Tu. references: Auerbach, 1943, DIS 17: 49. Lindsley, 1973, DIS 50: 21. Craymer, 1980, DIS 55: 197-200. phenotype: Dominant; larvae, pupae, and adults shorter and thicker than wild-type in both heterozygotes and homozygotes (not separable). Larvae distinguishable on basis of reduced length and tortuous tracheal trunks. Classification reliable in larvae and pupae but not adults. Both sexes viable and fertile. alleles: Two alleles, Tb, induced by chemicals, presumably nitrogen mustard (Auerbach, 1943) and *Tb2, induced by / rays (Lindsley, 1973). cytology: Salivary chromosomes normal (Lindsley, 1973). # tb-53: see mc #*tbd: tiny bristleoid location: 1-25. origin: Spontaneous. discoverer: Curry, 37g23. phenotype: Bristles short and thin, like a medium Minute. Fly somewhat smaller than wild type. Good viability and fertil- ity. RK2. cytology: Locus between 7C5 and 8C1 (Demerec, Kaufmann, Fano, Sutton, and Sansome, 1942, Year Book - Carnegie Inst. Washing- ton 41: 191). Further restricted to 8A1-C1 on the basis of its genetic location to the right of oc at 8A1-2 (Hinton and Welshons, 1955, DIS 29: 125-26). # tbl: tasteblind (J.C. Hall) location: 2- or 3-. origin: Induced by ethyl methanesulfonate. references: Isono and Kikuchi, 1974, Jpn. J. Genet. 49: 113- 24. Tanimura, Isono, and Kikuchi, 1978, Jpn. J. Genet. 53: 71-73. phenotype: Electrophysiological response of labellar hair sen- sory structures to D-glucose, maltose, and sucrose reduced compared to wild type; no response to D-mannose, D-xylose, and lactose. Response to D-fructose normal. # tbr: tracheae broken location: 3- (not located). origin: Spontaneous. discoverer: Slatis. synonym: tb (preoccupied). references: 1959, Genetics 44: 536. phenotype: Main tracheal trunks of larva have interruptions. Penetrance 17% at 16, 5% at 25. Does not seem to affect via- bility. RK3 . # tbs: thin bristles location: 2-81.6. origin: Spontaneous. synonym: Ho. references: Mostashfi and Koliantz, 1970, DIS 48: 104. phenotype: Thin and somewhat short bristles. # tc: tiny chaetae location: 1-51.6. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007) discoverer: Fahmy, 1954. references: 1958, DIS 32: 76. phenotype: Bristles extremely short and fine. Eclosion delayed. Viability and fertility good. RK1. cytology: Located in 13F since included in Df(1)sd72b = Df(1)13F1;14B1 but not in Dp(1;4)r+ = Dp(1;4)13F10;16A1-2 (Lefevre). # Tcp: Third chromosome cold-sensitive paralytic (J.C. Hall) location: 3-66.0. origin: Induced by ethyl methanesulfonate. synonym: TCP. references: S|ndergaard, 1980, Heredity 92: 335-40. phenotype: Tcp/+ mutants kept at 25 show an unsteady gait upon mechanical agitation, the more extreme alleles falling over and having difficulty in righting themselves. Surviving heteroallelic combinations have motor problems even when undisturbed. All heterozygotes reversibly paralyzed within 18 sec at 12 (more variable from 12 to 19). Homozygotes and heteroallelic combinations lethal for the most part; survivors more sensitive to cold than Tcp/+. During development, heterozygous embryos, but not larvae, are killed by exposure to temperatures less than 13. In extracts from mutant adults, assays of a mitochondrial enzyme show shifts in Arrhenius activation energy. alleles: Eleven alleles designated Tcp1 to Tcp11. Most alleles are recessive lethals. Tcp2 appears to be a hypomorph; Tcp9 survives as a homozygote, but is lethal in many heteroal- lelic combinations. # Tcr: Third chromosome resistant location: 3-39.6. origin: Induced by ethyl methanesulfonate. discoverer: Bishop, Sherald, and Wright. synonym: l(3)Tcr. references: Wright, 1987, Adv. Genet. 24: 127-222. phenotype: Tcr/+ heterozygotes resistant to dietary ( methyl dopa. Homozygous lethal. Heteroallelic combination Tcr40/Tcr45 partially lethal, 48.3% dying as late embryos, these unhatched larvae having underpigmented mouthparts like lethal Ddc/Ddc embryos; only 7.5% go through pupation and manage to eclose, but these adults die soon. Both pharate and hatched adults have cuticular abnormalities involving the eyes (rough, often small, with black, necrotic spots), ocelli (often missing), wings (notched), scutellum (reduced), bris- tles (missing or M-like), sex combs (reduced), and abdomen (grayish). Tcr/+ heterozygotes suppress the lethality of amd heteroallelic combinations; Tcr heteroallelic combinations are not rescued genetically by amd/+, but show increased embryonic mortality as a maternal effect of amd. alleles: Two partially complementing alleles described, Tcr40 and Tcr45. #*tdd: tiddler location: 1-0.0 (0/871 crossovers with sc). origin: Induced by ethyl methanesulfonate (CB. 1528). discoverer: Fahmy, 1956. references: 1958, DIS 32: 76. phenotype: Body small. Viability and fertility good. RK3. #*te: tenerchaetae location: 1-5.6. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1952. references: 1958, DIS 32: 76. phenotype: Bristles short and fine. Eyes dark and glistening. Wings frequently small, deformed in various ways. Eclosion delayed. Male viability, but not fertility, good. Female infertile. RK3. # technical knockout: see tko # ted: trapped location: 3- {47}. references: Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23. phenotype: Homozygous lethal; homozygotes attempt to eclose but cannot break the operculum seams. Rescue of fully viable and fertile adults can be effected by dissection from the puparium. alleles: Five mutant alleles have been described. allele origin discoverer synonym _______________________________________ ted1 EMS Grigliatti l(3)4.15 ted2 EMS Grigliatti l(3)5.12 ted3 EMS Cavener l(3)g8 ted4 EMS R. Lewis l(3)r5 ted5 EMS R. Lewis l(3)r12 cytology: Placed in 84C6-8 since in the region of overlap between the distal breakpoint of In(3R)Antp73b = In(3R)84B1- 2;84C5-6 and the proximal breakpoint of Df(3R)dsx-M29 = Df(3R)84C8-D1;84F6-7. other information: The rescuable mutant phenotype is the same as that observed in Gldn mutants (Cavener and MacIntyre, 1983, Proc. Nat. Acad. Sci. USA 80: 6286-88). # Tegula: see under shv in dpp entry # Tekele: see Fs(2)Sz10 # telegraph: see tg # telescope: see ts # temperature induced paralysis A: see tipA # Temporal protein 1: see Tp1 #*ten: tenuis chaetae location: 1-43.9. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1953. references: 1958, DIS 32: 76. phenotype: Bristles short and thin. Body small. Expression more extreme in female. Eclosion slightly delayed. Viability and fertility good. RK3. # tender little chaetae: see tlc # tenerchaetae: see te # tent: see tnt # tenuis chaetae: see ten # ter: terraced location: 2-36. origin: Spontaneous (terU appeared as cluster in mutable sc z wzmz stock). discoverer: Bridges, 29c12. references: Kalisch, 1970, Mol. Gen. Genet. 107: 321-35. 