# tu: tumor General term used to denote genes that lead to formation of single or multiple melanotic masses, either free or attached to internal organs in the abdomen or thorax. In most cases, these tumors (called "pseudotumors" by Barigozzi, 1968) appear in third instar larvae and may persist throughout pupal and adult life. They are formed by aggregation of hemocytes ("plasmatocytes") that have been transformed into flattened disk-like cells ("lamellocytes") which encapsulate other tis- sues (Rizki, 1957, J. Morphol. 100: 437-58; Rizki and Rizki, 1974, J. Invert. Path. 24: 37-40). Just before pupation, these masses of mutant location origin synonym discoverer ref ( comment ____________________________________________________________________________________________________________________________________ *tu-1a 2- spont Payne 60 in combination with tu-1b, produces melanotic tumors in 20% of larvae and 14% of adults; larval lethal in 57-81% *tu-1b 3- spont Payne 60 in combination with tu-1a, produces melanotic tumors in 20% of larvae and 14% of adults; larval lethal in 57-81% *tu-2 2- spont Payne 60 melanotic tumors in 20-100% of larvae; lethal in 41% tu-36e spont Skoog, 36e15 56 low penetrance tu-47 56 low penetrance tu-48 2-29.5 spont tu-48a Ghelelovitch 15, 23, 24, melanotic tumors in abdomen 56 of 3rd instar larvae; penetrance 96%; modifers on X and 4 (?) tu-4849h 2- spont tu-49h Brncic 7, 11, 13 penetrance 50-60%; fertility and viability good; modifier on 3 tu-48A2 2-(25.8- spont tu-A2 Barigozzi 1-3, 21 low penetrance 28.5) tu-48j 2-46 spont Herskowitz 11, 27, 28 melanotic tumors in 50% of larvae and in adult (abdomen) tu-49k 2- spont Oftedal 38, 39 black hemocyte aggregations (75-100) in late larvae; modifiers on X and 2 tu-53 1-41 neutrons tu-53l Darrow, 53l20 32 small melanotic tumors in 15- 20% of adults; wing abnormali- ties; egg hatch 65% of normal and delayed; lethality 50-70% tu-54e spont Haddox, 54e25 12 small melanotic tumors in 0.44% of adults under tergites 1 and 2 *tu-59h 2- spont Oshima 40 Small melanotic tumors in late larvae and adults *tu-be 3-25 spont *be-3 Stark, 16k 57-59 melanotic tumors in larvae and adults; nonlethal; modifiers tu-bw 2- spont mtA Morgan, 1922 8, 9, 11, 21 numerous melanotic tumors in (80.5-84) 26, 37, 52, larval hemocoel and in adults; 55 penetrance 59-86%; suppressed by su(tu-bw), affected by diet tu-bw36a 2- spont tu-36a Bridges, 36a16 11, 14, 50, melanotic tumors in late larvae; 51 penetrance 5-8% tu-bw50d 2- tu-50d 11, 14, 56 penetrance 12-27%; enhancer on X tu-bw50j 2- spont tu-50j Mittler, 1950 34-36 penetrance 5-10%; melanotic spots under ventral abdominal surface; mutant viable and fertile tu-bw55g 2- spont tu-55g Jacobs 21, 30 melanotic tumors in larvae and adults; almost 100% penetrance; usually in abdomen but may be in thorax or head (rare) tu-bwB3 2- spont tu-B3 Barigozzi; 2, 3, 15, suppressed by su(tu-bw); (85-90) Di Pasquale 21, 41, 56 penetrance 90% tu-bwe 2-88.0 spont e11 tu 22, 25, 31 melanotic tumors in posterior of larvae and abdomen and thorax of adults tu-C4 3- spont Barigozzi 2, 5, 6 incomplete dominance; (52-53) modifiers probably on 2 tu-D 2- spont Barigozzi 2 tu-e144 2- spont e144 Barigozzi 2, 4 tu-K 2- spont Sang,Burnet 8, 9, 16, small black nodules in hemo- 53-55 coel or with fat body in late larvae; penetrance low but can be increased by dietary changes tu-mt 3- mt 33 melanotic tumors in abdomen in 0-100% of larvae tu-mwh 2, 17 pupal lethal; 88% tumorous; lymph gland melanotic mass tu-pb 2- spont 18, 19, 20 melanotic tumors at base of 3- proboscis (62-70.7) *tu-R 1- spont Rosenberg 29 penetrance 40%; lethality 50%; bristles short tu-Soc spont 2, 42 melanotic masses in 33% of larvae and 5% of adults; semilethal tu-Szts | 1-34.3 EMS Suzuki 45, 46 melanotic tumors in caudal 48, 49 fat bodies of larvae at 26; none at 18 tu-W 2-66.2 dibenzan- Gowen 8, 9, 43, melanotic tumors in caudal thracene 44, 47, fat bodies; penetrance incomplete 56, 61 though raised to 100% by selection tu-Wg 2- tu-g 11, 13, 14 melanotic tumors in caudal 56, 62 fat bodies in late larvae; penetrance 50-100% tu-wps 10, 11, 14 penetrance up to 17% ( 1 = Barigozzi, 1962, Atti Assoc. Genet. Ital. 7: 9-76; 2 = Barigozzi, 1968, Nat. Canc. Inst. Monogr. 31: 277-90; 3 = Barigozzi and Di Pasquale, 1956, Rend. Inst. Lomb. Sci. Lett. 90: 484-509; 4 = Barigozzi, Castiglione, and Di Pasquale, 1960, Heredity 14: 151-62; 5 = Belt, 1971, J. Insect. Physiol. 17: 1217-23; 6 = Belt and Burnet, 1972, Genet. Res. 20: 115-35; 7 = Brncic, 1950, DIS 24: 57; 8 = Bryant and Sang, 1968, Nature (London) 220: 393-94; 9 = Bryant and Sang, 1969, Genetics 62: 321-36; 10 = Bur- dette, 1951, Acta Unio. Int. Cancrum 7: 670-74; 11 = Bur- dette, 1951, DIS 25: 101-02; 12 = Burdette, 1954, DIS 28: 73; 13 = Burdette, 1959, Univ. Texas Publ. 5914: 57- 68; 14 = Burdette and Carver, 1970, DIS 45: 151; 15 = Bur- net, 1966, DIS 41: 161; 16 = Burnet and Sang, 1964, Genet- ics 49: 599-610; 17 = Castiglione, 1958, DIS 32: 118; 18 = Di Pasquale and Cavolina, 1983, DIS 59: 31-33; 19 = Di Pasquale and Cavolina, 1984, DIS 60: 83-84, 84-86; 20 = Di Pasquale, Cavolina, Romano, and Ribaudo, 1987, DIS 66: 47- 48; 21 = Erk and Sang, 1966, DIS 41: 95; 22 = Friedman, Harnly, and Goldsmith, 1951, Cancer Res. 11: 904-11; 23 = Ghelelovitch, 1950, C.R. Hebd. Seanc. Acad. Sci., Paris 230: 1002-04; 24 = Ghelelovitch, 1958, Biologie Med. (Paris) 47: 711-810; 25 = Glassman, 1956, DIS 30: 116; 26 = Hartung, 1950, J. Hered. 41: 269-72; 27 = Herskowitz, 1949, DIS 23: 57; 28 = Herskowitz and Burdette, 1951, J. Exp. Zool. 117: 499-521; 29 = Hinton, 1957, DIS 31: 83; 30 = Jacobs, Bowman, and Walliser, 1958, DIS 32: 130; 31 = Kaplan, 1955, Trans. N.Y. Acad. Sci. 17: 289-93; 32 = King, 1955, DIS 29: 73; 33 = Mampell, 1967, Genetica 37: 449-65; 34 = Mittler, 1951, DIS 25: 74; 35 = Mittler, 1952, Science 115: 271-72; 36 = Mittler, 1952, Science 116: 657-59; 37 = Morgan, 1938, DIS 9: 108; 38 = Oftedal, 1951, DIS 25: 122-23; 39 = Oftedal, 1953, Z. Indukt. Abstamm. Vererbungsl. 85: 408-22; 40 = Oshima, 1959, DIS 33: 99; 41 = Perotti, Bairati, and Bairati, 1968, J. Invert. Path. 10: 122-38; 42 = Raimondi, 1956, DIS 30: 147; 43 = Rizki and Rizki, 1974, Experientia 30: 543- 46; 44 = Rizki and Rizki, 1974, J. Invert. Path. 24: 37-40; 45 = Rizki and Rizki, 1979, Genetics 91: s103-104; 46 = Rizki and Rizki, 1980, Wilhelm Roux's Arch. Dev. Biol. 189: 197-206; 47 = Rizki and Rizki, 1981, J. Hered. 72: 78-80; 48 = Rizki, Rizki, and Bellotti, 1985, Mol. Gen. Genet. 201: 7-13; 49 = Rizki, Rizki, Bebbington, and Roberts, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 1-7; 50 = Russell, 1940, J. Exp. Zool. 84: 363-79; 51 = Russell, 1942, Genetics 27: 612-18; 52 = Sang, 1969, Nat. Cancer Inst. Monogr. 31: 291-301; 53 = Sang and Burnet, 1963, Genetics 48: 235-53; 54 = Sang and Burnet, 1964, Genetics 49: 223-35; 55 = Sang and Burnet, 1967, Genetics 56: 743- 54; 56 = Sparrow, 1974, Genet. Res. 23: 13-21; 57 = Stark, 1919, Proc. Nat. Acad. Sci. USA 5: 573-80; 58 = Stark, 1935, DIS 4: 62; 59 = Stark and Bridges, 1926, Genetics 11: 249-66; 60 = Wilson, 1924, Genetics 9: 343-62; 61 = Wilson, King, and Lowry, 1955, Growth 19: 215-44; 62 = Yamazaki and Ohnishi, 1968, Genetics 59: 237-43. | cytology: Located in 10A9 to 10B8 since included in Df(1)KA7 = Df(1)10A9;10F6-7 but not in Df(1)N71 = Df(1)10B2-8;10D3-8. tumor cells become melanized. Some of the melanotic tumor mutants are larval lethals [for example, eight lethals in the Ddc region described by Wright, 1987 (Adv. Genet. 24: 127- 222)]; a few of the melanotic lethals are malignant, such as the mbn mutants of Gateff (1974, DIS 51: 21; 1977, DIS 52: 4) and the mutant Tum (Hanratty and Ryerse, 1981, Dev. Biol. 83: 238-49). In many cases, however, the melanotic tumors are benign and do not affect adult viability. Most of the genes designated tu are recessive and act in combination with modifying factors. The encapsulation and subsequent melanization (described for tu-bw, tu-bwB3, tu-C4, tu-K, tu- Szts and tu-W) seem to be a reaction to developmental abnor- malities in the mutants. General references for the tu mutants include: CP627. Sparrow, 1978, The Genetics and Biology of Drosophila (Ash- burner and Wright, eds.). Academic Press, London, New York, San Francisco, Vol. 2b, pp. 277-313. The preceding table describes the mutants and their alleles. # Tu: Turned-up wing location: 1-59. origin: X ray induced. discoverer: Muller, 46i19. references: Muller and Valencia, 1947, DIS 21: 70. phenotype: Wings curled; somewhat wrinkled in longitudinal direction. Heterozygous viability good; homozygote also viable. RK1. # Tu: see Tb # tu1: see tuh1 # TU36B: see Cyt-b # tub: tube location: 3-47. origin: Induced by ethyl methanesulfonate. references: Anderson and Nusslein-Volhard, 1984, Nature (Lon- don) 311: 223-27. Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal effect embryonic lethal. Embryos can be rescued with wild-type cytoplasm and RNA; however, none hatched (Anderson and Nusslein-Volhard, 1984). Dorsalization observed in the pattern of ftz stripes in tub embryos (Carroll et al., 1987). alleles: tub1 and tub2 recovered as tub118 and tub238. # Tub: Tubulin Tubulin proteins are found in a wide variety of species from unicellular organisms to man; their biochemical and molecular structure is highly conserved. The (- and |-subunits from different organisms can be combined in vitro into hybrid microtubule structures and there is a high level of primary amino acid sequence identity in the proteins (Sanchez, Natzle, Cleveland, Kirschner, and McCarthy, 1980, Cell 22: 845-54; Raff, 1984, J. Cell Biol. 99: 1-10). In Drosophila melanogaster, two multigene families, each made up of four members, code for (- and |-tubulins, each tubulin subunit being a 55,000 dalton polypeptide. Tubulins are the main structural components of microtubules in mitotic and meiotic spindles, cilia, flagella, neural processes, and the cytoskeleton; nontubulin proteins (MAPS or microtubule- associated proteins) are involved along with tubulins in the formation of specialized microtubules (Theurkauf, Baum, Bo, and Wensink, 1986, Proc. Nat. Acad. Sci. USA 83: 8477-81; Rudolph, Kimble, Hoyle, Subler, and Raff, 1987, Mol. Cell Biol. 7: 2231-42). The tubulin genes in each multigene fam- ily are dispersed in the second and/or third chromosomes rather than arranged in clusters. (1) (-Tubulin: Codes for the (-subunit; message of about 2000 bp. (2) |-Tubulin: Codes for the |-subunit; message of about 1800 bp. Variants of both (- and |-subunits have been detected. The following table summarizes current information in regard to these genes in Drosophila melanogaster. locus synonym location cytology comments _______________________________________________________________ (Tub67C (4t 3-{29} 67C4-6 maternal (Tub84B (1t 3-47.8 84B3-6 ubiquitous (Tub84D (3t 3-48 84D4-8 ubiquitous; except in adult male (Tub85E (2t 3-49 85E6-10 expressed from 7 hr through adult |Tub56D |1t;|4t 2-{87} 56D maternal; ubiquitous |Tub60D |3t 2-{107} 60D embryonic; pupal |Tub85D |2t 3-48.5 85D4-7 testis-specific |Tub97EF |4t;|1t 3-{92} 97E-F ubiquitous (Tub67C ((4t) references: Sanchez Natzle, Cleveland, Kirschner, and McCarthy, 1980, Cell 22: 845-54. Kalfayan and Wensink, 1981, Cell 24: 97-106. Kalfayan, Loewenberg, and Wensink, 1982, Cold Spring Harbor Symp. Quant. Biol. 46: 185-90. Kalfayan and Wensink, 1982, Cell 29: 91-98. Baum, Livneh, and Wensink, 1983, Nucleic Acids Res. 11: 5569-87. Natzle and McCarthy, 1984, Dev. Biol. 104: 187-98. Theurkauf, Baum, Bo, and Wensink, 1986, Proc. Nat. Acad. Sci. USA 83: 8477-81. Matthews, Miller, and Kaufman, 1989, Dev. Biol. 132: 45-61. Rees, Kaufman, and Matthews. phenotype: A structural gene for (-tubulin. It is transcribed into mRNA that is maternal in origin and is synthesized in the nurse cells; the transcript accumulates in 0- to 3-hr embryos and adult ovaries (Kalfayan and Wensink, 1982; Matthews et al., 1989). The protein is clearly different from the other (-tubulins of Drosophila melanogaster as well as from those of other animal species. A stable pool of (67C tubulin is found in ovaries, unfertilized eggs, and embryos, but synthesis of the protein probably only occurs in the ovary (Matthews et al., 1989). allele origin discoverer comments __________________________________________ (Tub67C1 EMS Matthews antimorph (Tub67C2 EMS Rees hypomorph (Tub67C3 X-ray Rees hypomorph (Tub67C4 DEB Rees hypomorph cytology: Located in 67C4-6 by in situ hybridization (Sanchez et al., 1980; Kalfayan and Wensink, 1981; Mischke and Pardue, 1982, J. Mol. Biol. 156: 449-66; Natzle and McCarthy, 1984); included in Df(3L)AC1 = Df(3L)67A5;67D9-13 (Carpenter). Sin- gle copy present (Kalfayan and Wensink, 1981). molecular biology: Gene cloned (Kalfayan and Wensink, 1981, 1982; Natzle and McCarthy, 1984), nucleotide sequences deter- mined, and transcript maps formulated (Theurkauf et al., 1986). (Tub67C tubulin differs markedly from the other three (-tubulins although it is similar in length and shares many sequences with the others; it ends with a carboxyl-terminal phenylalanine residue instead of the tyrosine characteristic of the other tubulins and differs from the (-tubulin of (Tub84B at 149 of the 450 residues (Theurkauf et al., 1986). The 3' end of (Tub67C is complementary to RNA bands on gels of 1.50, 1.70, 1.90, and 1.95 kb (Kalfayan and Wensink, 1982). A transcript of 1.5 kb was detected in early embryos and adult females (Matthews et al., 1989). (Tub84B ((1t) references: Sanchez, Natzle, Cleveland, Kirschner, and McCarthy, 1980, Cell 22: 845-54. Kalfayan and Wensink, 1981, Cell 24: 97-106. Kalfayan, Loewenberg, and Wensink, 1982, Cold Spring Harbor Symp. Quant. Biol. 46: 185-90. Kalfayan and Wensink, 1982, Cell 29: 91-98. Mischke and Pardue, 1982, J. Mol. Biol. 156: 449-66. Baum, Livneh, and Wensink, 1983, Nucleic Acids Res. 11: 5569-87. Mischke and Pardue, 1983, J. Submicrosc. Cytol. 15: 367-70. Natzle and McCarthy, 1984, Dev. Biol. 104: 187-98. Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23. Theurkauf, Baum, Bo, and Wensink, 1986, Proc. Nat. Acad. Sci. USA 83: 8477-81. Matthews and Kaufman, 1987, Dev. Biol. 119: 100-14. Matthews, Miller, and Kaufman, 1989, Dev. Biol. 132: 45-61. phenotype: A structural gene for (-tubulin; present in one copy per haploid genome; transcribed into mRNA in the oocyte and the embryo, reaching a maximum concentration 6-9 hr after the egg is laid (Kalfayan and Wensink, 1982). A variety of post- translational modifications of (Tub84b protein found in all tissues, some of which are tissue-specific (Matthews et al., 1989). The gene appears to be constitutively expressed, its functions being common to most cells; the resulting tubulins are very similar to those of other animal species (Theurkauf et al., 1986). Mutations in (Tub84B have been induced as lethals over Df(3R)Scx2. Alleles (Tub84B1 and (Tub84B3 produce proteins that are electrophoretic variants of the wild-type tubulin. Based on the extent of lethality and sterility found in interallelic heterozygotes and in heterozygotes over wild type, the severity of (Tub84B alleles can be ordered as follows: (Tub84B6 < (Tub84B1 < (Tub84B2 < (Tub84B4 < (Tub84B5 = (Tub84B3 (Matthews and Kaufman, 1987). Maternal-effect as well as zygotic lethality is shown by the more severe alleles. In the less severe hypomorphic alleles, heterozygotes die late in pupal life or early in adult life, the adults showing head, thoracic, or abdominal defects, bristle abnormalities, leg tremors, and sterility (Matthews and Kaufman, 1987). alleles: Seven alleles induced by ethyl methanesulfonate. allele discoverer synonym ref ( comments _______________________________________________________ (Tub84B1 Denell l(3)d10 1, 2 hypomorph (Tub84B2 Grigliatti l(3)5.10 1, 2 hypomorph (Tub84B3 Cavener l((3)g3 1, 2 null (Tub84B4 Matthews 2 hypomorph (Tub84B5 Matthews 2 null (Tub84B6 Matthews 2 hypomorph (Tub84B7 Kemphues (Tub84Bnc33 3 hypomorph ( 1 = Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23; 2 = Matthews and Kaufman, 1987, Dev. Biol. 119: 100-14. 