# ro: rough location: 3-91.1. references: Pilkington, 1941, Proc. Zool. Soc. London A 111: 199-222. Ready, Hanson, and Benzer, 1976, Dev. Biol. 53: 217-40 (fig.). Meyerowitz and Kankel, 1978, Dev. Biol. 62: 112-42 (fig.). Garen and Kankel, 1983, Dev. Biol. 96: 445-66. Tomlinson, Kimmel, and Rubin, 1988, Cell 55: 771-84. Renfranz, and Benzer, 1989, Dev. Biol. 136: 411-29. phenotype: Homozygotes have rough eyes; slightly smaller and narrower than wild type. Approximately normal numbers of facets but arrangement irregular; frequently have fewer and sometimes more than eight retinula cells; some facets missing such that three ommatidial bristles juxtaposed; other facets fused (Stemm-Tegethoff and Dicke, 1974, Theoret. Appl. Genet. 44: 262-65; Ready et al.). Fiber pathways through lamina and into medulla in considerable disarray; optic chiasma between the two replaced by parallel fibers; laminar cartridge and medullar columns deranged, ventral epithelial nuclear row absent; medulla displaced from normal position and rotated anteriorly. Mosaic studies demonstrate that phenotype is eye autonomous; i.e., the genotype of the eye dictates that of the underlying nervous elements. Expression, as determined by in situ hybridization found in the eye-antenna imaginal disk, especially in the region of the morphogenetic furrow, as well as in a specific area of the brain. No evidence of embryonic expression (Saint, Kalionis, Lockett, and Elizur, 1988, Nature (London) 334: 151-54). RK1. alleles: allele origin discoverer ref ( comments ___________________________________________________________________ ro1 | spont Muller, 13f 1, 5 insertion of middle- repetitive DNA into intron 5' to homeobox ro2 X ray Brosseau 2 ro3 X ray Brosseau 2 ro4 X ray Brosseau 2 ro64c X ray Puro 3, 4 recombination normal ro~~13 / P-element 6 rov1 X ray Brosseau 2 heterochromatin, 91D rearrangement rov2 X ray Brosseau 2 heterochromatin, 91E rearrangement row EMS 5 nonsense mutation in homeobox ( 1 = Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 93 (fig.). 2 = Brosseau, 1970, DIS 45: 100; 3 = Puro, 1980, DIS 58: 205; 4 = Puro and Nygren, 1982, Heredi- tas 81: 231-48; 5 = Saint, Kalionis, Lockett, and Elizur, 1988, Nature (London) 334: 151-54 (fig.); 6 = Tomlinson, Kimmel, and Rubin, 1988, Cell 55: 771-84. | Contains a >10 kb insertion homologous to 412 in intron 1 (Tomlinson et al., 1988). / Contains a P-element insertion in exon 3 (Tomlinson et al., 1988). P-element excised in a revertant of this allele. cytology: Placed in 97D1-9 based on its inclusion in Df(3R)ro- XB3 = Df(3R)97D1-2;97D9. Restricted to 97D5-7 by in situ hybridization (Tomlinson et al., 1988). molecular biology: Gene or part thereof isolated from a genomic library using a 33 base-pair homeobox consensus sequence as a probe. Isolated homeobox sequence shows 57 and 58% homology to those of Antp and Scr (Saint et al.). The complete ro gene was isolated by Tomlinson et al. (1988) by P-element transpo- son tagging. A mutant ro~~13 was rescued by transformation with an 8.6 kb genomic fragment carrying the gene. The ro locus contains three exons and two introns and the transcrip- tion unit spans about 4.3 kb. The homeobox domain is encoded in exon 2 and opa-like repeats are encoded in exons 1 and 3. The complete sequence of the ro gene was obtained, and the putative sequence of its 350-amino-acid homeobox protein determined (Tomlinson et al., 1988). # ro-63: see un3 # rod: rough deal location: 3-105.1 (to right of ca). origin: Induced by hybrid