1980, DIS 55: 206-07. phenotype: Eye abnormality varies from tiny facetless nick in anterior eye rim plus a horizontal seam of irregular facets to a large indentation in the anterior eye margin. Large tuft of bristles often found in facetless eye area. Penetrance in terU about 94% at 16-25. Viability good, but terU/terU homoz- ygotes show lower hatching rate than terU/+ heterozygotes. alleles: Two alleles of similar phenotype described: *ter (Bridges) and terU, terraced of Umea (Kalisch). # Term: Terminus location: 3- {45}. synonym: Bsg75C; ter; hid(?). references: Roark, Mahoney, Graham, and Lengyel, 1985, Dev. Biol. 109: 476-88. Baldarelli, Mahoney, Salas, Gustavson, Boyer, Chang, Roark, and Lengyel, 1988, Dev. Biol. 125: 85-95. phenotype: Blastoderm-specific locus whose function may involve binding to the DNA (see molecular biology section). In the syncytial blastoderm stage, Term RNA is distributed uniformly throughout the embryo. In late cellular blastoderm, it is concentrated at the posterior pole. At gastrulation, the RNA is found in the invagination that gives rise to the posterior midgut and proctodeum, the region that will form the ventral furrow, and the anterodorsal neurogenic region, but it disap- pears by the end of the period of germ band extension. cytology: Placed in 75C1-2 on the basis of in situ hybridiza- tion to the salivary chromosomes at 75C (Roark et al., 1985) and inclusion in Df(3L)W10 = Df(3L)75A6-10;75C2-4 (Baldarelli et al., 1988). molecular biology: Gene cloned (Roark et al.). A 5.8 kb. EcoRI fragment subcloned and restriction mapped and the nucleotide sequence of the Term coding region determined (Baldarelli et al., 1988). There are two transcription units, ( and ~, which appear to have identical coding regions and to be oriented in opposing directions with 3' ends adjacent. The longest open reading frame begins at the methionine codon at position 155 and extends without interruption to the tyrosine codon at 1436; it is believed to be the ORF that encodes the Term pro- tein. The RNA contains 150 nucleotides of untranslated sequences at its 5' end. A potential regulatory region between positions -387 and -431 contains two identical inverted repeats. The protein predicted from the nucleotide sequences has a TFIIIA-like finger which may bind to the DNA (Baldarelli et al., 1988). # terraced: see ter # tet: tetraltera location: 2- [located on 3 by Villee (1942); location later revised by Goldschmidt (1952, 1953), who considered tet to be multifactorial with the main factor on 2 and enhancing factors on X and 3; placed on 2 by E.B. Lewis and Garcia-Bellido]. origin: Spontaneous. dicoverer: Goldschmidt, 34l. references: 1940, Material Basis of Evolution, Yale University Press, p. 325 (fig.). Villee, 1942, Univ. Calif. Publ. Zool. 49: 125-84. Goldschmidt, Hannah, and Piternick, 1951, Univ. Calif. Publ. Zool. 55: 67-294. Goldschmidt, 1952, J. Exp. Zool. 119: 405-60. 1953, J. Exp. Zool. 123: 79-114. James and Bryant, 1981, Dev. Biol. 85: 39-54. phenotype: Wings reduced; may have tendency to be halterelike. Duplications of the notum as well as the costa and ventral hinge of the wing accompanied by deficiencies for the rest of the wing; outgrowths from wing formed by duplications of the costa; no evidence for wing to haltere transformation observed by James and Bryant (1981). Little cell death in third larval instar. Expression variable; overlaps wild type; enhanced by oss (E.B. Lewis). Penetrance temperature-sensitive (0-1% at 29, 35% at 15). RK3. alleles: tet (Goldschmidt; Villee); tet3 (Garcia-Bellido), *tetBd (Goldschmidt; Piternick). # tetanic: see tta # tetraltera: see tet # tetrapter: see ttr # tetrodotoxin-sensitive: see ttx # Tevel: see Fs(3)Sz21 #*tf: trefoil location: 2-55 (between 50 and 60). discoverer: Morgan, 13k. references: Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 244 (fig.). phenotype: Scutellum darkened. Base of trident pattern and back of head have extra areas of dark pigmentation. Classifi- cation uncertain. RK3. # tfd: two-faced (J.C. Hall) location: Complex; major components on 3. origin: Spontaneous. references: Lipschitz and Kankel, 1985, Dev. Biol. 107: 1-12. phenotype: Flies show variable expression of eye-antennal abnormalities on the dorsal head cuticle, ranging from cuticu- lar deformities with missing bristles and ocelli to duplica- tions of the antennae (frequent), eyes, and labial palps (infrequent). The extra antenna is usually a perfect copy of the normal one, but the extra eye is much smaller, with irreg- ular facets. In the late third instar, larvae often have extra tissue in their eye-antennal disks; in adults there is everted but not externalized disc tissue in the head. Nerves from extra antennae were traced with silver staining and Golgi and tannic acid and found to frequently connect to and make normal projections in the brain; no connections between the extra eyes and the brain were found. The infrequent palp duplications were not examined in detail. other information: The tfd phenotype originally appeared with low frequency (about 1%) in a In(3LR)DcxF, ru h D Sb sr es/Gl Ubx e4 stock, was separated from the DcxF chromosome and selected for until penetrance was almost complete and 20-40% of the flies showed strong tdf expression. Both penetrance and expression decreased rapidly when selection was relaxed except when tdf enhancer(s) had accumulated in the stock. #*tft: tufts location: 2-102 (between px and bw). origin: / ray induced. discoverer: R. M. Valencia, 1959. references: 1959, DIS 33: 99-100. phenotype: Sternopleural bristles form a dense tuft. Fully penetrant at 20, poorly so at 25. RK2. # Tft: Tufted location: 2-53.6; 1.2 cM to left of Bl (Tokunaga, 1967). origin: X ray induced. discoverer: Ritterhouse, 52f25. references: 1952, DIS 56: 68-69. Arnheim, 1967, Genetics 56: 253-63. Tokunaga, 1967, DIS 42: 40. Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85. Ghysen and Richelle, 1979, Dev. Biol. 70: 438-52. phenotype: Dominant mutation characterized by an increased number of bristles in the postalar, dorsocentral, and scutel- lar regions; tufts of bristles formed on mesothorax in both homo- and heterozygotes; bristles shorter in homozygotes. Extra bristles located dorsal to halteres at junction of thorax and abdomen. Posterior part of mesonotum appears wider than normal. Homo- and heterozygous females have a greatly reduced scutellum; scutoscutellar suture almost absent; heterozygous males have a nearly normal scutellum (Arnheim, 1967). Small to moderate amounts of fluid tend to remain between the epithelial layers of the wing. Penetrance of extra-bristle character 100%. Tft not suppressed by Df(1)sc19 = Df(1)1A1;1B4-5 but suppressed by Df(1)260-1 = Df(1)1A1;1B4-6 (Garcia-Bellido, communicated to Campuzano, Carramolino, Cabrera, Ruiz-Gomez, Villares, Boronat, and Modolell, 1985, Cell 40: 327-38). Cell autonomous in mosaics (Arnheim, 1967). Viability and fertility low. alleles: Single Tft allele and a viable point mutant revertant, Tftrv54 (Wright et al., 1976). cytology: Probably located in 37A3-6 since reverted to Tft+ by In(2L)47 = In(2L)37A2-B1;38A6-C1 (Wright et al., 1976). Uncovered by Df(2L)TW3 = Df(2L)36F7-37A1;37B2-8 and Df(2L)TW50 = Df(2L)36E4-F1;38A6-7. other information: Extra bristles often very close together; underlying neurons make functional contacts with the CNS (Ghysen and Richelle, 1979). Innervated bristles also found in the metanotum, which has no bristles in wild-type flies (Garcia-Bellido and Deak). # tg: telegraph location: 2-0.0. discoverer: Bridges, 16c27. references: Morgan, Bridges and Sturtevant, 1925, Bibliog. Genet. 