3 = Hayes, Deuring, Robertson, Prout, and Fuller, 1989, Mol. Cell Biol. 9: 875-84. cytology: Located in 84B3-6 by in situ hybridization (Sanchez et al., 1980; Kalfayan and Wensink, 1981; Mischke and Pardue, 1982; Natzle and McCarthy, 1984); cytologically located in 84B since included in Df(3R)Scx2 = Df(3R)84A4-5;84C1-2 (Matthews and Kaufman, 1987), but not in Df(3R)Win3 = Df(3R)84A4- 5;84B1-2 (Cavener et al., 1986) or Df(3R)dsx2M = Df(3R)84C1- 2;84D14 (B. Baker). The strongest hybridization among the (- tubulins is observed at the 84B site; cytological data suggest the presence of two copies of (Tub84B per haploid genome (Mischke and Pardue, 1982, 1983), the cloned DNA fragments hybridizing to salivaries and producing two rows of silver grains at 84B3-6. molecular biology: Gene cloned (Kalfayan and Wensink, 1981, 1982; Mischke and Pardue, 1982; Natzle and McCarthy, 1984), nucleotide sequences determined, and transcript maps formu- lated (Theurkauf et al., 1986). (Tub84B and (Tub84D show 92% nucleotide sequence identity within the protein coding region, the tubulins they encode differing by two substitutions, isoleucine-170 and cysteine II in the 84B tubulin being replaced by valine residues in the 84D tubulin. These (Tub genes also have blocks of identical sequences outside the cod- ing region (between nucleotides +27 and +147 of (Tub84B and nucleotides +354 and +503 of (Tub84D). The tubulin encoded by (Tub85E differs from the (Tub84B polypeptide at 21 of the 450 residues, while the tubulin encoded by (Tub67C differs from the polypeptide of (Tub84B at 149 residues. The (Tub84B tubu- lin, like most of the other (-tubulins except the (Tub67C pro- tein, ends with a tyrosine residue (Theurkauf et al., 1986). The 3' end of (Tub84B is complementary to an RNA band on a gel of approximately 1.8 kb (Kalfayan and Wensink, 1982). (Tub84D ((3t) references: Sanchez, Natzle, Cleveland, Kirschner, and McCarthy, 1980, Cell 22: 845-54. Kalfayan and Wensink, 1981, Cell 24: 97-106. Kalfayan, Loewenberg, and Wensink, 1982, Cold Spring Harbor Symp. Quant. Biol. 46: 185-90. Kalfayan and Wensink, 1982, Cell 29: 91-98. Mischke and Pardue, 1982, J. Mol. Biol. 156: 449-66. Baum, Livneh, and Wensink, 1983, Nucleic Acids Res. 11: 5569-87. Mischke and Pardue, 1983, J. Submicrosc. Cytol. 15: 367-70. Natzle and McCarthy, 1984, Dev. Biol. 104: 187-98. Fuller, 1986, Symp. Soc. Dev. Biol. 44: 19-41. Theurkauf, Baum, Bo, and Wensink, 1986, Proc. Nat. Acad. Sci. USA 83: 8477-81. Matthews and Kaufman, 1987, Dev. Biol. 119: 100-14. Matthews, Miller, and Kaufman, 1989, Dev. Biol. 132: 45-61. synonym: ms(3)nc33 (located in 84D). phenotype: A structural gene for (-tubulin. Coordinately expressed with (Tub84B at most developmental stages with the exception of the adult stage where no 84D mRNA can be detected in males (Matthews et al., 1989). alleles: (Tub84Dnc33 [=ms(3)nc33)] induced by ethyl methanesul- fonate, fails to complement certain |Tub mutant alleles for male fertility and is male sterile when homozygous (Fuller, 1986). cytology: Located in 84D4-8 by in situ hybridization (Sanchez et al., 1980; Kalfayan and Wensink, 1981; Mischke and Pardue, 1982; Natzle and McCarthy, 1984); cytologically located in 84C-D since included in Df(3R)dsx2D = Df(3R)84C1-3;84D14 (B. Baker), but not in Df(3R)Scx2 = Df(3R)84A4-5;84C1-2 (Matthews and Kaufman, 1987). Single copy present (Kalfayan and Wensink, 1981). molecular biology: Gene cloned (Kalfayan and Wensink, 1981, 1982; Mischke and Pardue, 1982; Natzle and McCarthy, 1984), nucleotide sequences determined, and transcript maps formulated (Theurkauf et al., 1986). The 3' end of (Tub84D is complementary to an RNA band on a gel of approximately 1.95 kb (Kalfayan and Wensink, 1982; Matthews et al., 1989). The transcript was found in both ovary and carcass RNA. (Tub85E ((2t) references: Sanchez, Natzle, Cleveland, Kirschner, and McCarthy, 1980, Cell 22: 845-54. Kalfayan and Wensink, 1981, Cell 24: 97-106. Kalfayan, Loewenberg, and Wensink, 1982, Cold Spring Harbor Symp. Quant. Biol. 46: 185-90. Kalfayan and Wensink, 1982, Cell 29: 91-98. Mischke and Pardue, 1982, J. Mol. Biol. 156: 449-66. Baum, Livneh, and Wensink, 1983, Nucleic Acids Res. 11: 5569-87. Mischke and Pardue, 1983, J. Submicrosc. Cytol. 15: 367-70. Natzle and McCarthy, 1984, Dev. Biol. 104: 187-98. Theurkauf, Baum, Bo, and Wensink, 1986, Proc. Nat. Acad. Sci. USA 83: 8477-81. Bo and Wensink, 1989, Development 106: 581-87. Matthews, Miller, and Kaufman, 1989, Dev. Biol. 132: 45-61. phenotype: A structural gene for (-tubulin. Only (-tubulin not expressed maternally. Transcripts present from 6-8 hr through adult. Protein found in support cells of chordotonal organs, developing muscles, and somatic component of the testis (Matthews, Miller, and Kaufman). cytology: Located in 85E6-10 by in situ hybridization (Sanchez et al., 1980; Kalfayan and Wensink, 1981; Mischke and Pardue, 1982; Natzle and McCarthy, 1984). Single copy present (Kal- fayan and Wensink, 1981). molecular biology: Gene cloned (Kalfayan and Wensink, 1981, 1982; Mischke and Pardue, 1982; Natzle and McCarthy, 1984), nucleotide sequences determined, and transcript maps formu- lated (Theurkauf et al., 1986). An (Tub85E-| galactosidase fusion gene was expressed in chordotonal organs (sensory organs in the peripheral nervous system) and in the testes (Bo and Wensink, 1989). Chordotonal expression occurs in males and females from late embryonic to early pupal stages. The 3' end of (Tub85E is complementary to bands on gels of approxi- mately 1.65 kb in pupae and adult males and 1.8 kb in larvae according to Kalfayan and Wensink (1982); the 1.8 kb tran- script was not found by Natzle and McCarthy (1984) or Matthews et al. (1989), who report a single 1.55 kb band. |Tub56D (|1t) references: Raff, Fuller, Kaufman, Kemphues, Rudolph, and Raff, 1982, Cell 28: 33-40. Bialojan, Falkenburg, and Renkawitz-Pohl, 1984, EMBO J. 3: 2543-48. Natzle and McCarthy, 1984, Dev. Biol. 104: 187-98. Raff, 1984, J. Cell Biol. 99: 1-10. Michiels, Falkenburg, Muller, Hinz, Otto, Bellmann, Glatzer, Brand, Biolojan, and Renkawitz-Pohl, 1987, Chromosoma 95: 387-95. Rudolph, Kimble, Hoyle, Subler, and Raff, 1987, Mol. Cell. Biol. 7: 2231-42. Gasch, Hinz, Leiss, and Renkawitz-Pohl, 1988, Mol. Gen. Genet. 211: 8-16. phenotype: A structural gene for |-tubulin. Its mRNA is mater- nally stored in the oocytes and expressed in the nurse cells and in early embryos (Natzle and McCarthy, 1984; Gasch et al., 1988); at this stage, the transcripts are evenly distributed throughout the embryo, but later in development they are con- centrated in the primordia of the nervous system and their derivatives (the supra-oesophageal ganglion and ventral nerve cord) and in the visceral mesoderm. Since |Tub56D is expressed throughout development and in all adult tissues (Rudolph et al., 1987), |Tub56D tubulin is probably involved in all the microtubular structures necessary for cell division and cell shape (Raff et al., 1982; Biolojan et al., 1984). It is the major |-tubulin of adult flies in all structures except the testis. cytology: Located in 56C (Bialojan et al., 1984) or in 56D (Natzle and McCarthy, 1984) by in situ hybridization. molecular biology: Gene cloned (Bialojan et al., 1984; Natzle and McCarthy, 1984); transcript of 1.8 kb present in all developmental stages (Raff, 1984); maximal expression in 6-9 hr embryos (Bialojan et al., 1984). Complete nucleotide sequences and predicted amino acid sequences of the protein- coding regions have been determined (Michiels et al., 1987; Gasch et al., 1988). A single intron of 2.6 kb is found between codons for amino acids 19 and 20. The 5' untranslated region is encoded in the same exon as the first 19 amino acids. There is a typical TATA box promoter element at -27. Transcription starts at an adenosine residue as in most eukaryotic genes, the initiation site being 110 bases upstream of the translation initiation codon (Gasch et al., 1988). The 3' untranslated region of |Tub56D mRNA is not identical to the 3' region of |Tub85D mRNA, but the protein coding regions show 95% identity at the amino acid level; there are 25 differences in amino acid sequence between these two tubulins (Michiels et al., 1987). |Tub60D (|3t) references: Sanchez, Natzle, Cleveland, Kirschner, and McCarthy, 1980, Cell 22: 845-54. Raff, Fuller, Kaufman, Kemphues, Rudolph, and Raff, 1982, Cell 28: 33-40. Bialojan, Falkenburg, and Renkawitz-Pohl, 1984, EMBO J. 3: 2543-48. Natzle and McCarthy, 1984, Dev. Biol. 104: 187-98. Raff, 1984, J. Cell Biol. 99: 1-10. Rudolph, Kimble, Hoyle, Subler, and Raff, 1987, Mol. Cell. Biol. 7: 2231-42. Gasch, Hinz, Leiss, and Renkawitz-Pohl, 1988, Mol. Gen. Genet. 