dysgenesis (rodH4.8) or / rays (rodX1-4). references: Karess and Glover, 1989, J. Cell Biol. 109: 2951- 61. phenotype: Mutants show mitotic abnormalities in larval neurob- lasts; there is a high frequency of both aneuploid cells and abnormal anaphase figures, with lagging chromatids, anaphase bridges, and stretched chromatid arms. Abnormal chromosome behavior also occurs in the second meiotic anaphase in male meiosis, although motile sperm are produced. All surviving homozygous females and 90% of surviving homozygous males are sterile and have roughened eyes, sparse abdominal bristles, and notched wings. alleles: allele % abnormal anaphases %homozygous viable ___________________________________________________ rodH4.8 20.2 25 rodX-1 42.5 0 rodX-2 20.7 27 rodX-3 15.0 49 rodX-4 13.9 73 cytology: Placed in 100B5-D1 based on the presence of the nor- mal allele in Dp(3;1)48 (=Df(3R)ca48) = Dp(3;1)100B7-8;100F as well as in Df(3R)tll-e = Df(3R)100A1-2;100B5-9 and Df(3R)Kpn-A = Df(3R)100D1;100E and a synthetic deficiency for 100D-F. # roe: roughened eye location: 3-47.6 [proximal to rn (Agnel, Kerridge, Vola, and Griffin-Shea, 1989, Genes Dev. 3: 85-95)]. references: Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23 (fig.). Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29. phenotype: Produces a slight roughening of the eye owing to the irregular disposition of the facets; interommatidial bristles lost from posterior portion of the eye. Extreme expression in mutant/deficiency heterozygotes and more so in deficiency homozygotes; enhanced roughening and posterior loss of ommati- dial bristles; in addition the eye is reduced in size and remaining interommatidial bristles are clumped. RK1. alleles: All alleles appear to be hypomorphic in that the phenotype of mutant/deficiency is more severe that of homozy- gous mutants. allele origin discoverer synonym ref ( comments ________________________________________________________ roe1 spont Markowitz, 61g 1, 2 roe2 EMS Grigliatti 1 roe3 EMS Grigliatti roe5.15 1 ( 1 = Lewis, Kaufman, Denell, and Tallerico, 1980, Genetics 95: 367-81; 2 = Markowitz, 1963, DIS 38: 31. cytology: Placed in 84D2 based on its inclusion in Df(3R)D6 = Df(3R)84D2-3;84F13-16 but not Df(3R)dsx10M = Df(3R)84D3;84F1- 2. Df(3R)D6/Df(3R)Scx4, which is deficient for both roe and rn, survives with an extreme roe phenotype. # Roi: Rough eye location: 2- [left arm, not separated from In(2L)t]. origin: Spontaneous in In(2L)t. discoverer: Ives, 47k18. references: 1952, DIS 26: 65. 1956, DIS 30: 72. Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29. phenotype: Eye facets of Roi/+ irregularly rounded, sometimes enlarged; eyes sometimes bulge. Roi/Roi lethal; Roi/S viable. Acts as a partial suppressor of B (E. H. Grell). Viability good. RK2A. cytology: Tentatively placed in 36F7-37B8 on the basis of its failure to survive in heterozygous combination with Df(2L)TW3 = Df(2L)36F7-37A1;37B2-8 (Voelker and Langley, 1978, DIS 53: 185). # rol: reduced optic lobes (J.C. Hall) location: 1-52. origin: Induced by ethyl methanesulfonate. discoverer: Heisenberg. references: Wolf and Heisenberg, 1986, Nature (London) 323: 154-56. Coombe, 1986, J. Comp. Physiol. 159: 655-65. Heisenberg and Wolf, 1988, J. Comp. Physiol. 