2: 237. Stern and Bridges, 1926, Genetics 11: 507 (fig.), 508-10. Carlson, 1966, Ohio J. Sci. 66: 340-46. 1970, Ohio J. Sci. 70: 365-71. Thompson, 1973, DIS 50: 59. phenotype: Vein L2 has one or more gaps or thin sections. Postscutellar bristles erect or misdirected. Overlaps wild type. RK3. alleles: Two alleles: tg of Bridges and tgC of Carlson (1966, 1970). # Tg: see under shv in dpp entry # th: thread location: 3-43.2. references: Ward and Alexander, 1957, Genetics 42: 42-54. Korge, 1972, DIS 48: 20. Mglinetz and Ivanov, 1975, Genetika (Moscow) 11: 88-96. Ashburner, Richards, and Velissariou, 1980, DIS 55: 196. phenotype: Aristae threadlike, without side branches. Mutation affects development of tarsal claws at 29 (Mglinetz and Ivanov, 1975). Deficiency for th homozygous lethal (Ward and Alexander, 1957; Korge, 1972). Mutant males and females less successful in mating than wild-type (Burnet, Connolly, and Dennis, 1971, Anim. Behav. 19: 409-15). alleles: Mutants and rearrangements (other than deficiencies) are described in the following table. allele origin discoverer ref ( cytology ___________________________________________________________________ th spont Bridges, 22j31 3 th3 | / ray Velissariou 1 *th293 / X ray Alexander 3 In(3L)72A2-B1;76A4-B1; 79A4-B1 thSS107 X ray 2 thSS108 X ray Smith 2 In(3L)63F3-5;72A3-4 + In(3L)68F5;73F ( 1 = Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91; 2 = Ashburner, Faithfull, Littlewood, Richards, Smith, Velissariou, and Woodruff, 1980, DIS 55: 193-95; 3 = Ward and Alexander, 1957, Genetics 42: 42-54. | Induced together with Df(3L)st3 = Df(3L)72E5-F1;73A4-5. / Homozygous lethal. cytology: Placed between 72A2 and 72C1-2 (Korge, 1972) since uncovered by Df(3L)th701 = Df(3L)72A2;72D and Df(3L)th70kI = Df(3L)71C3-4;72C1-2; probably in 72B1 according to Ashburner et al., 1980. # Th: Tyrosine-3-hydroxylase (K. White) location: 3-{21}. origin: Isolated as a cDNA clone using homology to rat tyrosine hydroxylase (TH). references: Neckameyer and Quinn, 1989, Neuron 2: 1167-75. cytology: Placed in 65B by in situ hybridization to the salivaries. molecular biology: Gene cloned and nucleotide sequence of the Drosophila cDNA and deduced amino acid sequence of the protein obtained (Neckameyer and Quinn, 1989). A 3.2 kb clone iso- lated from an adult Drosophila head library was analyzed. There is a single open reading frame that encodes a 58 kd pro- tein that is almost 50% identical to rat tyrosine hydroxylase. The protein is specifically recognized by an antibody made against bovine TH. The Drosophila gene is expressed in head tissue and first instar larvae. Transcripts of 3.2 and 3.65 kd were detected, the latter appearing to be adult-specific. other information: The Drosophila melanogaster mutant pale has been genetically mapped to the same region (65B) as the rat TH-homologous Drosophila cDNA clones, suggesting that ple may be a TH mutation. The ability of Th DNA to rescue ple mutants, however, has not been tested. #*tha: thin arched location: 1-27.8. origin: Induced by S-2-chloroethylcysteine (CB. 1592). discoverer: Fahmy, 1957. references: 1959, DIS 33: 93. phenotype: Fly small, has short thin bristles. Wings arched over abdomen or drooping at sides. Viability and fertility low. RK3. #*thb: thin bristle location: 1-48.0. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1951. references: 1958, DIS 32: 76. phenotype: Bristles thin, short in female. Occasionally, vibrissae abnormal and eyes rough. Vein L5 sometimes faint or missing beyond posterior crossvein. Viability and fertility good in male and reduced in female. RK2. # thg: throng location: 2-{0}. references: Shamanski and Orr-Weaver, 1989. Genetics: Maternal effect mutant. cytology: Located at 21B. # thi: thick head location: 2-72. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1983, DIS 59: 158-60. 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Homozygous lethal in embryo. Broad head. In combi- nation with Pc-like mutants, abdominal transformations occur. alleles: Two alleles, thi1 and thi2 isolated as HM and HN. # thic: thickened aristae location: 1- (to right of f). origin: Induced by ethyl methanesulfonate. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. Homyk, 1977, Genetics 87: 105-28. phenotype: Aristae and sex combs thickened; dark specks in eye. Lethal at 29. # thick: see tk # thick head: see thi # thick legs: see thl # thick legs-darker: see thl-d # thick vein: see thv # thick vein delta: see thvd # thick veins: see tkv # thickened arista: see thic # Thickened arista: see Ta # thickened veins: see thiv # thickoid: see tkd # thickset: see tht # thin: see tn # thin arched: see tha # thin bristle: see thb # thin bristles: see tbs # thin macros: see thm Third chromosome cold-sensitive paralytic: see Tcp # Third chromosome resistant: see Tcr # thiv: thickened veins location: 2-71.4. origin: Nuclear polyhedrosis virus of Galleria melonella. references: Shandala, 1985, Tsitol. Genet. 19: 179-83. phenotype: Wing veins thickened. Maximum penetrance at 16, minimum at 28; TSP for penetrance between second and third larval instars. #*thl: thick legs location: 1-60.7. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1955. references: 1959, DIS 33: 93. phenotype: Legs short and swollen, particularly posterior pair; swelling most pronounced in tibial and tarsal regions. Wings small and broad, divergent or slightly upheld. Body color slightly dusky and eye color a bit brownish. Male fertile; viability about 20% wild type. RK3. other information: One allele each induced by CB. 1506 and CB. 1528. # *thl-d: see *dkl #*thm: thin macros location: 1-48.9. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). references: Fahmy, 1958, DIS 32: 76. phenotype: Bristles slightly shorter and thinner than normal. Viability and fertility good. RK2. # thorny: see tny # thr: three rows location: 2-86. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1983, DIS 59: 158-60. 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Larval denticles sparse and arranged in few rows, all pointing posteriorly. Denticles larger than normal. Apparently no mitoses after the first post-blastoderm mitosis, resulting in embryos with fewer and larger cells than normal. TSP 4-9 h. Homozygous lethal in embryo. alleles: allele synonym comments ________________________________________ thr1 thrIB thr2 thrIL thr3 thrIIV temperature-sensitive thr4 thrBH hybrid dysgenic *thr5 *thr6 *thr7 *thr8 cytology: Placed in 55A-F. # thread: see th # thread bristle: see trb # three rows: see thr #*tht: thickset location: 1-42.1. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007) discoverer: Fahmy, 1953. references: 1959, DIS 33: 93. phenotype: Fly reduced in size, more in length than breadth, giving a stocky appearance. Eye shape slightly altered, has a few deranged facets. Viability about 10% wild type. Male fertile. RK3. # thv: thick vein location: 1-49.7. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1958, DIS 32: 76. phenotype: Veins thick, especially at junction of L1 and L2. Wings short and broad; marginal hairs irregular. Eyes small and dark. Body color rather pale. Eclosion delayed. Male viable and fertile. Female fertility subnormal. RK2. #*thvd: thick vein delta location: 1-55.2. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1955. synonym: dtv: delta vein. references: 1958, DIS 32: 69-70. phenotype: Wings slightly short and broad; has extra venation, especially around L2, which usually ends in a delta. Anal plates and genital arch deformed; genital region protruding. Male fertile but viability about 50% normal. RK3. #*ti: tarsi irregular location: 2-55.9. origin: Spontaneous. discoverer: Ives, 38k5. references: 1942, DIS 16: 48. phenotype: Third and fourth tarsal segments more or less fused and swollen. Eyes slightly rough. Viability subnormal. RK2. # tiddler: see tdd # tilt: see tt # tiny: see ty # tiny bristle: see tb # tiny bristle 2: see tyb2 # tiny bristleoid: see tbd # tiny chaetae: see tc # tiny eggs: see tne # tiny ovaries: see tov # tiny wing: see tyw # tinylike: see tyl # tipA: temperature induced paralysis A (J.C. Hall) location: 2-44.0. origin: Induced by ethyl methanesulfonate. references: Kulkarni and Padhye, 1982, Genet. Res. 40: 191-99. phenotype: Becomes paralyzed rapidly at 38C; time required for recovery (after return to 23) increases quickly with duration of exposure to high temperature. alleles: tipA1 and tipA2, the latter of which apparently leads to more rapid heat-induced paralysis and a longer recovery time. # TipB (J.C. Hall) location: 2-109.9. origin: Induced by ethyl methanesulfonate. references: Kulkarni and Padhye, 1982, Genet. Res. 40: 191-99. phenotype: Homozygous lethal; heterozygotes become rapidly paralyzed at 38C and recover fairly quickly when temperature is lowered. # tipC (J.C. Hall) location: 2-35.3. origin: Induced by ethyl methanesulfonate. references: Kulkarni and Padhye, 1982, Genet. Res. 40: 191-99. phenotype: Becomes paralyzed gradually at high temperatures (the higher the temperature, the faster the paralysis); recovery from paralysis, after temperature lowered, is some- what slow, and time required for this increases with longer heat exposure. # tipD (J.C. Hall) location: 2-110. origin: Induced by ethyl methanesulfonate. references: Kulkarni and Padhye, 1982, Genet. Res. 40: 191-99. phenotype: Becomes paralyzed rapidly at 38C; recovers fairly quickly when temperature is lowered. other information: Complemented lethality associated with TipB. tipD/TipB adults exhibit same heat-induced paralysis kinetics as does TipB/+; these mutations probably define separate genes in spite of similar map locations. # tipE (J.C. Hall) location: 3-13.5. origin: Induced by ethyl methanesulfonate. references: Kulkarni and Padhye, 1982, Genet. Res. 40: 191-99. Ganetzky, 1986, J. Neurogenet. 3: 19-31. Jackson, Wilson, and Hall, 1986, J. Neurogenet. 3: 1-17. phenotype: Mutant becomes paralyzed rapidly at 38; recovers within seconds when temperature is lowered. No apparent increase in recovery times with longer exposure to high tem- perature (Jackson et al., 1986). When in a double mutant com- bination with parats1, tipE results in action potential failures in recordings from larval motor neurons at 33, a tem- perature at which either parats1 or tipE alone seems to have normal nerve conduction (Ganetzky, 1986). Adult action poten- tial failures in napts;tipE double mutants occur at a lower temperature (31) than in wild type (Ganetzky, 1986); flies of this double-mutant genotype exhibit poorer viability and become paralyzed at lower temperatures than either mutant alone. The parats1; tipE double mutants also survive poorly, showing unconditional lethality in combinations with certain para alleles; In para/+; tipE/tipE mutants, para alleles become semi-dominant for heat-induced paralysis (Ganetzky, 1986). Biochemically, tipE leads to reduced levels of saxitonin binding activity (not temperature-dependent) in adult head extracts, but the dissociation constants for such binding is normal (Jackson et al., 1986). The mutant is slightly resis- tant to veratrine and shows enhanced tetrodotoxin sensitivity (Jackson et al., 1986). Sodium current density in cultured embryonic neurons is about half that recorded using "tight- seal" techniques from wild-type cells (O'Dowd and Aldrich, 1988, J. Neurosci. 8: 3633-43). When rather lengthy heat treatments are given to seits, the fairly long recovery times are partially suppressed by tipE. Partial suppression of Sh-induced leg shaking is also effected by tipE (Jackson et al., 1986). cytology: Located in 64A6-64B12 (L.M. Hall and colleagues) since included in Df(3L)HR277 = Df(3R)63B12-C1;64B12 but not in Df(3L)HR298 = Df(3L)63B6;64A6. # tipF (J.C. Hall) location: 3-15.2. origin: Induced by ethyl methanesulfonate. references: Kulkarni and Padhye, 1982, Genet. Res. 40: 191-99. phenotype: Kinetics of paralysis at a series of elevated tem- peratures like that associated with tipC, though tipF requires substantially longer times to recover after temperature lowered. other information: Complements tipE. # tk: thick location: 2-55.3. discoverer: Guthrie, 24k. references: 1925, Am. Naturalist 59: 479-80. phenotype: Legs and especially tarsi thick. Wings somewhat short and broad, has slight px-like effect. According to Wad- dington [1942, Proc. Zool. Soc. London Ser. A., 111: 181-88 (fig.)], these effects result from inadequate contraction of the legs and whole pupa after inflation period. RK2. cytology: Placed in region between 42A2 and 42B1 on the basis of its inclusion in inverted segment of In(2R)Cy = In(2R)42A2-3;58A4-B1 as well as in Df(2R)M41A-vg11 = Df(2R)40F-41A1;42A19-B1 (Morgan, Schultz, Bridges, and Curry, 1939, Carnegie Inst. Wash. Year Book 38: 273-77). # tkd: thickoid location: 2-40 (30 to 50). discoverer: Bridges, 33d25. phenotype: Fly large and thickset, has thick legs. Wings blunt at tip. Eyes large and slightly rough. Male genitalia some- times rotated. Fertile; viability about 50% wild type. RK3. # tko: technical knockout (J.C. Hall) location: 1-1.0 (.006 to left of z according to Judd et al., 1972). references: Judd, Shen, and Kaufman, 1972, Genetics 71: 139- 56. Shannon, Kaufman, Shen, and Judd, 1972, Genetics 72: 615-38. Lim and Snyder, 1974, Genet. Res. 24: 1-10. Liu and Lim, 1975, Genetics 79: 601-11. Ganetsky and Wu, 1982, Genetics 100: 597-614. Burg and Wu, 1987, Neurosci. Abstr. 13: 619. Royden, Pirotta, and Jan, 1987, Cell 51: 165-73. Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52. phenotype: Most tko alleles are lethal in all genetic combina- tions. In homo- and hemizygotes of the viable allele tko25t, however, mechanically shocked adults fall over and are briefly immobilized; after recovery, there is a refractory period dur- ing which sensitivity to further such shocks is reduced. tko25t is considered a semi-lethal by Judd, 1972, who finds that survivors exhibit a fine bristle phenotype. This allele is also a heat-sensitive paralytic (Burg and Wu, 1987). Its aberrent behavior is suppressed by napts when the latter is kept at its permissive temperature (Ganetzky and Wu, 1982). When heterozygous with deficiencies for the locus, most tko alleles are lethal. alleles: One viable and nine lethal alleles have been described. allele origin synonym ref ( comments __________________________________________________________________ tko1 EMS l(1)EC229 5 lethal tko2 EMS l(1)VA256 5 lethal tko3 EMS l(1)VE691 5 lethal tko4 | l(1)64k11 2 lethal tko15p NNG 4 lethal tko25t NNG 1, 3, 4, 8 quasi-viable and behaviorally defective; female hemizygotes lethal tkoe75 EMS 6 lethal tkok11 / dimethyl 4, 9 larval lethal sulfoxide + X rays tkom78 MMS 7 lethal tkom100 MMS 7 lethal ( 1 = Burg and Wu, 1987, Neurosci. Abstr. 