U: Upturned Edith M. Wallace, unpublished. # U: Upturned location: 2-70 (based on UH20, whose allelism is uncertain). Wings upturned like those of Cy but dark and waxy. Postscutel- lars crossed as in cu. Body color darker than normal. Eyes mottled with light flecks. RK2A. alleles: allele origin discoverer ref ( comments __________________________________________________________ U1 X ray Ball, 32a27 1, 2 homozygous lethal *UH20 Tanaka, 35a6 2, 3 homozygous viable ( 1 = Ball, 1935, DIS 3: 17; 2 = Bridges, 1938, DIS 9: 108; 3 = Tanaka, 1937, DIS 8: 11. cytology: U1 associated with In(2LR)U = In(2LR)40F;53A (Bridges and Li, 1935, Year Book - Carnegie Inst. Washington 35: 293; Bridges, 1938, DIS 9: 57). # u-shaped: see ush # U1: see snRNA # U2: see snRNA # U3: see snRNA # U4: see snRNA # U5: see snRNA # U6: see snRNA # u-shaped: see ush # Uab: see BXC # Ual: see ftzUal # UB3-D: see Ubi-m # UB597 location: 1-55.9. origin: Dysgenic cross of Berlin wild-type (M-cytotype) females with Harwich (P-cytotype) males (Campos-Ortega). references: Fischbach, Hoube, Boschert, Barleben, and Gschwander, 1987, J. Neurogenet. 4: 128-29 (abstract). phenotype: Eye mutant. When flies reared in normal light-dark cycle, rhabdomeres are about 40% normal length, not extending down to the basal membrane. Rhabdomeres R7 and R8 are split into two symmetrical halves in nearly all of the ommatidia. The proximal part of the eye is filled with pigment cells. No degeneration of lamina or medulla is observed. When flies are reared in the dark, both rhabdomeres and lamina show the beginnings of disintegration and the pigment cells are swelled. # UB883 location: 1- (between y and cv). origin: Dysgenic cross of Berlin wild-type (M-cytotype) females with Harwich (P-cytotype) males (Campos-Ortega). references: Fischbach, Hoube, Boschert, Barleben, and Gschwander, 1987, J. Neurogenet. 4: 128-29 (abstract). phenotype: Eye mutant. Inner optic chiasma in disorder. Bun- dles of fibers connecting medulla and lobula plate penetrate neuropil of lobula. # Ubi: Ubiquitin The ubiquitous and highly conserved protein ubiquitin binds to certain proteins within cells, marking them for degradation by various enzymes, and is later released after these proteins have been degraded. The proteins include histone H2A, H2B, and actin. Ubiquitin genes are found in Drosophila melanogas- ter as well as in many eukaryotes from yeast to man. The pro- teins encoded by these genes may be polyproteins that are later processed into monomeric units or they may be hybrid proteins, each of which is made up of a single unit fused to a nonhomologous tail sequence. Both protein types have been identified in yeast, man, and Drosophila melanogaster. # Ubi-m: Ubiquitin-monomeric location: 3-. synonym: UB3-D. references: Lee, Simon, and Lis, 1988, Mol. Cell Biol. 8: 4727-35. phenotype: Structural gene for ubiquitin (Lee et al., 1988). Ubi-m codes for a fusion protein whose single ubiquitin sequence is attached to a tail polypeptide with 65% identity to the yeast ubiquitin tail protein and 82% identity to the human ubiquitin tail protein. Ubiquitin-monomeric is not inducible by heat shock. molecular biology: Gene cloned and nucleotide and deduced amino acids sequences obtained (Lee et al., 1988). The fusion pro- tein is made up of a 76-amino-acid ubiquitin monomer (identi- cal to that of Ubi-p) and an 80-amino-acid basic tail polypep- tide. Ubi-m encodes a 0.9 kb mRNA whose expression is not detectably increased by heat shock. # Ubi-p: Ubiquitin-polymeric location: 3- {same map position