163: 373-88. phenotype: Relatively proximal portion of optic lobes, except for lamina, reduced in volume to approximately 40-50% normal; less severe reduction than in sol; rol sol double mutant has extremely small visual system (connecting eye to central brain), whose volume is some 12% of normal (Wolf and Heisen- berg, 1986) and whose lobula plate optic ganglion is absent (Heisenberg, unpublished); a triple mutant, with mnb added to the two just noted, has diminished amplitudes of light-on and light-off transient spikes in electroretinogram (Coombe, 1986). Behavioral experiments reported for rol sol [a single mutant involving only the former exhibits only subtle defects in visual behavior (Heisenberg, unpublished)]; the double mutant is blind in terms of standard optomotor responses to rotating vertical stripes, but it can respond to the positions of landmarks by making turning maneuvers (Wolf and Heisenberg, 1986); these optic-lobe-depleted flies can make use of the magnitudes, though not the directions, of moving patterns to stabilize the panorama presented to them; they do so apparently by sampling the optomotor torque value which has the effect of putting them in optomotor balance; thus, it is concluded that the double mutant's visual orientation is an operant behavior (Wolf and Heisenberg, 1986); same conclusion arrived at in experiments testing this double mutant's visu- ally mediated course control during tethered flight (Heisen- berg and Wolf, 1988). allele: One allele, rol1, isolated as rolKS221. # rolled: see rl # rolled up: see rlu # Roof: see Rf # roof wings: see rf # rosd: see Fs(3)Sz30 # rose: see rs # rosy: see ry # Rosy: see bwV4 # rotated abdomen: see rt # rotated penis: see rp # rotund: see rn # rough: see ro # rough deal: see rod # rough eye: see rey # Rough eye: see Roi # rough III: see dfi # Rough wing: see Rw # rough-64: see rg2 # roughened eye: see roe # Roughened: see R # roughest: see rst # roughestlike: see rstl # roughex: see rux # rougheye-like: see rey3 # roughish: see rg1 # roughish: see rh # roughoid: see ru # rox: see rg6 #*rp: rotated penis location: 3-41.7. origin: Spontaneous. discoverer: Bridges, 29c15. references: Morgan, Sturtevant, and Bridges, 1929, Year Book - Carnegie Inst. Washington 28: 339. phenotype: As viewed from behind, external genitalia of male rotated counterclockwise from 0 to 270, usually about 180; overlaps wild type in 30% of flies. Eyes rough. Fly small; legs weak; tergites ridged; abdomen narrowed. Male sterile, even when genitalia not rotated. RK3. # Rp21: Ribosomal protein 21 location: 3-{47}. references: Biessmann, Kuger, Schropfer, and Spindler, 1981, Chromosoma 82: 493-503. Kay, Zhang, and Jacobs-Lorena, 1988, Mol. Gen. Genet. 213: 354-58. phenotype: Cloned Rp21 DNA encodes a ribosomal protein of 26,000 daltons (Kay et al., 1988). When transformed into the Drosophila germ line using P elements, the Rp21 gene is expressed in the transgenic flies as an increase in the level of the corresponding mRNA. cytology: Rp21 located in 3L at 80 by in situ hybridization of the transformed copy to the salivaries. molecular biology: Gene coding for an abundant small RNA cloned by Biessman et al. (1981) and Kay et al. (1988) (see discus- sion under phenotype). Although mapped to the same region as M(3)80, the transformed Rp21 gene did not complement this Minute (Kay et al., 1988). # Rp49: see M(3)99D # RpA1: Ribosomal protein A1 location: 2-{78}. references: Kay and Jacobs-Lorena, 1985, Mol. Cell. Biol. 5: 3583-92. Qian, Zhang, Kay, and Jacobs-Lorena, 1987, Nucl. Acids Res. 15: 987-1003. Qian, Hongo, and Jacobs-Lorena, 1988, Proc. Nat. Acad. Sci. USA 85: 9601-05. phenotype: Encodes protein homologous to "A" family of eucaryotic ribosomal proteins involved in the initiation and