211: 8-16. Leiss, Hinz, Gasch, Mertz, and Renkawitz-Pohl, 1988, Develop- ment 104: 525-31. Gasch, Hinz, and Renkawitz-Pohl, 1989, Proc. Nat. Acad. Sci. USA 86: 3215-18. Kimble, Incardona, and Raff, 1989, Dev. Biol. 131: 415-29. Kimble, Dettman, and Raff, 1990, Genetics 126: 991-1105. phenotype: A structural gene for |-tubulin. The mRNA first appears in the mesoderm during mid-embryogenesis at about the time when synthesis of |-tubulin begins and later disappears from the embryo when synthesis of the tubulin ends; the tran- script reappears in the mesoderm during the pupal period (Raff et al., 1982; Natzle and McCarthy, 1984; Raff, 1984; Rudolph et al., 1987; Gasch et al., 1988; Kimble et al., 1989). Dur- ing embryogenesis, |Tub60C is only expressed in developing muscles; in pupae, it is expressed in adult muscles, imaginal discs, wing blades, optic lobes, ovaries and testes, but ceases (except in ovaries and testes) in adults. As compared to the tubulin encoded by |Tub56D, the product of |Tub60C is but a minor component of the total tubulin pool (Rudolph et al., 1987). When synthesis of the |Tub60C tubulin begins in the embryo, (-tubulin synthesis is increased (Raff et al., 1982). alleles: Five EMS-induced alleles (Kimble et al., 1990). allele synonym comments ( | ___________________________________________ (Tub60D1 |3t1 intermediate hypomorph (Tub60D2 |3t2 strong hypomorph (Tub60D3 |3t3 strong hypomorph (Tub60D4 |3t4 weak hypomorph (Tub60D5 |3t5 intermediate hypomorph ( Effect on viability: |3t2 > |3t3 > |3t4 > |t1 > |3t5. | Effect on fertility: |3t3 > |t2 > |3t4 > |3t1 > |t5. cytology: Located in 60D; also located in 60A-B (Sanchez et al., 1980), 60B (Bialojan et al., 1984), or 60C (Natzle and McCarthy, 1984) by in situ hybridization; placed in 60C6-8 by other molecular methods (see Raff, 1984). molecular biology: Gene cloned (Bialojan et al., 1984; Natzle and McCarthy, 1984); 2.3-2.5 kb transcript found in mid- embryogenesis and during pupation (Bialojan et al., 1984; Raff, 1984). The transcription initiation sites are identical in both of these developmental periods (Gasch et al., 1988). Gene structure, nucleotide sequences, and predicted amino acid sequences of the protein-coding regions have been determined (Rudolph et al., 1987; Gasch et al., 1988). The tubulin encoded by |Tub60C is longer and slightly more basic than that encoded by |Tub56D, and contains 454 amino acids (Rudolph et al., 1987). The first intron occurs between the codons for amino acids 19 and 20 and is about 4.5 kb long; the second intron occurs after the first nucleotide in the codon for amino acid 56 and is only 62 bp long; the third intron occurs between the codons for amino acids 137 and 138 and is about 56 bp long. Six amino acids not found in any other |-tubulin are positioned immediately after the 3' junction of the second intron in a highly variable region. The first and third introns occur in relatively conserved regions of the protein coding sequence (Rudolph et al., 1987). Upstream sequences of |Tub56D, |Tub60C, and |Tub85D are highly divergent, with the exception of the sequence common to |Tub60C and |Tub85D pro- moters (Gasch et al., 1988). Upstream of -1.2 kb (relative to the transcription start site) are regulatory elements required for expression of |Tub60C in the somatic muscles, the phar- yngeal muscles, and the dorsal vessel (Gasch et al., 1989). The first intron carries an enhancer element necessary for |Tub60C expression in the visceral muscles. |Tub85D (|2t) references: Kemphues, Raff, Kaufman, and Raff, 1979, Proc. Nat. Acad. Sci. USA 76: 3991-95. Kemphues, Raff, Raff, and Kaufman, 1980, Cell 21: 445-51. Sanchez, Natzle, Cleveland, Kirschner, and McCarthy, 1980, Cell 22: 845-54. Kemphues, Kaufman, Raff, and Raff, 1982, Cell 31: 655-70. Kemphues, Raff, and Kaufman, 1983, Genetics 105: 345-56. Bialojan, Falkenburg, and Renkawitz-Pohl, 1984, EMBO J. 3: 2543-48. Natzle and McCarthy, 1984, Dev. Biol. 104: 187-98. Fuller, 1986, Symp. Soc. Dev. Biol. 44: 19-41. Fuller, Caulton, Hutchens, Kaufman, and Raff, 1987, J. Cell Biol. 104: 385-94. Michiels, Falkenburg, Muller, Hinz, Otto, Bellmann, Glatzer, Brand, Biolojan, and Renkawitz-Pohl, 1987, Chromosoma 95: 387-95. Rudolph, Kimble, Hoyle, Subler, and Raff, 1987, Mol. Cell. Biol. 7: 2231-42. Fuller, Caulton, Hutchens, Kaufman, and Raff, 1988, J. Cell Biol. 107: 141-52. Gasch, Hinz, Leiss, and Renkawitz-Pohl, 1988, Mol. Gen. Genet. 211: 8-16. phenotype: A structural gene for |-tubulin. It is transcribed into mRNA that is testis-specific; the mRNA is translated into a |-tubulin subunit that is involved in the formation of microtubules in the sperm tail axoneme, the cytoplasmic micro- tubules, and the meiotic spindle (Kemphues et al., 1982; Fuller et al., 1988). Only the microtubules of the mitotic spindle are not affected by a null mutation in |Tub85D. The first mutant discovered, |Tub85DD (Kemphues et al., 1979, 1980, 1982, 1983), codes in males for an electrophoretic vari- ant of |2-tubulin that causes disruption of microtubule func- tion in all stages of spermatogenesis (beginning with meiosis) and shows abnormal spindle formation, abnormal chromosome movement, and no cytokinesis. This phenotype is expressed in males in both homo- and heterozygotes; mutants heterozygous over wild type contain both wild-type and mutant |2-tubulins; mutants over a deficiency for the locus contain only mutant |2-tubulin. Severity of effect on meiosis is as follows: |Tub85DD/|Tub85DD > |Tub85DD/+ > |Tub85DD/+/+, the first two genotypes being sterile and the last weakly fertile. All females are fertile. Chromosome replication and condensation appear normal. Recessive male-sterile mutations have also been induced, two of them in |Tub85DD chromosomes and the rest in |Tub85D+ chromosomes. Testes of flies homozygous for the recessives |Tub85D3, |Tub85D4, |Tub85DDrv1, and |Tub85DDrv2 synthesize, but later degrade, both (-tubulin and |-tubulin and show abnormalities in meiotic divisions, nuclear shaping, and formation of the flagellar axoneme (Kemphues et al., 1982, 1983; Fuller, 1986). The most extreme recessive allele, |Tub85Dn, is male sterile but female fertile when homozygous (Fuller et al., 1988); heterozygotes raised at 25 are male fertile, but those raised at 18 are male sterile. Recessive alleles |Tub85D6 - |Tub85D10 seem to accumulate normal amounts of |-tubulin but the |-tubulin subunits are defective. |Tub85D6, |Tub85D7, and |Tub85D8 cause different defects in spermatogenesis. |Tub85D8 is unable to form normal closed microtubules (Fuller et al., 1987); in homozygous males it is defective in meiosis, nuclear shaping, and flagellar elonga- tion. This allele is semi-dominant; heterozygous males with one normal and one abnormal tubulin subunit, form some func- tional sperm. Transheterozygotes between ms(3)nc (second site non-complementing) mutations and certain |Tub85D alleles are male sterile even if wild-type copies of both genes are present (Fuller, 1986); a deletion of a ms(3)nc mutation in a heterozygote over |Tub85Dn, however, is fertile in males. alleles: allele origin synonym ref ( comments _____________________________________________________________________________ |Tub85D3 EMS |2t3; T|23 1, 4, 5 male fertile in heterozygote, sterile in homozygote |Tub85D4 EMS |2t4; T|24 1, 4, 5 same phenotype as above |Tub85D6 EMS |2t6; T|26 1, 3 same phenotype as above |Tub85D7 EMS |2t7; T|27 1, 3 same phenotype as above |Tub85D8 EMS |2t8; T|28 1, 2, 3, 8 same phenotype as above |Tub85D9 EMS |2t9; T|29 9 same phenotype as above | |Tub85D10 EMS |2t10; T|210 9 same phenotype as above / |Tub85D11 EMS |2t11; T|211 9 same phenotype as above / |Tub85DD EMS ms(3)KKD; 1, 4-7 male sterile in homo- |2tD; T|2D and heterozygote |Tub85DDrv1 EMS |2tD+R1; 1, 4, 5 male fertile in heterozygote, TB2D+R1 sterile in homozygote |Tub85DDrv2 EMS |2tD+R2; 1, 4, 5 same phenotype as above T|2D+R2 |Tub85Dn EMS |2tn; T|2n 1 null allele; no protein synthesized ( 1 = Fuller, 1986, Symp. Soc. Dev. Biol. 44: 19-41; 2 = Fuller, Caulton, Hutchens, Kaufman, and Raff, 1987, J. Cell Biol. 104: 385-94; 3 = Fuller, Caulton, Hutchens, Kaufman, and Raff, 1988, J. Cell Biol. 107: 141-52; 4 = Kemphues, Kaufman, Raff, and Raff, 1982, Cell 