as an early ecdysone-induced puff; see Ashburner, 1982, Developmental Studies on Giant Chromosomes (Berman, ed.). Springer-Verlag, Berlin, pp. 101- 51}. synonym: polyubiquitin. references: Lis, Neckameyer, Dubensky, and Costlow, 1981, Gene 15: 67-80. Izquierdo, Arribas, Galceran, Burke, and Cabrera, 1984, Biochim. Biophys. Acta 783: 114-21. Simon, Sutton, and Lis, 1985, Chromosoma 93: 26-30. Arribas, Sampedro, and Izquierdo, 1986, Biochim. Biophys. Acta 868: 119-27. Lee, Simon, and Lis, 1988, Mol. Cell Biol. 8: 4727-35. phenotype: Structural gene for ubiquitin (Arribas et al., 1988); structure and expression described by Lee et al. (1988). Threefold increase in level of gene by heat shock. An Ubi-p - lacZ fusion gene introduced by germ line transfor- mation has been expressed at high levels at all life stages tested (embryonic, larval, pupal, and adult). cytology: Ubi-p has been localized to 63F, previously identi- fied as the early ecdysone and heat-shock puff region (Ash- burner, 1972; Lis et al., 1981; Izquierdo et al., 1984; Simon et al., 1985). In the Canton-S strain, the gene contains 18 repeats of a 228-base pair ubiquitin-encoding unit, all arranged in tandem (Lee et al., 1988). molecular biology: Intact Ubi-p genes have been cloned. The nucleotide sequences of several monomeric and dimeric repeats have been independently determined (Arribas et al., 1986; Lee et al., 1988). These sequences varied, especially at the third position of the codon. The predicted amino acid sequences of the repeats, however, were identical to those of five of the nine ubiquitin-encoding repeats previously reported. The Ubi-p gene encodes a major 4.4 kb mRNA in all tested in vivo and in vitro Drosophila melanogaster cells; the expression of this mRNA is increased by heat shock. The nucleotide sequences of Ubi-m and Ubi-p are about 83% identi- cal. # Ubl: see RpII215Ubl # Ubx: see BXC # uex: unextended location: 2-55. references: Maeda, 1962, DIS 36: 39. Hilliker, 1976, Genetics 83: 765-82. Maeda, 1984, Jpn. J. Genet. 59: 249-57. phenotype: Wings incompletely expanded as in a newly emerged fly, about one-half normal length, and frequently inflated. Tibiae and tarsi of third legs irregularly shortened and gnarled. Posterior scutellars convergent. The rare uex2 - uex7 hemizygous survivors may also have etched tergites and small bodies. alleles: Original allele found by Maeda, 58l3, has not been lost (Maeda, 1984); the six hemizygous late-pupal lethals induced by Hilliker are inferred to be allelic to uex1 on the basis of map position and phenotype. allele origin synonym ref ( comments __________________________________________________________________ uex1 spont unexpanded 2, 3 low male viability uex2 EMS l(2)EMS34-07 1 late lethal, few escapers uex3 EMS l(2)EMS45-01 1 late lethal, few escapers uex4 EMS l(2)EMS45-17 1 late lethal, few escapers uex5 EMS l(2)EMS45-37 1 late lethal, few escapers uex6 EMS l(2)EMS45-40 1 late lethal, few escapers uex7 EMS l(2)EMS45-73 1 late lethal, few escapers ( 1 = Hilliker, 1976, Genetics 83: 765-82; 2 = Maeda, 1962, DIS 36: 39. 3 = Maeda, 1984, Jpn. J. Genet. 59: 249-57. cytology: Located in 41A; included in Df(2R)A" but not in Df(2R)A. # Uf: Unfolded location: 2- (to the left of b). origin: X ray induced. discoverer: Belgovsky, 36c29. phenotype: Wings spread in homozygote and heterozygote. Via- bility and fertility good. RK3. # Ugra: see Fs(2)Sz12 # Ultrabar: see BB # Ultrabithorax: see BXC # ultraspiracle: see usp # un: uneven location: 1-54.4. references: Mohr, 1927, Nyt Mag. Naturv. 