elongation steps of protein synthesis (Qian et al., 1987). mRNA of the RpA1 gene is regulated at the level of transla- tion; it is associated with polysomes during oogenesis and late embryonic stages (Kay and Jacobs-Lorena, 1985). An antisense RpA1 gene (carrying a heat shock promoter), transformed into the fly genome, disrupts oogenesis and results in female sterility (Qian et al., 1988). cytology: Located in 53C1-6 by in situ hybridization to the salivaries (Socolitch). Single copy gene indicated. molecular biology: Cloned DNA sequence coding for RpA1 protein identified; complete nucleotide sequence and deduced amino acid sequence determined (Qian et al., 1987). RpA1 gene has no introns. The amino acid sequence of RpA1 shows significant identity to the amino acid sequences of the r-proteins of rat, shrimp, and yeast; all of these r-proteins are acidic. other information: Not allelic to M(2)53. # RpII140: RNA polymeraseII-140 kd subunit location: 3- {54}. origin: Recovered by cross hybridization with yeast gene clone. synonym: wimp. references: Faust, Renkawitz-Pohl, Falkenburg, Gasch, Bialojan, Young, and Bautz, 1986, EMBO J. 5: 741-46. phenotype: The structural gene for the 140-kd subunit of RNA polymerase II [RNA nucleotidyl transferase (EC 2.7.7.6)]. The gene is highly conserved judging from shared sequence homology with the yeast 150-kd subunit gene. alleles: Mutants selected by Mortin, (1990, Proc. Nat. Acad. Sci. USA 87: 4864-68) as extragenic suppressors of RpII215K1. cytology: Placed in 88A-B by in situ hybridization. molecular biology: Clone isolated from a genomic library using as a probe the gene for the yeast 150-kd subunit of RNA polym- erase II. Antibodies raised to a fusion protein made in an expression vector react with Drosophila RNA polymerase II, and the fusion protein has spots in common with RNA polymerase II in peptide maps. Polyadenylated RNA of 3.9 kb transcribed by gene; very little space for untranslated sequences. High degree of homology in conceptual amino-acid sequence between yeast and Drosophila subunits. # RpII215: RNA polymeraseII-215 kd subunit location: 1-35.66 [based on 320 recombinants between v and m (Greenleaf et al., 1980)]. synonym: l(1)L5. references: Greenleaf, Borsett, Jiamachello, and Coulter, 1979, Cell 18: 13-22. Greenleaf, Weeks, Voelker, Ohnishi, and Dickson, 1980, Cell 21: 785-92. Greenleaf, 1983, J. Biol. Chem. 258: 13403-06. phenotype: The structural gene encoding the 215 kd subunit of RNA polymerase II [RNA nucleotidyl transferase (EC 2.7.7.6)]. This subunit highly conserved as inferred from the cross reac- tion of antiserum from the large subunit of calf RNA polym- erase II with enzyme isolated from Drosophila as well as that from yeast and wheat germ (Carrol and Stollar, 1983, J. Mol. Biol. 170: 777-90); also amino-acid sequence homology detected with the |' subunit of E. coli RNA polymerase (Biggs, Searles, and Greenleaf, 1985, Cell 42: 611-21). Dosage com- pensated at the level of transcription (Faust, Penkawitz-Pohl, Falkenberg, Gasch, Biabjah, Young, and Bautz, 1986, EMBO J. 5: 741-46). alleles: Most alleles are recessive lethals; however several viable alleles and others with dominant phenotypes are described at the end of this entry. These alleles all enhance expression of Ubx in RpII215/+ heterozygotes with the effect of + (no effect) < RpII215H1 < RpII2157 < RpII215K2 < RpII2154 < RpII215Ubl. Heteroallelic combinations of these mutants produce either a reduced effect when RII215Ubl is involved or no effect