31: 655- 70; 5 = Kemphues, Raff, and Kaufman, 1983, Genetics 105: 345-56; 6 = Kemphues, Raff, Kaufman, and Raff, 1979, Proc. Nat. Acad. Sci. USA 76: 3991-95; 7 = Kemphues, Raff, Raff, and Kaufman, 1980, Cell 21: 445-51; 8 = Rudolph, Kim- ble, Hoyle, Subler, and Raff, 1987, Mol. Cell. Biol. 7: 2231-42; 9 = Regan and Fuller, 1988, Genes and Develop- ment 2: 82-92. | Fertile in transheterozygotes with haync2. / Sterile in transheterozygotes with haync2. cytology: Placed in 85D by in situ hybridization of cloned DNA (Sanchez et al., 1980; Bialojan et al., 1984; Natzle and McCarthy, 1984); placed in 85D7-11 by deficiency testing since in the 84F1-85E deletion of In(3R)MscLAntpBR but not in Df(3R)p46 = Df(3R)84D4-6;85D6 or Df(3R)by10 = Df(3R)85D8- 12;85E7-F1 (Kemphues et al, 1983). molecular biology: Gene cloned (Bialojan et al., 1984; Natzle and McCarthy, 1984); clone contains one complete |-tubulin gene and the 3' end of another tubulin-like sequence; 2.0-2.2 kb transcript specifically expressed in spermatogenesis (Bialojan et al., 1984; Raff, 1984). Complete nucleotide sequences and predicted amino acid sequences of the protein- coding regions have been determined (Rudolph et al., 1987; Gasch et al., 1988). The proteins encoded by |Tub85D and |Tub60C show 87% overall identity in amino acid sequence; the |Tub85D tubulin contains 446 amino acids while the |Tub60C tubulin contains 454 amino acids. The |Tub85D gene has a sin- gle intron of 61 bases and the mRNA contains a 5' untranslated region of 175 bases. The first exon comprises this 5' region, the translation initiation codon ATG, and codons up to amino acid 131; the second exon includes the codons for amino acids from 132 to the stop codon. Transcription starts at an adeno- sine residue. The sequence for the mutant |Tub85D8 is identi- cal to that of the wild-type in both intron and protein-coding regions, except that at nucleotide 862 there is a single nucleotide substitution resulting in a change from glu to lys at amino acid residue 288 (Rudolph et al., 1987). P-element mediated germline transformation using the |Tub85D-lacZ fusion gene resulted in |Tub85D expression in the testis only (Michiels, Gasch, Kaltschmidt, and Renkawitz-Pohl, 1989, EMBO J. 8: 1559-65). 53 bp of upstream sequences are necessary for correct testis expression. |Tub97EF (|4t) references: Natzle and McCarthy, 1984, Dev. Biol. 104: 187-98. Raff, 1984, J. Cell Biol. 99: 1-10. Gasch, Hinz, Leiss, and Renkawitz-Pohl, 1988, Mol. Gen. Genet. 211: 8-16. phenotype: A structural gene for |-tubulin. It is transcribed into mRNA that occurs ubiquitously throughout development. |Tub97EF is expressed coordinately with |Tub56D, but the |Tub97EF transcripts are much less prevalent. They occur at highest concentration during the first half of embryogenesis and the first and second larval instars (Natzle and McCarthy, 1984). No protein variant has been described (Gasch et al., 1988). cytology: Located in 97E-F by in situ hybridization (Natzle and McCarthy, 1984). molecular biology: Gene cloned (Natzle and McCarthy, 1984); 1.8 kb transcript obtained (Raff, 1984). # Tubby: see Tb # tube: see tub # Tubulin: see Tub # tud: tudor (T. Schupbach) location: 2- {97}. origin: Induced by ethyl methanesulfonate. discoverer: Wieschaus and Nusslein-Volhard. references: Boswell and Mahowald, 1985, Cell 43: 97-104. Degelmann, Hardy, Perrimon, and Mahowald, 1986, Dev. Biol. 115: 479-89. Schupbach and Wieschaus, 1986, Roux's Arch. Dev. Biol. 195: 302-17. Nusslein-Volhard, Frohnhofer, and Lehmann, 1987, Science 238: 1675-81. O'Donnell, Boswell, Reynolds, and Mackay, 1989, Genetics 121: 273-80. Schupbach and Wieschaus, 1989, Genetics 121: 101-17. phenotype: Maternal-effect mutant; embryos from homozygous mothers exhibit a so-called "grandchildless-knirps" phenotype: all eggs lack polar granules and no pole cells are formed; most of the embryos show variable deletions of abdominal seg- ments, whereby segment A4 is deleted most frequently; larger deletions may include segments A2 through A7; in extreme cases anterior parts of segment A1 become fused to posterior part of segment A8, but telson elements are always present and rela- tively normal. Around 30% of all embryos survive and grow into sterile adults. Analysis of germline clones indicates that the mutation is germline autonomous (Schupbach and Wieschaus, 1986, Dev. Biol. 113: 443-48). alleles: allele origin discoverer synonym ref ( comments | __________________________________________________________________________ tud1 EMS Wieschaus tudWC 1, 2, 3 Nusslein-Volhard tud2 EMS Boswell 1 tud3 EMS Boswell 1 tud4 EMS Boswell 1 tud5 EMS Boswell 1 tud6 EMS tudB46 2, 3 In(2R)B46 = In(2R)53D2-E1;57B6-D11 ( 1 = Boswell and Mahowald, 1985, Cell 43: 97-104; 2 = Schup- bach and Wieschaus, 1986, Roux's Arch. Dev. Biol. 195: 302-17; 3 = Schupbach and Wieschaus, 1989, Genetics 121: 101-17. | Eight alleles, l(2)57Ce1-l(2)57Ce8, complement both lethal and grandchildless phenotypes of tud (O'Donnell et al., 1989). cytology: Located in 57C7-9 by O'Donnell et al., 1989, since not complemented by Df(2R)PF1 = Df(2R)57C5;57D1 but comple- mented by deficiencies with distal break proximal to 57C6-7. molecular biology: Gene has been cloned and found to encode a 8.0 kb transcript which is expressed most strongly in early embryos and in pupae (Golumbeski, O'Rourke, and Boswell, 1989, New Orleans Drosophila meeting). # tuf: tufted location: 2-59 (Ashburner). references: Sturtevant, 1948, DIS 22: 56. Nusslein-Volhard and Wieschaus, 1980, Nature (London) 287: 795-801. Nusslein-Volhard, Wieschaus, and Kluding, 1983, DIS 59: 158- 60. 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Carroll and Scott, 1986, Cell 45: 113- 26. Nakano, Guerrero, Hidalgo, Taylor, Whittle, and Ingham, 1989, Nature (London) 341: 508-13. synonym: ptc, patched. phenotype: The tuf gene is involved in patterning within seg- ments in Drosophila. The viable first-identified mutant has a small tuft of hairs between eyes and antennae and shows basal twinning of the anterior halves of wings; it overlaps wild type. tuf/T(2;3)dp has an extreme form of this mutant pheno- type. Other mutants are embryonic lethals of the segment- polarity type. There is a mirror-image duplication of segment boundaries and adjacent cuticle of all segments with deletion of the remainder of the segment. Defect visible during extended-germ-band stage (6 hr) (Nusslein-Volhard and Wieschaus, 1980). Normal number of denticle bands; duplicated region of embryo includes some naked cuticle anterior to den- ticle bands. Pattern of neurons underlying affected epidermal region is altered (Patel, Schafer, Goodman, and Holmgren, 1989, Genes Dev. 3: 890-904). This mutant has no effect on the spatial expression of the "pair-rule" mutant ftz (Carroll and Scott, 1986). tuf embryos cultured in vivo produced derivatives of the eye-antennal and thoracic discs, the latter being abnormal in morphology and in en expression (Simcox, Roberts, Hersperger, Gribbon, Shearn, and Whittle, 1989, Development 107: 715-22). alleles: One viable allele and numerous lethal alleles reported. allele origin synonym ref ( comments ___________________________________________________________ tuf1 spont 3 viable tuf2| EMS 5 homozygous lethal; extreme allele tuf3 EMS ptc6C 4 homozygous lethal tuf4 EMS ptc6P 4 homozygous lethal tuf5 EMS ptc7M 4 homozygous lethal tuf6 EMS ptc8H 4 homozygous lethal tuf7 EMS ptc9B 4 homozygous lethal tuf8 EMS ptcIF 4 homozygous lethal; temperature-sensitive tuf9 EMS ptcIN 1,4 homozygous lethal tuf10 EMS ptcIIB 4 homozygous lethal tuf11 EMS ptcIIC2 4 homozygous lethal tuf12 EMS ptcIIC8 4 homozygous lethal tuf13 EMS ptcIIE 4 homozygous lethal tuf14 EMS ptcIIR 4 homozygous lethal; weak tuf15 EMS ptcIIU 4 homozygous lethal; weak tuf16 EMS ptcIIW 4 homozygous lethal tuf17 EMS ptcIIX 4 homozygous lethal tuf18 HD ptcP78 2 homozygous lethal tuf19 HD 2 homozygous lethal tuf20 HD 2 homozygous lethal tuf21 HD 2 homozygous lethal tuf22 HD 2 homozygous lethal tuf23 HD 2 homozygous lethal tuf24 HD 2 homozygous lethal tuf25 HD 2 homozygous lethal tuf26 X ray ptcRX67 1 homozygous lethal ( 1 = Hooper and Scott, 1989, Cell 59: 751-65; 2 = Nakano, Hidalgo, Taylor, Whittle, and Ingham, 1989, Nature (London) 341: 