13: 619; 2 = Garcia-Bellido and Robbins, 1983, Genetics 103: 235-47; 3 = Ganetsky and Wu, 1982, Genetics 100: 597-614; 4 = Judd, Shen, and Kaufman, 1972, Genetics 71: 139-56; 5 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 6 = Lim and Snyder, 1974, Genet. Res. 24: 1-10; 7 = Liu and Lim, 1975, Genetics 79: 601-11; 8 = Royden, Pirotta, and Jan, 1987, Cell 51: 165-73; 9 = Shannon, Kaufman, Shen, and Judd, 1972, Genetics 72: 615-38. | Discovered by Geer. / Discovered by Alexander (Judd et al., 1972). cytology: Placed in 3A2 (Judd et al., 1972) based on uncoverage of lethality by Df(1)w-rJ1= Df(1)3A1-2;3C2-3, Df(1)X12 = Df(1)2F5-3A1;3B5-3C1, and Df(1)62g18 = Df(1)3A1-2;3A4-5, and complementation by Df(1)64c4 = Df(1)3A3-4;3C2-3. molecular biology: tko region cloned, originally by micro- dissection (Mariani, Pirrotta, and Manet, 1985, EMBO J. 4: 2045-52) and identified molecularly by transformation res- cue. A 3.1 kb XhoI/BamHI fragment covers lethality caused by tkok11 and behavioral defects of tko25t (Royden et al., 1987). This genomic DNA fragment encodes one detectable transcript of 0.68 kb. Predicted protein shows considerable sequence simi- larity to ribosomal protein S12 from Euglena gracilis chloro- plasts and E. coli (Royden et al., 1987). # Tkr: Tyrosine kinase related location: 2- {107}. origin: Induced by ethyl methanesulfonate. synonym: dTKR (Haller et al., 1987); g2 (Cote et al., 1987). references: Cote, Preiss, Haller, Schuh, Kienlin, Seifert, and Jackle, 1987, EMBO J. 6: 2793-2801. Haller, Cote, Bronner, and Jackle, 1987, Genes Dev. 1: 862- 67. phenotype: No mutant phenotype identified as yet. Transcripts initially expressed in the syncytial blastoderm stage (Haller et al., 1987; Cote et al., 1987), accumulating temporarily at dorsal-lateral positions in the embryo. At the end of blasto- derm, the transcripts accumulate unevenly and are restricted to the dorsal region along 20-85% of the egg length. During gastrulation they are found in the dorsal region of the cephalic furrow and cover the neurogenic ectoderm in the pro- cephalic region, disappearing from anterior to posterior dur- ing the extended germband stage. Later Tkr is expressed anew in the developing nervous system, including the brain, but disappears completely at the end of embryogenesis (Haller et al., 1987). cytology: Located in 60F1 on the basis of in situ hybridiza- tion. Also, Tkr included in Df(2R)IIX62 = Df(2R)60E9- 10;60F1-2 (Cote et al., 1987). molecular biology: To determine the molecular structure of the Tkr gene, the cDNA clone, the corresponding genomic DNA, and the genomic DNA upstream of the 5' end of the cDNA were sequenced and the amino acids predicted. There is a single open reading frame of three exons (a 5' exon of 1357 bp, a small exon of 132 bp and a 3' exon of 1895 bp separated by two introns of 2500 and 3800 bp, respectively) which would encode a 753-amino-acid polypeptide. A single major transcript (4 kb long) is indicated by northern blot analysis (Cote et al., 1987). other information: Weak homology has been demonstrated between the putative Tkr protein and various serine, threonine, and tyrosine kinases and related oncogenes. The presence of puta- tive ATP-binding and tyrosine autophosphorylation sites in the tkr sequence also suggests a tyrosine kinase function (Haller et al., 1987). tkv: thick veins Edith M. Wallace, unpublished. # tkv: thick veins location: 2-16. references: Kotarski, Pickert, and MacIntyre, 1983, Genetics 105: 371-86. Reuter and Szidonya, 1983, Chromosoma, 88: 277-85. Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. Szidonya and Reuter, 1988a, DIS. 67: 77-79. 1988b, Genet. Res. 51: 197-208. phenotype: Two types of mutants have been described, recessive lethals and visibles (viable as adults ). Some of the reces- sive lethals die as embryos, lacking dorsal hypoderm (Nusslein-Volhard et al., 1984). The wing veins of the viable mutants are thickened and branched in the region of crossveins, near end of L2, and elsewhere. Sometimes there is a blister near the posterior crossvein in female flies; L4 sometimes shortened, especially in females. Expression more extreme at 19 than at higher temperatures and in females than in males. Some heteroallelic combinations are lethal; others are viable with thick veins and thoracic abnormalities (Szi- donya and Reuter, 1988b). alleles: Lethal and viable alleles are listed in the following table. Deficiences for tkv are described in the rearrangement section. alleles origin discoverer synonym ref ( comments ____________________________________________________________________________ tkv1 spont Nichols-Skoog, homozygous viable 33b25 with thick veins tkv2 spont Bridges, 34e20 homozygous viable with thick veins tkv3 EMS Szidonya tkvSz3 1 homozygous viable with thick veins; Tp(2;3)25A2-3;25D5-E1;69C tkv4 | EMS Szidonya tkva12 1, 2 homozygous lethal tkv5 EMS Szidonya tkva33 1, 2 homozygous lethal tkv6 | EMS Szidonya tkvSz15 1, 2 homozygous lethal; hemizygous viable with thick veins; tkv7 / EMS Nusslein-Volhard strIO 3 homozygous lethal tkv8 / EMS Nusslein-Volhard strIIB 3 homozygous lethal ( 1 = Szidonya and Reuter, 1988a, DIS 67: 77-79; 2 = Szidonya and Reuter, 1988b, Genet. Res. 51: 197-208; 3 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. | Viable with strong tkv phenotype over Tp(2;3)tkv3 (Szidonya and Reuter, 1988b). / Allelism with tkv indicated by location, failure to comple- ment lethal and viable tkv alleles, and thick vein and abnormal thorax phenotype over Tp(2;3)tkv3 (Szidonya and Reuter, 1988b). cytology: Located in 25D5-E1 (Szidonya and Reuter, 1988a, 1988b); in the region of overlap of Df(2L)tkv-Sz3 = Df(2L)25A2-3;25D5-E1 and Df(2L)cl-h2 = Df(2L)25D5-6;26A7-8. # Tl: Toll location: 3-91. discoverer: Wieschaus and Nusslein-Volhard. synonym: Fs(3)Tl (dominant allele); mel(3)9, mel(3)10 (reces- sive alleles). references: Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 317-26. Anderson and Nusslein-Volhard, 1984, Nature 311: 223-27. Anderson, Jurgens, and Nusslein-Volhard, 1985a, Cell 42: 779-89. Anderson, Bokla, and Nusslein-Volhard, 1985b, Cell 42: 791- 98. Anderson and Nusslein-Volhard, 1986, Symp. Soc. Dev. Biol. 44: 177-94. Anderson, 1987, Trends Genet. 