in other combinations. allele origin discoverer synonym ( ref | comments / _____________________________________________________________________________________________________________________ RpII2151 X ray Lefevre l(1)L5, Ubln 5, 10 RpII2152 ` EMS RpII215A9 12 heat sensitive, haplospecific RpII2153 ` EMS RpII215A11 12, 4 haplospecific RpII2154 EMS RpII215C4 1, 3, 4, 12 viable RpII2155 EMS RpII215C8 12, 4 RpII2156 EMS RpII215C9 12, 4 RpII2157 EMS Baker RpII215C11-138 12 cold sensitive RpII2158 ` EMS RpII215C20 12, 4 heat sensitive, haplospecific RpII2159 dysgenesis RpII215D50 11 P insert at 0.1 RpII21510 - EMS RpII215D150 12 RpII21511 - EMS RpII215D308 12 RpII21512 ` EMS RpII215E28 12 heat sensitive, haplospecific RpII21513 EMS RpII215F4 12 RpII21514 ` EMS RpII215F6 12 RpII21515 EMS RpII215F7 12 RpII21516 ` EMS RpII215F8 12 RpII21517 EMS RpII215F9 12 RpII21518 EMS RpII215F12 12 RpII21519 ` EMS RpII215F36 12 RpII21520 EMS RpII215F48 12 RpII21521 ` EMS RpII215F50 12 RpII21522 EMS RpII215F51 12 RpII21523 ` EMS RpII215F60 12 RpII21524 EMS RpII215F69 12 RpII21525 EMS RpII215F76 12 RpII21526 EMS RpII215F89 12 RpII21527 ` EMS RpII215F90 12 RpII21528 EMS RpII215F103 12 RpII21529 EMS RpII215F106 12 RpII21530 EMS RpII215F118 12 RpII21531 EMS RpII215F125 12 RpII21532 EMS RpII215F128 12 RpII21533 EMS RpII215F129 12 RpII21534 EMS RpII215F134 12 RpII21535 EMS RpII215G1 12 RpII21536 EMS RpII215G2 12 RpII21537 EMS RpII215G3 12 RpII21538 EMS RpII215G8 12 RpII21539 ENU RpII215H2 12 heat sensitive RpII21540 ENU RpII215H14 12 heat & cold sensitive *RpII21541 ENU RpII215H19 12 RpII21542 ENU RpII215H20 12 RpII21543 ENU RpII215H21 12 RpII21544 ENU RpII215H22 12 RpII21545 ENU RpII215H24 12 RpII21546 ENU RpII215H25 12 RpII21547 ENU RpII215H26 12 RpII21548 ENU RpII215H33 12 RpII21549 ENU RpII215H34 12 RpII21550 ENU RpII215H35 12 RpII21551 ENU RpII215H36 12 RpII21552 ENU RpII215H37 12 RpII21553 ENU RpII215H38 12 RpII21554 ENU RpII215H101 12 RpII21555 ENU RpII215H445 12 RpII21556 ENU RpII215H1239 12 RpII21557 ENU RpII215H1717 12 RpII21558 ENU RpII215H3006 12 RpII21559 ENU RpII215H3116 12 RpII21560 EMS RpII215K6 12 RpII21561 EMS RpII215K8 12 heat & cold sensitive RpII21562 EMS RpII215K12 12 RpII21563 EMS RpII215K17 12 RpII21564 EMS RpII215K18 12 RpII21565 EMS RpII215K21 12 RpII21566 EMS RpII215K26 12 heat sensitive RpII21567 ENU RpII215M1 12 RpII21568 ENU RpII215M3 12 RpII21569 ENU RpII215M8 12 RpII21570 ENU RpII215M17 12 RpII21571 ENU RpII215M18 12 RpII21572 ENU RpII215M42 12 RpII21573 ENU RpII215M43 12 RpII21574 ENU RpII215M45 12 RpII21575 ENU RpII215M47 12 RpII21576 ENU RpII215M48 12 heat & cold sensitive RpII21577 ENU RpII215M49 12 RpII21578 ENU RpII215M54 12 RpII21579 ENU RpII215M66 12 RpII21580 ENU RpII215M69 12 RpII21581 ENU RpII215M81 12 RpII21582 dysgenesis RpII215W21 11, 12 P insert 0 to 0.9 RpII21583 dysgenesis RpII215W38 11, 12 P insert -5 to -7 RpII21584 dysgenesis RpII215W42 11, 12 P insert 0 to 0.9 *RpII21585 dysgenesis RpII215W49 12 RpII21586 dysgenesis RpII215W81 11, 12 P insert -5 to -7 RpII21587 dysgenesis RpII215W83 12 RpII21588 dysgenesis RpII215W86 12 RpII21589 dysgenesis RpII215W94 12 RpII21590 dysgenesis RpII215W105 12 RpII21591 dysgenesis RpII215W110 12 RpII21592 dysgenesis RpII215W151 12 RpII21593 dysgenesis RpII215W173 12 RpII21594 dysgenesis RpII215W182 12 RpII21595 dysgenesis RpII215W183 12 RpII21596 EMS l(1)v8 2 RpII21597 EMS l(1)v9 2 RpII21598 EMS l(1)v10 2 RpII21599 EMS l(1)v83 2 RpII215100 EMS l(1)v84 2 RpII215101 EMS l(1)v216 2 RpII215102 EMS l(1)v219 2 RpII215103 