65: 266. Bateman, 1951, DIS 25: 78. Krivshenko, 1956, DIS 30: 75. Garen and Kankel, 1983, Dev. Biol. 96: 445-66. phenotype: Eyes smaller than normal, surface rough. Hemi- and homozygotes have retinas with slight to moderate disorganiza- tion of the ommatidial array, with occasional fused or aber- rant ommatidia and missing or condensed rhabdomeres (Garen and Kankel, 1983). There is some variation in the structure of the individual neurons of the optic lobe. Within the retina, un behaves in a nonautonomous way as indicated by analysis of genetic mosaics. alleles: The three surviving and three lost alleles are described in the following table: allele origin discoverer ref ( comments __________________________________________________________________________ un1 spont Mohr, 25a14 2, 4 RK1 *un3 | X ray Demerec, 28f30 wing margins frayed, eyes like un1; RK1 un4 X ray Dubinin, 1928 less extreme, more viable than un1 or un3; RK2 unC Craymer 2 *unK / spont Krivshenko, 56b9 3 eyes small, bulging, rough; scutellum long, narrow, with thin, deformed bristles; good viability, fertility; RK1 *unP ` 32P Bateman 1 eyes like un1; RK2 ( 1 = Bateman, 1951, DIS 25: 78; 2 = Garen and Kankel, 1983, Dev. Biol. 96: 445-66; 3 = Krivshenko, 1956, DIS 30: 75; 4 = Mohr, 1927, Nyt Mag. Naturv. 65: 266. | Synonym: ro-63. / Cytology: Salivary chromosomes appear normal. ` Other information: Allelism inferred from phenotype and genetic location. cytology: Located in 14D1;15A4 since included in Df(1)r-D1 = Df(1)14D1-2;15D1-2 but not covered by Dp(1;3)f+71b = Df(1;3)15A4;16C2-3;80-81 (Schalet, 1986, Mutat. Res. 163: 115-44). # unc: uncoordinated location: 1-65.9 (reduced from Fahmy's value of 68.9 to fit on map). references: Fahmy, 1960, DIS 34: 49. Schalet, 1972, DIS 49: 36-37, 64-66. Schalet and Lefevre, 1973, Chromosoma 44: 183-202. Schalet and Lefevre, 1976, The Genetics and Biology of Droso- phila (Ashburner and Novitski, eds.). Academic Press, Lon- don, New York, San Francisco, Vol. 1b, pp. 847-902. Miklos, Healy, Pain, Howells, and Russell, 1984, Chromosoma 89: 218-27. Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31. phenotype: Fly unable to walk because of lack of coordination in moving legs. Wings held up and frequently curled at tips. Death usually takes place after eclosion. alleles: unc1, the original allele induced by Fahmy, has been lost. 22 mutants identified as male lethals or semi-lethals were found to be allelic to unc1. allele origin discoverer synonym ( ref | comments ___________________________________________________________________________ *unc1 CB. 3025 Fahmy, 1954 1 dies shortly after eclosion; RK3 unc2 / neutrons Munoz l(1)16-3-212 6, 7, 9 unc3 EMS Baldwin l(1)LB17 8, 9 *unc4 3HT Kaplan l(1)LV7 9, 11 unc5 EMS Lifschytz l(1)M169 5 on y+Ymal+ unc6 EMS Lifschytz l(1)R-9-31 4 unc7 EMS Lifschytz l(1)R-10-1 4, 8, 10 unc8 EMS Lifschytz l(1)W1 4, 8, 10 also run8 unc9 EMS Lifschytz l(1)W5 4, 8, 10 unc10 X ray Lefevre l(1)GE230 2 unc11 X ray Lefevre l(1)GE250 2 unc12 X ray Lefevre l(1)HA28 2 unc13 X ray Lefevre l(1)HF329 2 unc14 X ray Lefevre l(1)JA69 2 T(1;A)19F3;h? unc15 X ray Lefevre l(1)RC60 2 unc16 X ray Lefevre l(1)RF7 2 unc17 X ray Lefevre l(1)S86 2 unc18 / EMS Lefevre l(1)DC803 3, 7 unc19 EMS Lefevre l(1)VA288 3 In(1)17E-F;19E unc20 EMS Lefevre l(1)VE715 3 Tp(1;2)19E;27A unc21 EMS Lefevre l(1)VE797 3 unc22 EMS Lefevre l(1)VE799 3 unc23 EMS Lefevre l(1)VE824 3 unc24 / X ray Schalet l(1)27E2 7 ( Synonym for unc locus = l(1)19Ef. | 1 = Fahmy, 1960, DIS 34: 49; 2 = Lefevre, 1981, Genetics 99: 461-80; 3 