3: 91-97. Carroll, Winslow, Trombly, and Scott, 1987, Development 99: 327-32. Gerttula, Jin, and Anderson, 1988, Genetics 119: 123-33. Hashimoto, Hudson, and Anderson, 1988, Cell 52: 269-79. Erdelyi and Szabad, 1989, Genetics 122: 111-27. phenotype: Maternal expression of the Toll gene is required for the normal production and distribution of positional informa- tion in the embryo (Anderson et al., 1985); zygotic expression is required to maintain viability in early larvae (Gerttula et al., 1988). Toll mutants and deficiencies occurring in the mother result in lethal abnormalities in the pattern of gas- trulation and the differentiation of cuticular structures in the offspring. When null alleles and deficiencies are homozy- gous in the zygote, delayed development and early lethality result. Females heterozygous for dominant Toll alleles are sterile, their lethal embryos being partially ventralized regardless of their genotype. Dorsoventral polarity is present; a furrow is formed in the midventral region, but the lateral cephalic fold is shifted to the dorsal side and the normal dorsal folds are missing. The cuticle lacks dorsal hairs, filzkorper, spira- cles, head sensory organs, and a head skeleton; there are patches of denticles extending around the entire dorsoventral circumference of the embryo (Anderson et al., 1985a). The ventral nervous system is also expanded (Campos-Ortega, 1983). Embryos produced by females hemizygous for some dominant alleles (Tl1/Df; Tl3/Df) are ventralized, but the embryos of other hemizygotes (Tl2/Df; Tl4/Df) are dorsalized, all cells behaving at gastrulation and in differentiation like wild-type dorsal cells. In embryos derived from Tl/+ females, virtually the entire ectoderm capable of neurogenesis in response to absence of Dl function (Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 317-26). Whereas females heterozygous for recessive alleles of Tl are fertile, homozygous Tl-recessive females are viable but sterile, their lethal embryos lacking dorsoventral polarity and forming no ventral furrow at gastrulation. In most reces- sive alleles (Tlr5, Tlr6, Tlr7), the embryos are partially dorsalized with laterally derived structures (Anderson et al., 1985a); for example, Tlr6 embryos differentiate dorsal hairs, filzkorper, and ventral denticle bands of nearly normal width, but lack mesoderm (Anderson and Nusslein-Volhard, 1986). In one allele (Tlr4), however, embryos have no dorsal hairs and show rings of denticles as in TlD embryos (Anderson et al., 1985a). Hemizygotes for the Toll-recessives resemble the corresponding homozygotes in phenotype. A number of Toll alleles were obtained as reversions of the Toll-dominant phenotype (see table). When crossed to wild- type males, females heterozygous for a null-type reversion are fully fertile; however, when crossed to males who are also heterozygous for a Toll null, these females produce Tl- homozygotes who are zygotic lethals, dying as early larvae and producing no Toll transcript. Heteroallelic combinations of reversions such as Tlrv1/Tlrv2 produce sterile females with lethal dorsalized embryos. Females carrying combinations of certain reversions and Toll-dominant (or Toll-recessive) alleles produce embryos with phenotypes like those of Toll- dominant (or Toll-recessive) hemizygotes. Most of the rever- sions, when in trans to deficiencies, result in females with dorsalized embryos, but a few hemizygous reversion females (Tlrv21, Tlrv22, Tlrv23) produce ventralized embryos (Hashi- moto et al., 1988). The lethal embryos of Df(3R)Tl-X/Df(3R)ro-XB3 (null) females (Hashimoto et al., 1988), are completely dorsalized, never making ventral furrows, filzkorper, or denticles; their germ bands fail to extend; no Toll transcript is produced in these embryos except when contributed by wild-type fathers (Gerttula et al., 1988). The 97D1-2 breakpoint of the Toll deficiency Df(3R)Tl-X maps within the 6.0 kb EcoRI fragment of a Toll clone (Hashimoto et al., 1988). Injection of wild-type cyto- plasm into embryos of Toll-deficient females restores the wild-type dorsoventral pattern, the site of the injection determining the midventral part of the pattern (Anderson et al., 1985b); (also see molecular biology section). alleles: Dominant, recessive, and revertant Toll alleles are listed in the following table. Six HD-induced revertants are mentioned but not named (Hashimoto, Hudson, and Anderson, 1988, Cell 52: 269-279). Deficiencies are listed in the rearrangement section. allele origin allele ref ( comments cytology _____________________________________________________________________________ Tl1 EMS 2,5 dominant Tl2 EMS Tl5B 1,2,5 dominant Tl3 EMS Tl9Q 1,2,5,6 dominant Tl4| EMS Tl84C 2,5 dominant Tl5/ HD Tl9QRPBR14 4,6 dominant Tl6 EMS Tl2b 4 semidominant Tl7 EMS Tl3c 4 dominant Tl8 EMS Tl10b 4 dominant Tl9 EMS Tl18a 4 dominant Tl10 EMS Tl20i 4 semidominant Tlr1`- EMS Tlr26 2,5 recessive Tlr2- EMS Tlr444 2,5 recessive Tlr3- EMS Tlr632 2,3,5 recessive Tlr4 EMS Tlrm9 2,4 recessive Tlr5 EMS TlLB1 4,5 recessive . Tlr6 EMS TlrB1 4,5 recessive Tlr7 EMS TlrB2 4,5 recessive . Tlrv1 X ray TlRXA 2 revertant Tlrv2 X ray TlRXD 2 revertant Tlrv3 X ray TlRXE 2 revertant T(2;3)40-41;97D Tlrv4 X ray TlRXH 2,5 null revertant Tlrv5 X ray TlRXJ 2 revertant In(3R)97D;98F Tlrv6 X ray TlRXZ 2 revertant In(3R)97D;99E-F Tlrv7 EMS Tl5BREF 2 null revertant Tlrv8 EMS Tl5BREH 2 null revertant Tlrv9 EMS Tl5BREJ 2 null revertant Tlrv10 EMS Tl5BREL 2 null revertant Tlrv11 EMS Tl5BREM 2 null revertant Tlrv12 EMS Tl5BREN 2 null revertant In(3R)97D;99B Tlrv13 EMS Tl5BREQ 1,2,5 null revertant Tlrv14 EMS Tl5BRER 2 null revertant Tlrv15 EMS Tl5BRES 2 null revertant Tlrv16 EMS Tl5BREV 1,2,5 null revertant Tlrv17 EMS Tl5BREW 2 null revertant In(3R)97A;97D + Df(3R)97B;97D Tlrv18n X ray Tl5BRXV 2,5 null revertant In(3R)74A;97D Tlrv19 EMS Tl9QRE 1,2,5 null revertant In(3R)97D;98C-D Tlrv20 X ray Tl84CRXB 2 revertant Tlrv21- HD Tl9QRPA 6 null revertant Tlrv22- HD Tl9QRPB 6 null revertant Tlrv23- HD Tl9QRPL 6 null revertant Tlrv24 Tl9QRPS 5 null revertant Tlrv25 Tl9QRPU 5 null revertant ( 1 = Anderson, Bokla, and Nusslein-Volhard, 1985, Cell 42: 791- 98; 2 = Anderson, Jurgens, and Nusslein-Volhard, 1985, Cell 42: 779-89; 3 = Carroll, Winslow, Trombly, and Scott, 1987, Development 99: 327-32; 4 = Erdelyi and Sza- bad, 1989, Genetics 122: 111-27; 5 = Gerttula, Jin, and Anderson, 1988, Genetics 119: 123-33; 6 = Hashimoto, Hud- son, and Anderson, 1988, Cell 52: 269-79. | Pattern normalized by extra copy of wild-type allele. All Tl4/+/+ embryos make dorsal hairs and one quarter of these embryos make filzkorper. / Derivative of Tlrv22 that has restored the dominant Tl3 phenotype; apparently associated with precise excision of the P element (Hashimoto et al., 1988). ` Isolated on the basis of a leaky dominant dorsalized pheno- type. - Temperature sensitive for the maternal effect, showing stronger dorsalization of the embryonic pattern at 29 than at 18; also temperature sensitive for viability. TSP for the maternal effect begins slightly before pole cell forma- tion and ends in midsyncytial blastoderm in the offspring of Tlr7 females. TSP for zygotic viability begins late in embryogenesis and extends into the second larval instar in Tlr5 and Tlr6 mutants. Discovered by T. Rice, who named it mel(3)9. Unique lateralized pattern. Cuticular phenotype of embryos resem- ble that of Toll-dominant embryos, but denticles finer and less heavily pigmented and body shape often an elongated tube. n 97D breakpoint located in the 6.0 kb EcoR1 fragment of the Toll clone Tp1 (Hashimoto et al., 1988). - All HD-induced revertants are derivatives of Tl3. cytology: Placed in 97D1-2 since