EMS l(1)v221 2 RpII215104 X ray Lefevre l(1)HC212 6 RpII215105 X ray Lefevre l(1)N40 6 RpII215106 EMS Lefevre l(1)DC783, Ublh 7, 10 RpII215107 EMS Lefevre l(1)DC811 7 RpII215108 EMS Lefevre l(1)DF912, Ubln2 7, 10 RpII215109 EMS Lefevre l(1)DF940, Ublm 7, 10 RpII215110 EMS Lefevre l(1)VA113 7 RpII215111 EMS Lefevre l(1)VE778 7 RpII215112 EMS Lefevre l(1)VE811 7 RpII215113 EMS Lefevre l(1)VE819 7 RpII215114 EMS Lefevre l(1)VE851 7 RpII215115 EMS Lefevre l(1)VE895 7 RpII215116 EMS Lefevre l(1)VE919 7 RpII215H1 EMS Huang RpII215JH1 9 viable RpII215K1 EMS Kim RpII215WJK1 9 t.s. lethal RpII215K2 EMS Kim RpII215WJK2 9 viable; female sterile RpII215ts EMS l(1)Fb40, Ublts 1, 8 RpII215Ubl EMS l(1)MGM179, Ubl 10 ( Alleles with synonymic designations A through F, except RpII2154 and RpII2157, are derivatives of RpII2154. | 1 = Coulter and Greenleaf, 1982, J. Biol. Chem. 257: 1945- 52; 2 = Geer, Lischwe, and Murphy, l983, J. Exp. Zool. 225: 107-18; 3 = Greenleaf, Borsett, Jiamachello, and Coulter, 1979, Cell 18: 613-22; 4 = Greenleaf, Weeks, Voelker, Ohnishi, and Dickson, 1980, Cell 21: 785-92; 5 = Lefevre, l971, Genetics 67: 497-513; 6 = Lefevre, 1981, Genetics 99: 461-80; 7 = Lefevre and Watkins, 1986, Genet- ics 113: 869-95; 8 = Mortin and Kaufman, 1982, Mol. Gen. Genet. 187: 120-25; 9 = Mortin, Kim, and Huang, 1988, Genetics 119: 863-73; 10 = Mortin and Lefevre, 1981, Chro- mosoma 82: 237-47 (fig.); 11 = Searles, Jokerst, Bingham, Voelker, and Greenleaf, l982, Cell 31: 585-92; 12 = Voelker, Wisely, Huang, and Gyurkovics, l985, Mol. Gen. Genet. 201: 437-45. / Haplospecific lethals survive, at least with a low fre- quency, as homozygotes, but are lethal as hemizygotes. ` Lethal derivatives of RpII2154 that retain alpha-amanitin resistance. - Derivatives of RpII2154 chosen for reduced resistance to alpha amanitin. P-element insertion in 10B-C. cytology: Placed in 10C2-5 based on its being in the region of overlap between Df(1)m259 = Df(1)10C2-3;10E1-2 and Df(1)vN48 = Df(1)9F;10C3-5 (Voelker, Wisely, Huang, and Gyurkovics, 1985, Mol. Gen. Genet. 201: 437-45). molecular biology: Region cloned and restriction mapped (Searles, Jokerst, Bingham, Voelker, and Greenleaf, 1982, Cell 31: 585-92) and a 7 kb transcript identified as that encoding RpII215 polypeptide (Ingles, Biggs, Wong, Weeks, and Green- leaf, 1983, Proc. Nat. Acad. Sci. USA 80: 3396-3400); four exons separated by three relatively small introns; 5' exon of 500 bp followed by 600 bp intron; the next three introns larger (2.3, 2.1, and 1.8 kb) separated by introns of 100 and 50 bp. 0 coordinate of walk is SstI site within the small 5' exon of RpII215; polarity with respect to chromosome not determined. RpII215 transcript extends from 0.2 at the 5' end to -7.2; first large exon sequenced (Biggs, Searles, and Greenleaf, 1985, Cell 42: 611-21). # RpII2154 synonym: RpII215C4. references: Greenleaf, Borsett, Jiamachello, and Coulter, 1979, Cell 18: 13-22. Greenleaf, Weeks, Voelker, Ohnishi, and Dickson, 1980, Cell 21: 785-92. Mortin, Kim, and Huang, 1988, Genetics 119: 863-73. phenotype: This allele was selected as an amanitin resistant mutation; RpII2154/+ females produce equal amounts or amanitin-sensitive and -resistant enzyme and are themselves amanitin resistant. Generally a viable allele, but survival in combination with RpII21563 and RpII21586 reduced, and with RpII21551 and RpII21578 survival is zero. RNA polymerase iso- lated from embryos homozygous for this allele is 250 times less sensitive to inhibition by alpha