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 4 = Lifschytz and Falk, 1968, Mut. Res. 8: 147-55; 5 = Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84; 6 = Miklos, Healy, Pain, Howells, and Russell, 1984, Chromosoma 89: 218-27; 7 = Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31; 8 = Schalet, 1972, DIS 49: 36-37, 64-66; 9 = Schalet and Lefevre, 1973, Chro- mosoma 44: 183-202; 10 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902; 11 = Schalet and Singer, 1971, DIS 46: 131-32. / Lethal phase during pupation or after emergence; unc gene not maternally required (Perrimon, Smouse, and Miklos, 1989). cytology: Placed in 19E7-F1 (Schalet and Lefevre, 1973, 1976; Miklos et al., 1984) since included in Df(1)Q539 = Df(1)19E6;19F6-20A1 but not in Df(1)DCB1-35b = Df(1)19F1- 2;20E-F or Df(1)A118 = Df(1)19E4-5;19E7-8. molecular biology: A cloned entry point into the transition zone between the euchromatic and heterochromatic regions of the X chromosome was mapped to the near vicinity of unc (Mik- los et al., 1984). # uncl: uncoordinatedlike location: 1- {66} (between wap and fog). references: Lifschytz and Falk, 1968, Mut. Res. 6: 235-44. Lifschytz and Falk, 1969, Mut. Res. 8: 147-55. Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84. Schalet, 1972, DIS 49: 36-37, 64-66. Schalet and Lefevre, 1973, Chromosoma 44: 183-202. Schalet and Lefevre, 1976, The Genetics and Biology of Droso- phila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 848-902. Lefevre and Watkins, 1986, Genetics 113: 869-95. Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31. phenotype: Most flies die before eclosion, but the ones that hatch have uncoordinated leg movements and soon die. Females that are hemizygous have the same abnormal phenoype as homozy- gotes. Viability of various allele heterozygotes is only 1- 12%. alleles: allele origin discoverer synonym ( ref | comments _____________________________________________________________________________ uncl1 X ray Lifschytz l(1)B83 3, 4, 6-8 uncl2 l(1)J14 uncl3 EMS Lifschytz l(1)M82 5 on y+Ymal+ uncl4 EMS Lifschytz l(1)Q456 4, 6-8 uncl5 EMS Lifschytz l(1)R-10-10 4, 6-9 pupal lethal *uncl6 X ray Lefevre l(1)HC175 1 uncl7 X ray Lefevre l(1)RF7 1 uncl8 EMS Lefevre l(1)DF905 2 uncl9 EMS Lefevre l(1)GA137 2 uncl10 EMS Lefevre l(1)VA228 2, 6 early larval lethal uncl11 spont Schalet l(1)16-66 10 ( Synonym for uncl locus = l(1)20Ae. | 1 = Lefevre, 1981, Genetics 99: 461-80; 2 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 3 = Lifschytz and Falk, 1968, Mutat. Res. 6: 235-44; 4 = Lifschytz and Falk, 1969, Mut. Res. 8: 147-55; 5 = Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84; 6 = Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31; 7 = Schalet, 1972, DIS 49: 36-37, 64-66; 8 = Schalet and Lefevre, 1973, Chro- mosoma 44: 183-202; 9 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902. 10 = Schalet, 1986, Mutat, Res. 163: 115-44. cytology: Placed in 20A4-5 (Schalet and Lefevre, 1976; Lefevre and Watkins, 1986); since included in Df(1)17-439 = Df(1)20A;20B (Schalet and Lefevre, 1976) and in Df(1)GA33 (Lefevre), which also includes unc (Perrimon et al., 1989), but not in Df(1)17-257 = Df(1)19F3;20A1-2 or Df(1)16-3-22 = Df(1)19D1;20A2. # uncoordinated: see unc # uncoordinatedlike: see uncl # undersized: see us # uneven: see un # Uneven wing: see Bg2 # unexpanded: see unp # unexpanded irregular: see unr # unextended: see uex # unfolded: see uf # unp: unexpanded location: 1-63.1. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1959, DIS 33: 94. phenotype: Wings always unexpanded, frequently droop. Two sym- metrical grooves occur on the pronotum immediately anterior to wing base. Postscutellar bristles often crossed. Eclosion delayed. Male fertile; viability about 10% normal. Female extremely inviable. RK3. alleles: One allele each induced by CB. 1356 and X rays. # unpaired: see upd #*unr: unexpanded irregular location: 1-52.3. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1959, DIS 33: 94. phenotype: Wings usually unexpanded to some degree; if expanded, they are short, broad, and slightly drooping or divergent. Fertility reduced in both sexes. RK3. # Uo: see Uro # up: upheld (J.C. Hall) location: 1-41.0 [between s and g (Deak et al., 1982)]. references: Fahmy, 1958, DIS 32: 77. Hotta and Benzer, 1972, Nature (London) 240: 527-35. Grigliatti, Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-14. Deak, 1977, J. Embryol. Exp. Morphol. 40: 35-63. Fekete and Szidonya, 1979, Acta Biol. Acad. Sci. Hung. 30: 47-57. Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. Vasudev, Krishnamurthy, and Gayathri, 1980, DIS 55: 211. Mogami, Nonomura, and Hotta, 1981, Jpn. J. Genet. 56: 51-65. Deak, Bellamy, Bienz, Dubuis, Fenner, Gollin, Rahmi, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81. Hall, 1982, Quart. Rev. Biophys. 15: 223-479. Homyk and Emerson, 1988, Genetics 119: 105-21. phenotype: Wings held upright and mutants unable to jump or fly when homo- or hemizygous. The indirect flight muscles of the thorax are abnormal, with many mitochondria in the muscle fiber envelopes but with defective myofibrils (Hotta and Benzer, 1972; Deak, 1977); electron microscope and electro- phoresis studies indicate that these muscles lack internal structure in the Z-bands and Z-band proteins (Fekete and Szi- donya, 1979; Mogami et al., 1981). Although wings are held in normal position, wild-type heterozygotes of certain mutant alleles are unable to jump or fly; their muscles contain half the normal amount of Z-band proteins. Fate maps of the behavioral and morphological foci of up and up2 indicate that the gene has its site of action in the presumptive musculature of the ventral mesoderm (Hotta and Benzer, 1972; Deak, 1977). Viability and fertility of up is good. RK1. alleles: up alleles are listed in the following table. int3 may be an up allele since the two genes are close together and do not complement each other, but int3 is not listed in the table because its homozygotes show a different pattern of mus- cle abnormalities than do up homozygotes (Deak et al., 1982; Homyk and Emerson, 1988). allele origin ref ( wing phen. able to fly? up/up up/+ up/up up/+ ______________________________________________________________________ up1 | CB. 3007 1-3, 6 abnormal normal - - up2 / EMS 1, 2, 7-10 abnormal normal - - up3 EMS 2, 7 abnormal normal - - up101 ` EMS 4, 7, 8 abnormal normal - + upwg amino-naphthol- 11 abnormal sulfonic acid upwhu - EMS 4, 5, 7, 8 3 normal: normal - +/- 1 abnormal upx EMS 7 abnormal normal - + ( 1 = Deak, 1977, J. Embryol. Exp. Morphol. 40: 35-63; 2 = Deak, Bellamy, Bienz, Dubuis, Fenner, Gollin, Rahmi, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81; 3 = Fahmy, 1958, DIS 32: 77; 4 = Fekete and Szidonya, 1979, Acta Biol. Acad. Sci. Hung. 30: 47-57; 5 = Grigliatti, Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-14; 6 = Hall, 1982, Quart. Rev. Biophys. 15: 223-479; 7 = Homyk and Emerson, 1988, Genetics 119: 105-21; 8 = Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65; 9 = Hotta and Benzer, 1972, Nature (London) 240: 527-35; 10 = Mogami, Nonomura, and Hotta, 1981, Jpn. J. Genet. 