uncovered by Df(3R)Tl-X = Df(3R)97B;97D1-2 and Df(3R)ro-XB3 = Df(3R)97D1-2;97D9. molecular biology: Toll has been cloned using P element tagging and the nucleotides have been sequenced (Hashimoto et al., 1988). The Toll clone Tp1 contains 15 kb of DNA flanking the P element insertion. Nucleotide sequencing reveals one long open reading frame, with the initiation codon at nucleotide 575 and the termination codon at 3866; it could encode a pro- tein of 1097 amino acids [thought to be a transmembrane pro- tein made up of a cytoplasmic domain and an extracytoplasmic domain containing multiple copies of a 24-amino-acid leucine- rich sequence in two blocks (Hashimoto et al., 1988)]. This mRNA is transcribed (Hashimoto et al., 1988) and also zygoti- cally (Gerttula et al., 1988); no transcript is found when Tl- females are mated to Tl- males, but the 5.3 kb mRNA appears in the embryo when either or both parents carry Tl+. A 5.3 kb hybrid-selected RNA abundant in young embryos (and also in older embryos and pupae) rescues the Tl- mutant phenotype when injected at a posterior ventral site; a wild-type gastrulation pattern and ventral and lateral cuticular structures are pro- duced in these injected Tl- embryos. The sequence of cDNAs indicates that Tl encodes an integral membrane protein with a cytoplasmic and an extracytoplasmic domain, the latter con- taining 15 repeats of a 24 amino acid leucine-rich sequence occurring in both human and yeast membrane proteins (Hashimoto et al., 1988) and the former showing striking homology to human interleukin-1 receptor (Gay and Kieth, 1991, Nature 351: 355-56). other information: Females carrying the dominant allele Tl3, when combined with the mutants gd, ndl, pip, snk, or ea, pro- duce embryos that are lateralized like embryos derived from Tlr8 females; these embryos lack dorsalmost and ventralmost pattern elements, and have rings of denticles (Anderson et al., 1985a). Some alleles of ea increase the probability that the temperature-sensitive alleles Tlr5, Tlr6, and Tlr7 will survive. An interaction has been reported between the reces- sive allele Tlr7 and dpp (Irish and Gelbart, 1987, Genes and Development 1: 868-79). Double mutants of Tl3 and dl produce embryos that are completely dorsalized and indistinguishable from the embryos of dl homozygotes. Females carrying Tl2 or Tl4 in combination with gd, ndl, or dl also produce dorsalized embryos. # tlc: tender little chaetae location: 1- {0.5}. phenotype: Short thin bristles. alleles: Four alleles induced. allele origin discoverer synonym comments _____________________________________________________ tlc1 ( EMS Lefevre l(1)DA654 lethal tlc2 ( EMS Lefevre l(1)VDM30 viable tlc3 EMS Lefevre _247 viable tlc4 spont Schalet l(1)11-76-1 lethal ( References: Lefevre and Watkins, 1986, Genetics 113: 869- 95. cytology: Placed in 2B15 (Lefevre). # tld: tolloid location: 3-85. 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. Partially ventralized. Cephalic furrow shifted dorsally; defects in germband extension. Den- ticle belts extended laterally. alleles: allele synonym comments ____________________________________________ tld1 tld5H weak tld2 tld6B tld3 tld6P4 tld4 tld6P7 tld5 tld7H tld6 tld7M tld7 tld7O tld8 tld8L tld9 tld9B tld10 tld9D temperature-sensitive tld11 tld9K tld12 tld9Q1 tld13 tld9Q7 tld14 tld10E strong tld15 tld10F tld16 tldFF tld17 tldT cytology: Located in 96B-D based on segmental aneuploidy of translocations (Jurgens et al., 1984). # tll: tailless (J. A. Lengyel) location: 3-102. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. Strecker, Kongsuwan, Lengyel, and Merriam, 1986, Dev. Biol. 113: 64-76. Mahoney and Lengyel, 1987, Dev. Biol. 122: 464-70. Strecker, Merriam, and Lengyel, 1988, Development 102: 721- 34. Pignoni, Baldarelli, Steingrimsson, Diaz, Patapoutian, Mer- riam, and Lengyel, 1990, Cell 62: 151-63. phenotype: Recessive; zygotic lethal with pattern deletions in anterior and posterior of embryo (but body of normal length due to increase in length of non-deleted pattern elements). Anteriorly, dorsal portion of cephalopharyngeal skeleton is defective (dorsal arms shortened, dorsal bridge unfused), dor- sal pouch shortened and scleritized, much of brain missing. Posteriorly, eighth abdominal segment and telson, Malpighian tubules, hindgut and much of posterior midgut missing. alleles: The alleles can be arranged in a series as follows: tlll49 > tll1 > tlla = tlll29 > tll2 > tllle3, where tlll49 has almost the amorphic phenotype, and tllle3 is missing only part of the anal pads and part of the hindgut (Strecker et al, 1988; Pignoni et al, 1990; Pignoni and Lengyel, unpublished). The extant tll alleles and rearrangements (other than defi- ciencies) are listed in the following table. allele origin ref ( comments ___________________________________________________ tll1| EMS 1-3 leaky tll2 spont 2-4 In(3R)85F10-86A1;100A6-B1 tlla X ray 2, 3 tlll29 X ray 5 tlll49 X ray 4 tllle3 EMS 5 ( 1 = Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95; 2 = Strecker, Kongsuwan, Lengyel, and Merriam, 1986, Dev. Biol. 113: 64- 76; 3 = Strecker, Merriam, and Lengyel, 1988, Development 102: 721-34; 4 = Pignoni, Baldarelli, Steingrimsson, Diaz, Patapoutian, Merriam, and Lengyel, 1990, Cell 62: 151-63; 5 = Merriam, unpublished. | Originally named tllL10. cytology: Placed between 100A5-6 and 100B1-2 on the basis of in situ hybridization of the cloned tll gene and mapping of tll into the synthetic deficiency produced by combining 3PYD of T(Y;3)A113 = T(Y;3)100A with Dp(3;1)150P = Dp(3;1)20F;100B1-2 (Strecker et al., 1988; Pignoni et al., 1990). molecular biology: Gene cloned and sequenced (Pignoni et al., 1990). The 2.0 kb tll mRNA is maximally expressed in the blastoderm stage embryo. Initial activation of tll transcrip- tion is in two mirror image symmetrical caps at the poles of the embryo; this expression resolves into a posterior cap and an anterodorsal stripe, consistent with the position on the blastoderm fate map of anlagen which give rise to structures deleted in tll embryos. The tll gene is also expressed in cells which appear to be neuroblasts of the brain and sensil- lum precursors of the peripheral nervous system. The concep- tual tll protein has significant similarity to both the DNA- binding and ligand-binding domains of the members of the steroid receptor superfamily (Pignoni et al., 1990). Tran- scription of the tll gene during early embryogenesis is apparently activated via a phosphorylation cascade containing the membrane-bound, tyrosine kinase receptor-like tor gene product and the serine-threonine kinase phl gene product. The tll gene has a positive effect on gene expression in that it is required for appearance of the seventh stripe of expression of at least two pair-rule genes, h and ftz (Mahoney and Len- gyel, 1987) and for specific domains of expression of cad, hb, and fkh (Mlodzik and Gehring, 1987, Development 101: 421-35; Schroder, Tautz, Seifert, and Jackle, 1988, EMBO J. 7: 2881- 87; Weigel, Jurgens, Klingle, and Jackle, 1990, Science 248: 495-98). The tll gene also has negative effects on gene expression; thus kni expression expands posteriorly in tll embryos [Pankratz, Hock, Seifert, and Jackle, 1989, Nature (London) 341: 337-40] and tll is required for the repression of Kr and ftz expression that occurs in tor gain-of-function embryos [Klingler, Erdelyi, Szabad, and Nusslein-Volhard, 1988, Nature (London) 335: 295-77; Strecker, Halsell, Fisher, and Lipshitz, 1989, Science 243: 1062-66]. # Tm1: Tropomyosin 1 (J.C. Hall) location: 3- {55}. Closely linked to Tm2. origin: Naturally occurring. synonym: mTmII; cTm(isoform). references: Bautch, Storti, Mischke, and Pardue, 1982, J. Mol. Biol. 162: 231-50. Basi, Boardman, and Storti, 1984, Mol. Cell. Biol. 4: 2828- 36. Karlik, Mahaffey, Coutu, and Fyrberg, 1984, Cell 37: 469-81. Basi and Storti, 1986, J. Biol. Chem. 261: 817-27. Karlik and Fyrberg, 1986, Mol. Cell Biol. 6: 1965-73. Tansey, Mikus, Dumoulin, and Storti, 1987, EMBO J. 6: 1375- 85. phenotype: Structural gene for tropomyosin, a 34,000-dalton protein that acts as a regulator of motility in muscle and nonmuscle cells. At least five tropomyosin isoforms are encoded by Tm1, some in embryos (during myogenesis) and myo- genic cell culture and others in the myofibrils of adult indirect flight muscles and leg muscles. cytology: Located in 88F4-5 by in situ hybridization with cloned DNA (Bautch et al., 1982). Tm1 proximal to Tm2. molecular biology: Gene cloned (Bautch et al., 1982; Karlik et al., 1984). The constant proximal coding region (codons 1- 257) and the variable distal coding region (codons 258-284) have been restriction-mapped and sequenced (Basi et al., 1984; Karlik et al., 1984; Karlik and Fyrberg, 1986). Transcripts of 2.0, 2.3 and 2.8 kb accumulate in the cytoplasm of early embryos, while transcripts of 1.3, 1.4, 1.6, 1.7, 1.8, and 1.9 kb accumulate in muscles of later embryos and adults, the 1.7 and 1.9 kb transcripts being restricted to the indirect flight muscle. The proximal coding region at the 5' end occupies about 18 kb and is made up of five exons and four introns (according to Basi et al., 1984) or five to nine exons and up to eight introns (according to Karlik and Fyrberg, 1986). The distal coding region at the 3' end includes four variable exons and three introns, the first exon coding for cytoplasmic tropomyosin, and the second and third for heavy tropomyosins found in the indirect flight muscles (Karlik and Fyrberg, 1986). As a result of the variable splicing at least five developmentally-regulated isoforms are specified. Tropomyosin in the cytoplasmic (cytoskeletal) form of early embryos and Kc cells (a form originally believed to be encoded by a separate gene) has been found to be an alternatively spliced product of Tm1 (Hanke, Lepinske and Storti, 1987, J. Biol. Chem. 262: 17370-73; Hanke and Storti, 1988, Mol. Cell Biol. 8: 3591-3602. # Tm2: Tropomyosin 2 (J.C. Hall) location: 3- {55} (closely linked to Tm1). origin: Naturally occurring and induced by ethyl methanesul- fonate. synonym: mTmI; lfm(3)3. references: Mogami and Hotta, 1981, Mol. Gen. Genet. 183: 407-17. Bautch, Storti, Mischke, and Pardue, 1982, J. Mol. Biol. 162: 231-50. Basi, Boardman, and Storti, 1984, Mol. Cell Biol. 4: 2828-36. Basi and Storti, 1986, J. Biol. Chem. 261: 817-27. Karlik and Fyrberg, 1986, Mol. Cell Biol. 6: 1965-73. Fyrberg and Karlik, 1987, Mol. Cell Biol. 7: 2977-80. Tansey, Mikus, Dumoulin, and Storti, 1987, EMBO J. 6: 1375- 85. phenotype: Structural gene for tropomyosin that is active in particular muscle lineages in late embryos and adult flies (Basi et al., 1984). A dominant flightless mutant lfm(3)3 was induced by Mogami and Hotta (1981); this mutant, which was unable to jump or fly, turned out to be a Tm2 allele, Tm23. Although arranged in sarcomeres, the myofibrils of Tm23 are structurally weak (Karlik and Fyrberg, 1986). The flightless phenotype can be rescued by P-element mediated transformation with two copies of the wild-type allele of Tm2 (Fyrberg and Karlik, 1987); the ability to jump can be restored with one copy of Tm2+ (Tansey et al., 1987). alleles: One mutant allele Tm23 [=lfm(3)3]. cytology: Located in 88F2-3 by in situ hybridization with cloned DNA (Bautch et al., 1982). Tm2 distal to Tm1. molecular biology: Gene cloned (Bautch et al., 1982). The con- stant proximal coding region (codons 1-257) includes two exons and occupies 833 nucleotides that are interrupted by a single 62-nucleotide intron between codons 198 and 199 (Karlik and Fyrberg, 1986). The variable distal coding region (codons 258 to 284) includes two alternate exons with large untranslated regions. The proximal coding region of Tm2 is 1/20th the size of the corresponding Tm1 coding region, presumably due to deletion of introns in Tm2 and duplication of exons in Tm1 (Karlik and Fyrberg, 1986). The complete nucleotide sequence of Tm2 has been given by Basi and Storti (1986). In the flightless mutant Tm23, pupae lack the 1.7 and 1.9 kb indirect-flight-muscle transcripts, but accumulate the 1.3 and 1.6 kb transcripts (Karlik and Fyrberg, 1986; Tansey et al., 1987). There is an 8.8 kb insertion of middle-repetitive copia-like DNA in the mutant, interrupting the exon believed to be involved in the synthesis of the indirect flight muscle isoform (Tansey et al., 1987). #*tmc: tonomacrochaetae location: 1-17.5. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1955. references: 1958, DIS 32: 76. phenotype: Bristles thin. Abdomen underpigmented, especially in female. Eclosion slightly delayed. Viability and fertil- ity good. RK2. #*tms: tumorous location: 1-58.7. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1954. references: 1959, DIS 33: 93. phenotype: Many small, diffuse tumors. Fly slightly small. Both sexes viable and fertile. RK3. # tn: thin location: 2-85.6 (between c and px). origin: Spontaneous. synonym: l(2)tn. references: Ball, Ball, and Sparrow, 1985, Dev. Genet. (Amster- dam) 6: 77-92. phenotype: Fully penetrant recessive lethal (no homozygous adults recovered). Hatching occurs late and second/third instar moult is delayed. Third instar larvae are long, thin, and rather slow-moving; histological examination shows abnor- mal muscle structure. Puparium also long and thin. Pupal development of homozygotes incomplete. Since mutants are unable to perform movements necessary for pupation, they die prior to eclosion. cytology: Placed within 55F. Gene lies between the transposing elements TE55DE (=TE178) and TE56B (=TE124) and is not lethal over Df(2R)PC4 = Df(2R)55A;55F. # tne: tiny eggs location: 3-91. origin: Induced by ethyl methanesulfonate. discoverer: Anderson. phenotype: Female sterile. Very small eggs. alleles: Four alleles induced. cytology: Located in 97D9-15; it is uncovered by Df(3R)ro80b = Df(3R)97D1;97D15 but not by Df(3R)roXB3 = Df(3R)97D1-2;97D9. #*tnt: tent location: 1-18.0. origin: X ray induced. discoverer: Fahmy, 1956. references: 1959, DIS 33: 93. phenotype: Wings droop to variable extent. Bristles thin. Fly small. Male sterile. RK2. #*tny: thorny location: 1-33.5. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1959, DIS 33: 93. phenotype: Fly grossly deformed, extremely inviable. Eyes small, very rough, and dull red. Thoracic bristles very short. Wings abnormal, spread, incompletely expanded. Male sterile. RK2.