amanitin than that from wild type; resistance attributable to reduced amanitin bind- ing; otherwise RNA polymerase normal in all respects except that there is some reduction in activity in the presence of Mg2+; stable to thermal denaturation (Coulter and Greenleaf, 1982, J. Biol. Chem. 157: 1945-52). Flies carrying both RpII2154 and RpII215+ display an Ultrabithorax-like phenotype, with enlarged halteres, and an enhancing effect on expression of Ubx [Greenleaf et al., 1980; Voelker, Wisely, Huang, and Gyurkovics, 1985, Mol. Gen. Genet. 201: 437-45 (fig.)]. Measurements of haltere size in TM6/+ females of various con- stitutions produced the following: 4/+/+ > 4/+ > 4/4/+ > 4/4 = 4/0 = +/+. The haltere effect of RpII2154 is abolished in heteroallelic combination with RpII2157, RpII215H1, and RpII215K2. RpII2154 decreases the Ubx effect of RpII215Ubl. Heterozygotes also exhibit increased numbers of duplicated bristles in Dl/+ (Mortin et al.). Males carrying RpII2154 on their X plus a normal allele on Dp(1;Y)BS-v+y+ are nearly sterile, and those carrying the normal allele instead on Dp(1;2)v65b are sterile (Voelker et al.). # RpII2157 synonym: RpII215C11-138, UblC11. references: Voelker, Wisely, Huang, and Gyurkovics, 1985, Mol. Gen. Genet. 201: 437-45. Mortin, Kim, and Huang, 1988, Genetics 119: 863-73. phenotype: Cold-sensitive lethal; survives at 28 with nearly wild-type viability, but is lethal at lower temperatures. Surviving males are fertile, whereas homozygous females are sterile. Displays slight increase in haltere size in RpII2157/+; Ubx/+ females. Lethal in combination with RpII215Ubl. Ubx effect inhibited in trans heterozygotes with other interacting alleles. In viable heterozygotes, causes an increase in the number of duplicated bristles in Dl/+ and, in males carrying a duplicated normal allele, produces sex combs on the middle legs. # RpII215106 synonym: Ublh. references: Mortin and Lefevre, 1981, Chromosoma 82: 237-47. phenotype: Homozygous lethal; RpII215106/RpII215106 females with a duplication for RpII215+ display about 50% normal via- bility, and are fertile when crossed to wild type, but nearly sterile in crosses to RpII215Ubl males with a duplication for RpII215+; all surviving progeny of the latter cross display a hyperabdominal-like phenotype; the females lack metathoracic legs and/or halteres in addition to having extra abdominal tissue; this phenotype barely detectable in offspring of crosses to normal males. # RpII215109 synonym: Ublm. references: Mortin and Lefevre, 1981, Chromosoma 82: 237-47. phenotype: Homozygous lethal; RpII215109/RpII215109 /Dp(1;1)RpII215+ females display about 50% normal viability, are fertile when crossed to wild type, but fertility only 50% normal in crosses to RpII215Ubl/Dp(1;1)RpII215+ males; offspr- ing from the latter cross have darkened eyes, thin bristles, and are sterile. # RpII215H1 phenotype: Homozygous and hemizygous viable. Exhibits slight enhancement of Ubx when heterozygous to + but not in heteroal- lelic combination with any of the interacting mutant alleles; it decreases the enhancing effects of RpII215Ubl. Increases the number of duplicated bristles of Dl/+ in all genotypes. # RpII215K1 phenotype: Temperature-sensitive recessive lethal; flies sur- vive at 19 but not at 29. Although not displaying the Ubx- enhancing effect in combination with +, it does inhibit the effect of RpII2154 at 29 but not at 25 or 19. # RpII215K2 phenotype: Homozygous and hemizygous viable; homozygous females sterile. Exhibits slight enhancement of Ubx when heterozygous to + but not in heteroallelic combination with any of the interacting mutant alleles; it decreases the enhancing effects of RpII215Ubl. Increases the number of duplicated bristles of Dl/+ in all genotypes. Temperature-sensitive period for effects on both Ubx and Dl from third larval instar until mid-pupal stage. # RpII215ts synonym: Ublts. references: Mortin and Kaufman, 1982, Mol. Gen. Genet. 