56: 51-65; 11 = Vasudev, Krish- namurthy, and Gayathri, 1980, DIS 55: 211. | All mutant flies raised at 29 hold their wings in a vertical position, while 60% of those raised at 18 hold their wings in a ventrolateral position (Deak, 1977); all flies are flightless and have abnormal muscles regardless of tempera- ture. up1 shows more muscle abnormalities than up2. / Synonym: wupB. Flight muscles lack cross-striations (Hotta and Benzer, 1972). "jump" muscle absent or very small. Extracts of indirect flight muscles do not show a 54 kd polypeptide that may be a Z-band component (Deak et al., 1982). Shows electron-dense structures instead of normal Z-bands (Deak et al., 1982). ` Synonym: wupB101. Although allele previously reported as semidominant for flightlessness (Homyk et al., 1980), heterozygotes found to be able to hop and fly about as well as wild type (Fekete and Szidonya, 1979; Homyk and Emerson, 1988). - Semidominant for flightlessness (Homyk and Emerson, 1988). cytology: Located in 12A1-7; between the proximal end of Df(1)C246 = Df(1)11D-E;12A1-2 and the distal end of Df(1)HA92 = Df(1)12A6-7;12D3 (Deak et al., 1982), a region thought to be haplolethal since it is not uncovered by known deficiencies (Stewart and Merriam, 1973, DIS 50: 167-70). Although up2/+ females show the dominant flightless phenotype, up2/+/+ females carrying a duplication for 11E-12A can hop and fly as well as wild type (Homyk and Emerson, 1988). other information: Two alleles, up101 and upx, that show a wild-type flight phenotype as heterozygotes, are flightless when also heterozygous for the wing mutants hdp (hdp-a and hdp-b not distinguished) or rsd (Homyk and Emerson, 1988). up2/+;rsd/+ are not only flight-defective, but about 1/3 of them have abnormal wing positions (Deak et al., 1982). up101;Tm2/+, int3;Tm2/+, upx;Tm2/+, up101;Mhc5/+, and up101;Mhc16/+ are lethal. Double heterozygotes involving up101, int3, or upx and Mhc5 cannot fly and have abnormal wing postures. These alleles over hdp-a2 show the same phenotype. # upd: unpaired location: 1-58.7. origin: Induced by ethyl methanesulfonate. references: Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. Carroll and Scott, 1986, Cell 45: 113-26. Gergen and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 49-62. Wieschaus and Noell, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 63-73. Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52. phenotype: Embryonic lethal. Mutants show variable larval cuticular phenotype with defects predominantly in the mesothorax and the fifth abdominal segment (Nusslein-Volhard et al., 1984; Gergen and Wieschaus, 1986); also some head defects and fourth, sixth, seventh, and eighth abdominal seg- ment defects. Heterozygotes show 88-93% viability (Wieschaus and Noell, 1986). alleles: allele synonym ref ( comments _______________________________________________________________________ upd1 updC43 1,3 T2 and A5 defects; no effect on ftz upd2 updM5 3 upd3 updYC43 2 T2, A5, A8 denticle belts deleted; A6 and A7 denticle belts fused; abnormal posterior spiracles upd4 updYM55 2 T2 defect; rudimentary filzkorper and posterior spiracles; A6 and A7 denticle belts fused; A8 denticle belt reduced ( 1 = Carroll and Scott, 1986, Cell 45: 113-26; 2 = Gergen and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 49-62; 3 = Wieschaus and Noell, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 63-73. cytology: Located in 17A-B (Perrimon et al., 1989). other information: Determined to be allelic