508-13; 3 = Sturtevant, 1948, DIS 22: 56; 4 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26; 5 = Whittle, 1980, DIS 55: 211. | Wings of tuf1/tuf2 grossly foreshortened and shaped like a ping-pong paddle; these flies also show duplications and triplications of anterior wing structures, lack costal bris- tles, and have more head abnormalities than tuf1 homozy- gotes. cytology: tuf (= ptc) placed in 44D3-4 by in situ hybridization to P-element-free polytene chromosomes (Nakano et al., 1989). Located in 44B-E based on uncoverage by the deficiency segre- gant of Tp(2;3)eve1.18 but not by the deficiency segregant of Tp(2;3)eve2.28 (Nusslein-Vollard et al., 1984; Tearle and Nusslein-Vollard, 1987, DIS 66: 209-26); located in 44D1-2 to 44E1-4 since included between the centromere-proximal breaks of Df(2R)P14TE (a synthetic deficiency) and Df(2R)44CE (Hooper and Scott, 1989). molecular biology: Gene cloned; transcription unit of about 17-30 kb encodes a 5.8 to 7 kb transcript (Hooper and Scott, 1989, Cell 59: 751-65; Nakano et al., 1989). At blastoderm, tuf transcribed uniformly except in pole cells and A-D region; later expressed as 14 and then 28 stripes. Expression in lar- vae occurs in the imaginal disks. Nucleotide sequence of tuf and predicted amino acid sequences obtained (Nakano et al., 1989). There is a single open reading frame of 4152 bases (Hooper and Scott, 1989). Predicted protein is large (1286 amino acids) with at least seven putative transmembrane ( hel- ices. # Tufted: see Tft # tufts: see tft # tuh1: tumorous head in chromosome 1 location: 1-65.3 (Woolf). origin: Spontaneous. discoverer: Griffen. references: Gardner, 1949, DIS 23: 57. Gardner and Woolf, 1949, Genetics 34: 573-85. Newby, 1949, J. Morphol. 85: 177-95. Newby and Thelander, 1950, DIS 24: 89-90. Gardner, 1959, Genetics 44: 471-81. Woolf, 1966, Genetics 53: 295-302. 1968, Genetics 60: 111-21. Gardner, 1970, Adv. Genet. 15: 115-46. Postlethwait, Bryant, and Schubiger, 1972, Dev. Biol. 29: 337-42. Pyati, 1976, Mol. Gen. Genet. 146: 189-90. Bournias-Vardiabasis and Bownes, 1978, J. Embryol. Exp. Mor- phol. 44: 227-41. Bournias-Vardiabasis and Bownes, 1979, Wilhelm Roux's Arch. Dev. Biol. 186: 87-90. Kuhn, Zust, and Illmensee, 1979, Mol. Gen. Genet. 168: 117- 24. Woolf and Passage, 1980, Mol. Gen. Genet. 178: 423-27. Kuhn, Woods, and Andrew, 1981, Genetics 99: 99-107. Kuhn and Packert, 1988a, Dev. Biol. 125: 8-18. 1988b, Genetics 118: 103-07. phenotype: Maternal effect gene with no phenotypic expression of its own; presence of gene indicated by difference in results obtained from reciprocal crosses between phenotypi- cally tumorous head and inbred wild-type flies, the mutant phenotype only appearing in the offspring when the mother comes from the tuh stock (Gardner, 1959). There seems to be an interaction involving maternal effect substances between tuh1 (or tuh1+) and iab9tuh3, an allele of the most distal gene in the BXC; the homoeotic effects of homo- or heterozy- gous iab9tuh3 flies are strongly enhanced by the tuh1 allele. One type of abnormality in tumorous head mutants involves homoeotic changes, deficiencies, and duplications in the eye, antenna, or rostralhaut regions that transform parts of these structures into tergite-like, leg-like, or genital-like growths in the adult (Postlethwait et al., 1972). In the mutant larvae, patches of aldehyde oxidase positive tissue can be demonstrated within the aldehyde oxidase negative eye discs, where, presumably, transformed tissue will occur (Kuhn et al., 1979). Penetrance of these head abnormalities is increased by high temperature during oogenesis and early embryogenesis (Gardner, 1970; Bournias-Vardiabasis and Bownes, 1979) and also by the presence of E(tuh1) an enhancer of the mutant phenotype on 3R (Kuhn and Dorgan, 1974, Genetics 77: s37; Kuhn and Packert, 1988a). Modifiers on the first, second, and third chromosomes in certain lines likewise increase the maternal effect of tuh1 (Gardner, 1970; Woolf and Passage, 1980). The other type of abnormality occurring in tumorous head stocks involves genital disc defects that result in missing or undeveloped testes and associated organs, both in males and in transformed females (Gardner and Woolf, 1949; Woolf, 1966, 1968; Kuhn et al., 1981). Viability of stocks showing head abnormalities is about 70%; lethality may occur in the egg, larval, or pupal periods (Bournias-Vardiabasis and Bownes, 1978). alleles: allele synonym ref ( phenotype with iab9tuh3 | __________________________________________________________________________ tuh1 tuh1h, tu-1 1, 2 homeotic leg, tergite, or genital tissue in 3, 4 eye-antenna region (penetrance up to 90%) tuh1+ tuh1g 2, 3 defects in male genital disc or complete 5, 6 absence of disc (penetrance up to 60%) ( 1 = Gardner and Woolf, 1949, Genetics 34: 573-85; 2 = Kuhn and Packert, 1988a, Dev. Biol. 125: 8-18; 3 = Kuhn and Packert, 1988b, Genetics 118: 103-07; 4 = Kuhn, Zust, and Illmensee, 1979, Mol. Gen. Genet. 168: 117-24; 5 = Woolf, 1966, Genetics 53: 295-302; 6 = Woolf, 1968, Genetics 60: 111-21. | Effect with tuh1 semidominant; effect with tuh1+ recessive (Kuhn and Packert, 1988a and 1988b). cytology: Located in 20A1-2 since uncovered by Df(1)JC4 = Df(1)20A1-2;20E-F and Df(1)mal6 = Df(1)19C3;20A2-3, but not by Df(1)Q539 = Df(1)19E6;19F6-20A1 (Pyati, 1976). other information: A third chromosome EMS-induced mutant I127, when homozygous or when heterozygous over iab9tuh3, produces head abnormalities involving genital and abdominal transforma- tions under the influence of the tuh1 maternal effect (Bownes, Roberts, Demster, and Bournias-Vardiabasis, 1981, Mol. Gen. Genet. 183: 158-62; Kuhn and Packert, 1988a); may be an allele of iab9tuh3. # tuh3: see iab9tuh3 # Tul: Turneduplike location: 1-50 (between g and f). origin: Spontaneous. references: Muller, 1965, DIS 40: 35. phenotype: Like Tu. Wing tips of heterozygote turned up slightly but definitely not twisted. Male and homozygous female more extreme with wrinkled wings sometimes held some- what apart; viable and fertile. RK2. # Tum: Tumorous location: 1-35.8. origin: Induced by ethyl methanesulfonate. references: Corwin and Hanratty, 1976, Mol. Gen. Genet. 144: 345-47. Hanratty and Ryerse, 1981, Dev. Biol. 83: 238-49. phenotype: Dominant tumorous gene that is a temperature- sensitive lethal at 29 in hemizygous males and homozygous females; about two-thirds of the hemizygous males survive at 18 and one-quarter of these have melanotic tumors. Males raised at 26 and heterozygous females raised at 29 survive to adulthood, but show melanotic masses in the abdominal cavity or small black specks in the legs, wings, or thorax. Mutant larvae kept at 29 show enlargement of the lymph glands in the late second- or early third-instar larvae, but no melanotic masses. By mid third-instar, the lymph glands are large and diffuse and the gastric caeca have become encapsulated and melanized. By late third-instar, the larvae have melanotic masses in the body cavity, lack lymph glands, and have reduced, encapsulated and melanized gastric caeca as well as encapsulated and melanized muscles and fat bodies. These mutants do not survive beyond the late third-instar or the early pupal stage. When lymph glands from Tum larvae are injected into adult female hosts, transplantable neoplasms are produced. Melanization, at first associated with the leg joints and later with the head, thorax, and abdomen, takes place; also abdominal bloating. The lymph glands become melanotic and the abdomen is filled with encapsulated masses before the premature death of the injected individuals. Injection of Tum tissue other than lymph glands fails to pro- duce these effects. The melanotic neoplasms can be tran- splanted into a succession of hosts in which they produce the same abnormalities. The neoplastic cells resemble hemocytes; some cell lines are melanotic and others are unpigmented, but in both types, the tissue, when transplanted, grows rapidly in the hosts and kills them. other information: Shown to be allelic to hop too late to be included in the hop entry (Dearoff). # tumor: see tu # tumor head 63: see eytu # tumorous: see tms # Tumorous: see Tum # tumorous head in chromosome 1: see tuh1 # tup: tailup location: 2-54. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. phenotype: Embryonic lethal. Head broad. Germband shortening apparently ceases early, resulting in the posteriormost three segments remaining on dorsal side of the embryo. alleles: tup1 and tup2, isolated as tupIIIB and tupIIIe. # tur: turnip (J.C. Hall) location: 1- (proximal to f, distal to car). origin: Induced by ethyl methanesulfonate. references: Aceves-Pina and Quinn, 1979, Science 206: 93-96. Quinn, Sziber, and Booker, 1979, Nature 277: 212-114. Booker and Quinn, 1981, Proc. Nat. Acad. Sci. USA 78: 3940-44. Duerr and Quinn, 1982, Proc. Nat. Acad. Sci. USA 79: 3645-50. Tully and Quinn, 1985, J. Comp. Physiol. 157: 253-77. Tully, 1987, Trends Neurosci. 10: 330-35. 1989, Adaptation, Learning, and Affect (Madden, Matthysse, and Barchas, eds.). Raven, New York, pp. 1989. phenotype: Homozygotes or hemizygotes are blocked or impaired in learning, with respect to certain of the conditioning tests used on groups of flies or larvae or on individual adults, e.g. tests involving olfactory "shock-avoidance" learning (Acevas-Pina and Quinn, 1979; Quinn et al, 1979), leg- shock/leg-lift learning (Booker and Quinn, 1981); "courtship conditioning" (Gailey, Jackson, and Siegal, 1982, Genetics 102: 771-82; 1984, Genetics 106: 613-23), and habituation to sugar stimuli when applied to tarsus (Duerr and Quinn, 1982). When the original shock-odor testing system is modified by redesigning the choice chamber, homozygous and hemizygous mutants show about 60% of the control wild-type values when tested just post-training (Tully and Quinn, 1985; Tully, 1987), but the mutant shows very rapid short-term and slower long-term memory losses. tur/+ heterozygous females show seemingly normal levels of shock-odor conditioned behavior when tested immediately after training, but very rapid memory losses (Quinn et al., 1979). Homozygous tur flies are said to have a deficiency in (and possibly absence of) protein kinase C (PKC) (Smith, Choi, Tully, and Quinn, 1986, Soc. Neurosci. Abstr. 12: 399), and tur flies are almost totally deficient in phosphorylation of a 76 kd head membrane protein which is a major substrate for PKC (Choi, Smith, Marler, and Quinn, 1989), but the lowered PKC levels and abnormal learning do not map to the same cytogenetic location (see cytology). cytology: Df(1)JA27 = Df(1)18A5;18D1-2, which uncovers the PKC deficiency and the non-phosphorylation of head membrane pro- tein phenotypes, did not uncover any deficit in classical con- ditioning in one series of tests (Tully and Quinn, 1985; Tully, 1989). Another series, however, revealed 15% reduction in learning scores for classical conditioning tests and 70% reduction in scores for shock-avoidance tests in tur/Df(1)JA27 females (Choi et al., submitted). Other proximal X deletions [Df(1)N19, Df(1)mal8, Df(1)16-3-22, and Df(1)DCB1-35B] have not uncovered any classical conditioning deficits. # Turned-up wing: see Tu # Turneduplike: see Tul # turnip: see tur # tw: twisted location: 1-0.4 (tw); 1-0.1 (tw3). references: Demerec, Kaufmann, Fano, Sutton, and Samsome, 1942, Year Book - Carnegie Inst. Washington 41: 191. Davis, 1975, Genetics 80: s25. 1980, DIS 55: 29-31, 31-33. Kramers, Schalet, Paradi, and Huiser-Hoogteyling, 1983, Mutat. Res. 107: 187-201. Lefevre and Watkins, 1986, Genetics 113: 869-95. phenotype: Abdomens of males and females twisted about 30 clockwise, as viewed from the posterior. Body tends to be dwarfed. Viability reduced; hatching delayed. Males usually fertile. 1% nondisjunction for homologs in males (Davis, 1975, 1980). alleles: 13 alleles are listed in the following table. Pheno- types of tw2 and tw3 are given in more detail in subsequent sections. allele origin discoverer synonym ref ( viability _______________________________________________________________ tw1 X ray Demerec 1, 3 60% tw2 spont Mohr 50% tw3 EMS Davis tricky dicky 2, 3 tw4 EMS Lefevre l(1)DAM7 low tw5 EMS Lefevre l(1)VAM201 low tw6 ENU Voelker l(1)A23 low tw7 ENU Voelker l(1)B9 low tw8 ENU Voelker l(1)B19 low tw9 ENU Voelker l(1)B32 low tw10 ENU Voelker l(1)B39 low tw11 ENU Voelker l(1)B44 low tw12 ENU Voelker l(1)B47 low tw13 EMS Voelker l(1)C6 low ( 1 = CP627; 2 = Davis, 1975, Genetics 80: s25; 3 = Davis, 1980, DIS 55: 29-31, 31-33. cytology: Located at 1C5-1D4. # tw2 phenotype: Abdomens of males and females twisted 30-60 clock- wise, as viewed from the posterior; more extreme than tw. Male genitalia often twisted counter-clockwise. Viability reduced. Males usually fertile. tw2/tw flies resemble tw2/tw2. # tw3 phenotype: Abdomens of males and females twisted up to 90, as viewed from the posterior. Male genitalia and anal plate often twisted clockwise or counter-clockwise (misalignment up to 180). Males and females often sterile, although male geni- talia appear normal and sperm are motile. 1% nondisjunction for homologues in males (Davis, 1975, 1980). #*twg: twisted genitals location: 1-48.1. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1959, DIS 33: 93-94. phenotype: External genitalia abnormally positioned on extreme tip of abdomen. Tergites often notched at mid-dorsal line. Eyes large, abnormally shaped, and slightly rough. Wings vary from almost normal to small, deformed structures with very abnormal venation. Bristles frequently waved or bent. Male viability and fertility subnormal. RK2. # twi: twist location: 2-100. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1983, DIS 59: 158-60. Simpson, 1983, Genetics 105: 615-32. Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32. Thisse, Stoetzel, El Messal, and Perrin-Schmitt, 1987, Genes and Development 1: 709-15. Thisse, Stoetzel, Gorostiza-Thisse, and Perrin-Schmidt, 1988, EMBO J. 7: 2175-83. phenotype: The wild-type allele of twi is involved in the establishment of germ layers. Mutants are embryonic lethals (zygotic), partially dorsalized, and without mesodermal dif- ferentiation. A normal blastoderm is formed; at gastrulation, no ventral furrow is visible, but the endoderm invaginates, a cephalic furrow is formed, and the germband elongated. The embryo is twisted or coiled in the egg case, often with poste- rior side up. There are few mesodermally derived internal tissues. Some embryos fail to make a properly differentiated cuticle, although 40-100% make normal ectodermal derivatives (Simpson, 1983). There is no maternal effect in germline chimeras. twi/+ heterozygous embryos have delayed ventral furrow formation. The TSP of the twi gene is around gastrula- tion (Thisse et al., 1987). alleles: allele synonym comments ____________________________________________ twi1 twiID twi2 twiIIE twi3 twiIIH twi4 twiD5 twi5 twiO5 twi6 twiX10 twi7 twiey63 twi8 twiIG temperature-sensitive cytology: Placed in 59C3-D2; uncovered by Df(2R)twi = Df(2R)59C3-4;59D1-2. molecular biology: Region containing twi cloned (Thisse, El Messal and Perrin-Schmidt, 1987, Nucleic Acids Research 15: 3439-53) and the nucleotide sequence obtained (Thisse et al., 1988). The sequence is a simple transcription unit, with an unique 5' end and a 120 bp intron near its 3' end. The mature twist mRNA is 1878 bp long excluding the poly(A) tail, and contains one large open reading frame that generates a protein of 490 amino acids that is present at the anterior and posterior poles and in the midventral region at the cellular blastoderm stage. The twi protein is localized in the nucleus (Thisse et al., 1988). Translation apparently occurs just after the transcription process. other information: Mutations in dl, pll, ea, or Tl abolish the expression of twi. At least one dose of dl+ in females is necessary for transcription of twi (Thisse et al., 1987). twi shows extensive identity to a pair of myc-related polypeptides whose dimerized products bind to a sequence in the immunoglo- bulin kappa chain enhancer; the identical regions have the potential to form two amphipathic helices separated by an intervening loop (Murre, McCaw, and Baltimore, 1989, Cell 56: 777-83). # twirl: see twl # twirled tips: see twt # twist: see twi # twisted: see tw # twisted bristles roughened eye: see twr # twisted gastrulation: see tsg # twisted genitals: see twg # twl: twirl location: 2-63.5. origin: Ultraviolet induced. discoverer: Meyer, 54d. references: 