to os too late to be included in the os entry (Perrimon). # upheld: see up # upi: see Pu #*ups: upright scutellars location: 1-40.8. origin: Spontaneous. discoverer: Fahmy, 1955. references: 1958, DIS 32: 77. phenotype: Posterior scutellar bristles held vertically. Fly small. Eyes dull, small, and abnormally shaped. Wings short and folded. Male sterile; viability about 20% normal. RK2. # upt: upturned bristles location: 2- (between dp and pr). origin: Spontaneous. discoverer: Bryan, 63f. references: Whittinghill and Clancy, 1967, DIS 42: 37. phenotype: Dorsocentral and/or anterior scutellar bristles curled upwards. Increase in penetrance as temperature raised (40% at 21; 60% at 25). Variable expression. # Upturned: see U # upturned bristles: see upt #*upw: upward location: 2-62. discoverer: Bridges, 33k21. phenotype: Wings turned up at tips. More extreme at higher temperatures. Veins sometimes have lumps. RK3. # uq: see bruq # Urate oxidase: see Uro # urd: urdur (J.A. Kennison) location: 3-53. origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1983. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Isolated as a dominant suppressor of Pc mutations. Also suppresses Pcl and Msc alleles. Recessive larval lethal. alleles: urd2 induced by ethyl methanesulfonate. cytology: Placed in 87F12-88A1 based on the cytology of Df(3R)urd, which lacks several bands in 87F; also its exclu- sion from Df(3R)126c = Df(3R)87D14-E1;87F11-12 and its inclu- sion within Df(3R)red31 = Df(3R)87F12-14;88C1-3 and Df(3R)ry85 = Df(3R)87B15-C1;87F15-88A1. # Uro: Urate oxidase location: 2- {22}. synonym: Uo. references: Friedman and Johnson, 1977, Science 197: 477-79. Friedman and Barker, 1982, Insect Biochem. 12: 563-70. Kral, Johnson, Wing, and Friedman, 1982, Dev. Genet. (Amster- dam) 3: 213-15. phenotype: Structural gene for urate oxidase [UO (E.C. 1.7.3.3)], the enzyme involved in the oxidation of uric acid to allantoin. Enzyme confined to the Malpighian tubules and only expressed in third-instar larvae and adults. Rapid decline in urate oxidase activity in late third-instar larvae attributed to the accumulation of 20-hydroxyecdysone for puparium formation; ecd larvae, when kept at 29, fail to accu- mulate 20-hydroxyecdysone and, unless fed 20-hydroxyecdysone, retain high urate oxidase activity (Kral et al., 1982). cytology: Located in 28C by in situ hybridization. molecular biology: Gene cloned (Kral, Johnson, Burnett, and Friedman, 1986, Gene 45: 131-37). Highest concentration of mRNA in third instar larvae; decline in enzyme activity accom- panied by disappearance of mRNA. Sequence and expression pat- tern described by Walbrath, Burnett, and Friedman (1990, Mol. Cell. Biol. 10: 5114-27). #*us: undersized location: 1-52.5. origin: X ray induced. discoverer: Fahmy, 1956. references: 1959, DIS 33: 94. phenotype: Body small. Viable and fertile. RK3. alleles: One allele each induced by CB. 1506 and CB. 1528; two by X rays. # ush: u-shaped location: 2-0.1. origin: Induced by ethyl methanesulfonate. synonym: l(2)19. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. phenotype: Embryonic lethal. No shortening of the germ band. Lateral fusion of anterior and posterior hypoderm. alleles: ush1 and ush2, both strong alleles, recovered as 19 and IIa. cytology: Located in 21C since uncovered by Df(2L)al = Df(2L)21B8-C1;21C8-D1. # usp: ultraspiracle (A. E. Oro) location: 1- {0.5}. discoverer: Lefevre. synonym: XR2C (Oro et al., 1990); Cf1 (Shea et al., 1990). references: Perrimon, Engstrom, and Mahowald, 1984, Dev. Biol. 105: 404-14. 1985, Genetics 111: 23-41. Perrimon and Mahowald, 1986, Symp. Soc. Dev. Biol. 44: 221- 35. Henrich, Sliter, Lubahn, MacIntyre, and Gilbert, 1990, Nucleic Acids Res. 18: 4143-48. Oro, McKeown, and Evans, 1990, Nature 347: 298-301. Shea, King, Conboy, Mariani, and Kafatos, 1990, Genes Dev. 4: 1128-40. phenotype: Mutants are recessive lethals. usp/usp or usp// progeny of usp/+ mothers die during the first larval instar or in the molt to the second instar. Those that die during the molt to the second instar sometimes have incompletely molted the first instar set of larval spiracles and thus have two sets of spiracles (Perrimon et al., 1985; Oro, McKeown and Evans, in prep.). usp/Y embryos derived from usp/usp germ cells die just prior to or just after hatching with an oval scar on the ventral surface of the posterior eighth abdominal or ninth abdominal segment. The spiracles of these animals appear normal as does the rest of the cuticle and the ventral nervous system. Paternally supplied usp+ completely rescues this phenotype and allows survival to adulthood (Perrimon et al., 1985; Oro, McKeown, and Evans, in prep.). Use of a con- ditional expression system for rescue of the first/second instar lethal phase results in survival into the third instar and early pupal periods, with no animals surviving beyond pupal stage P4 (Oro, Mckeown, and Evans, in prep.). usp/0//usp+ gyandromorphs do not survive suggesting that the gene is required in multiple parts of the body and not just in the terminal regions. /-ray induced usp/usp clones survive in the female germline, abdomen, thorax and head, showing that usp is not a general cell lethal. Clones in the head are associated with defects in rhabdomere and ommatidial morphol- ogy (Oro, McKeown, and Evans, in prep.). Expression of a usp cDNA at high levels throughout development rescues the usp- phenotype and has no deletenous effect on usp+ animals, suggesting that any necessary spatial or temporal regulation of usp action occurs by regulation of some other factor such as a ligand. alleles: allele origin synonym ref ( comments ________________________________________________________ usp1 X ray l(1)HF346 1 T(1;4)2C1-2;101 usp2 X ray l(1)KA21 1, 2 Tp(3;1)2C9;66B;67E usp3 EMS l(1)VE653 1-3 usp4 EMS l(1)VE849 1-3 ( 1 = Lefevre; 2 = Oro, McKeown, and Evans, 1990, Nature 347: 298-301; 3 = Perrimon, Engstrom, and Mahowald, 1985, Genetics 111: 23-41. cytology: Placed in 2C1-2D1 since covered by Dp(1;3)wvco = Dp(1;3)2B17-C1;3C5-6 but not by Dp(1;Y)w+303 = Dp(1;Y)2D1- 2;3D3-4 (Perrimon et al., 1970). molecular biology: Cloning and nucleotide and putative amino acid sequencing of the 2C region indicates that the protein product of usp (= XR2C) is a homologue of the human retinoid X receptor, (Oro et al., 1990). Factors with the same putative DNA-binding domain as usp have been cloned and sequenced by Shea et al. (1990) and Henrich et al. (1990). usp produces a single 2.4-kb transcript with higher levels in adults and embryos than in larvae. The colinearity of the cDNA and the genomic DNA indicates that there are no introns. In the mutant usp2, the coding region has been disrupted by insertion of a 66B-67E fragment from the third chromosome. The structure of the cloned breakpoints of this transposition [Tp(3;1)usp4] has been determined. The lethal mutants usp2, usp3, and usp4 are rescued by germ-line transformation with an 8-kb EcoR1 fragment carrying the XR2C transcription unit, the transformed flies being as viable as wild-type (usp+) flies (Oro et al., 1990). # Uw: see Bg2