1955, DIS 29: 74-75. phenotype: Wings strongly curled. Good viability; easy to classify. RK2. other information: Possibly an allele of upw (2-62). #*Two-b: Two bristles location: 3-58.3. origin: Spontaneous. discoverer: Bridges, 16b22. references: Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 155. phenotype: Two postvertical bristles always and two anterior dorsocentrals usually absent. Heterozygote viability excel- lent. Homozygous lethal. RK1. # two-faced: see tfd # twr: twisted bristles roughened eye location: 3-{47}. references: Merrill, Diederich, Turner, and Kaufman, 1989, Dev. Biol. 135: 376-91. phenotype: Most alleles lethal; few escapers display twisted bristles and rough eyes; survivors female sterile. alleles: allele origin discoverer synonym ______________________________________ twr1 EMS Wakimoto EfW5 twr2 EMS Wakimoto EfW9 twr3 EMS Wakimoto EfW27 twr4 EMS Kaufman k1 twr5 EMS Kaufman k4 twr6 EMS Fornili f17 twr7 EMS Fornili f37 twr8 EMS Fornili f66 twr9 EMS Fornili f68 twr10 EMS Fornili f70 twr11 EMS Lambert c33 cytology: Placed in 84A1-6 based on its inclusion in Df(3R)Scr = Df(3R)84A1-2;84B1-2 but not in Dr(3R)Antp17 = Df(3R)84A6;84D13-14. #*twt: twirled tips location: 1-37.1. origin: Induced by 1:4-dimethanesulfonoxybut-2-yne (CB. 2058). discoverer: Fahmy, 1951. references: 1959, DIS 33: 94. phenotype: Wings completely or partially unexpanded; tips fre- quently twisted. Male inviable, dies shortly after eclosion, and does not breed. RK3. # tx: taxi (J.C. Hall) location: 3-91. origin: Spontaneous. phenotype: Wings held out at about 75 from body axis, often arched or wavy, somewhat narrow and dusky. Unable to fly because of shape and posture of wings. RK2. alleles: allele discoverer ref ( ___________________________________ tx1 Collins, 24j30 1, 2 tx52j Tsukamoto, 52j 3 ( 1 = Chiarodo, Reing, and Saranchak, 1971, J. Exp. Zool. 178: 325-30; 2 = Collins, 1928, Am. Nat. 62: 127-36; 3 = Tsukamoto, 1956, DIS 30: 79. tx: taxi From Collins, 1928, Am. Naturalist 62: 127-36. # ty: tiny location: 1-44.5. discoverer: Bridges, 25k1. references: King and Koch, 1963, Quart. J. Microscop. Sci. 104: 297-320. King, 1970, Ovarian Development in Drosophila melanogaster, Acad. Press, New York. King and Mohler, 1975, Handbook of Genetics (R.C. King, ed.). Plenum Press, New York and London, Vol. 3, pp. 757-91. Perrimon and Gans, 1983, Dev. Biol. 100: 365-73. phenotype: Bristles small. Body small. Eclosion delayed. Viability excellent. Female sterile; eggs rarely found and only in a few ovarioles (Perrimon and Gans, 1983). Yolk for- mation in oocytes inhibited [King and Burnett, 1957, Growth 21: 263-80 (fig.)]. Follicular cells form abnormal deriva- tives of endoplasmic reticulum and migrate abnormally or form excess of normal endoplasmic reticulum derivative [King and Vanoucek, 1960, Growth 24: 333-38; Falk and King, 1964, Growth 28: 291-324 (fig.)]. ty ovaries in ty+ host develop autonomously (King and Bodenstein, 1965, Z. Naturforsch. 20B: 292-97). RK2. The heteroallelic combination ty/tyl5 exhibits the visible phenotypes described for ty homozygotes (Schalet, 1986, Mutat. Res. 163: 115-44), and, in addition, may show a reduction in thoracic hairs and abnormally-shaped rough eyes; viability severely reduced in some cultures. alleles: A spontaneous lethal, l(1)4-103, was found to be allelic to ty (Schalet, 1986). cytology: Located in 12A6-12D3. #*tyb2: tiny bristle 2 location: 1-19.5. origin: Spontaneous. discoverer: Neel, 41i9. references: 1942, DIS 16: 52. phenotype: Bristles small and thin. Viability and fertility good. RK1. # tyl: tinylike location: 1-36. origin: X ray induced in In(1)dl-49. discoverer: Oliver, 28k4. references: 1935, DIS 3: 28. 1942, DIS 16: 53. phenotype: Bristles short, fine, and stubblelike. Eclosion delayed. Both sexes viable and fertile. RK2A. alleles: allele origin discoverer synonym ref ( comments _________________________________________________________ tyl1 X ray Oliver 1, 2 tyl2 EMS Voelker l(1)A8 3 tyl3 ENU Voelker l(1)M14 3 leaky ( 1 = Oliver, 1935, DIS 3: 28; 2 = Oliver, 1942, DIS 16: 53; 3 = Voelker, Wisely, Huang, and Gyurkovics, 1985, Mol. Gen. Genet. 201: 437-45. cytology: Located in 10C3-5 since included in the transposed region of Tp(1;1)vN48 = Tp(1;1)9F;10C3-5;20, but not in Df(1)GA112 = Df(1)10A11-B1;10C2. # tyr1: tyrosine 1 (J.C. Hall) location: 2-54.5 (Huntly, 1978, Ph.D. Thesis, University of Virginia); inseparable so far from pr. origin: Spontaneous. discoverer: H.W. and H.S. Lewis. synonym: (: alpha; tyrosinase-1. references: 1960, DIS 34: 51. H.W. and H.S. Lewis, 1961, Proc. Nat. Acad. Sci. USA 47: 78- 86. H.W. Lewis, 1962, Biol. Bull. 123: 464. H.W. and H.S. Lewis, 1963, Ann. N.Y. Acad. Sci. 100: 827-39. Rizki, Rizki, and Bellotti, 1985, Mol. Gen. Genet. 201: 7-13. Wright, 1987a, Results and Problems in Cell Differentiation (Hennig, ed.). Springer-Verlag, Berlin, Heidelberg, Vol. 14, pp. 95-119. 1987b, Adv. Genet. 24: 127-222. Pentz, Black, and Wright, 1990, Biochem. Genet. 28: 151-71. phenotype: tyr1 originally thought to be a structural gene for phenol oxidase (Lewis and Lewis, 1963); the mutant reported to be heat stable relative to wild type, but this differential heat stability in the original mutant strain has not been con- firmed (Wright, 1987b). Rizki et al. suggest that tyr1 acts as a regulator of phenol oxidase activity. Mutant homozygotes have about 10% of the phenol oxidase activity of most wild- type strains. 50 h mutant pupae lack activity for the proen- zyme PHOX and have detectable but reduced amounts of the diphenol oxidase components A1, A2, and A3 as compared to Samarkand wild-type pupae (Wright, 1987b; Warner, Grell, and Jacobson, 1974, Biochem. Genet. 11: 359-65); result confirmed by Pentz, Black, and Wright, 1987, who also showed that activator preparations from tyr1 were as efficient as those from wild type (Wright, 1987b). Homozygous tyr1 adults slightly underpigmented; less so than qs which has more phenol oxidase activity. Males (normal or tyr1) have three times higher dopamine levels than females (normal or mutant); the mutants (males or females) have 70% normal dopamine levels [Burnell and Daly, 1982, Advances in Genetics, Development, and Evolution of Drosophila (Lakovaara, ed.). Plenum Press, New York, pp. 361-70)]. Homozygous viable and fertile. Hemolymph of tyr1 mutant larvae will turn black but hemolymph from mutant adults will not. alleles: Only one mutant allele identified so far. cytology: Placed in salivary chromosome region 38B3 to 38B6 based on lack of recombinant with pr (Pentz et al, 1990); uncovered by Df(2L)TW150 = Df(2L)37F5-38A1;38B2-C1 which also uncovers pr (Huntley, 1978). # Tyr2: Tyrosine 2 (J.C. Hall) location: 2-66.3 (between cn and L; Homyk and Pye, 1989). origin: Spontaneous in In(2L)Cy and In(2R)Cy or induced by ethyl methanesulfonate. discoverer: H.W. and H.S. Lewis. synonym: |: beta; Tyrosinase-2. references: H.W. Lewis, 1962, Biol. Bull. 123: 464. H.W. and H.S. Lewis, 1963, Ann. N.Y. Acad. Sci. 100: 827-39. Homyk and Pye, 1989, J. Neurogenet. 5: 37-58. phenotype: Tyr2/+ heterozygotes show about 50% of the diphenol oxidase activity of wild-type strains; modifiers involved in this dominant effect. Tyr2P208, isolated as a recessive light-on/light-off transient-minus mutant by Pak, also affects electroretinograms when in heteroallelic combination with the original Tyr2 (Homyk and Pye, 1988). Tyr2 homozygotes also show this ERG defect. alleles: Two alleles, Tyr2 and Tyr2P208 (the latter not characterized biochemically). # Tyr3: Tyrosine 3 location: 3- (right arm) synonym: Tyrosinase-3. references: H.W. Lewis, 1962, Biol. Bull. 123: 464. H.W. and H.S. Lewis, 1963, Ann. N.Y. Acad. Sci. 100: 827-39. phenotype: Tyr3 heterozygotes show 35% of the diphenol oxidase activity of wild-type strains; modifiers involved in this dom- inant effect. # tyrosinase-1: see tyr1 # Tyrosinase-2: see Tyr2 # Tyrosinase-3: see Tyr3 # tyrosine 1: see tyr1 # Tyrosine 2: see Tyr2 # Tyrosine 3: see Tyr3 # Tyrosine hydroxylase: see Th # Tyrosine kinase related: see Tkr #*tyw: tiny wing location: 3-0. discoverer: Bridges, 18c9. phenotype: Wings small. Postscutellars divergent, curling upward and forward. Extra bristles on head and thorax. Viability 60% wild type. RK3.