187: 120-25. Mortin and Kaufman, 1984, Dev. Biol. 103: 343-54 (fig.). phenotype: Encodes a heat labile RNA polymerase subunit, as measured in vitro (Coulter and Greenleaf, 1982, J. Biol. Chem. 157: 1945-52) and by sterilizing effects on females and lethal effects on embryos. Females shifted from 22 to 29 become sterile, although their eggs laid during the first 24 hr appear normal morphologically; after 24 hr, embryonic development is visibly abnormal. Embryonic abnormalities include holes in the ventral cuticle and abnormal pharyngeal structures. Partial rescue of the sterility can be achieved by shifting newly laid eggs to 22 or by fertilization of eggs of RpII215ts females with wild-type sperm; the degree of res- cue decreases as the time that the females have been held at 29 increases. Abnormalities of embryos dying despite rescue attempts mimic the phenotypes of pair-rule and segment- polarity mutants; surviving adults resemble Hab in lacking one or both halteres and metathoracic legs. In RpII215ts/+//RpII215ts/0 gynandromorphs, the RpII215ts/0 tis- sue appears to occupy more territory than expected, as though it had a proliferative advantage over the RpII215ts/+ tissue (Mortin, Perrimon, and Bonner, 1985, Mol. Gen. Genet. 201: 437-45). # RpII215Ubl: Ultrabithorax-like synonym: Ubl. references: Mortin and Lefevre, 1981, Chromosoma 82: 237-47. Mortin, Kim, and Huang, 1988, Genetics 119: 863-73. phenotype: Homozygous and hemizygous lethal. Heterozygotes mimic Ubx in adding several hairs to and enlarging the capi- tellum of the haltere; females homozygous for RpII215Ubl, sur- viving by virtue of a duplication for RpII215+, more severely affected with capitellum approximately three times the size of that observed in RpII215Ubl/+ and with two or more rows of bristles; about 10% normal viability; poorly fertile in crosses to wild type; sterile when crossed to RpII215Ubl males with a duplication of RpII215+. Similarly males with one mutant and one normal allele are more extreme than females with one mutant and two normal alleles. Acts as a dosage sen- sitive enhancer of Ubx, transforming halteres into wing-like structures; enhancement by RpII215Ubl/RpII215Ubl/+ > RpII215Ubl/+ > RpII215Ubl/+/+. RpII215Ubl/+ interacts with heterozygotes for bx3 and bx7 but not bx1 to produce enlarged capitellum, and with bxd100/+ to transform halteres into wing-like structures; extra doses of Ubx+ counteract the enhancing effects of RpII215Ubl. A second interaction with Ubx/+ is the production of miscadestral-like pigmentation. Ubx enhancement by RpII215Ubl reduced in trans heterozygotes with other interacting alleles (Mortin et al.). Furthermore in RpII215Ubl/+//RpII215Ubl/0 gynandromorphs, the X0 tissue is without any RpII215Ubl phenotype, displaying neither enlarged halteres nor enhancement of Ubx expression, whereas the XX tissue exhibits both enlarged halteres and Ubx enhancement (Mortin, Perrimon, and Bonner, 1985, Mol. Gen. Genet. 201: 437-45). RpII215Ubl/+ also display increased frequen- cies of duplicated bristles in Dl/+, and in some crosses causes Sb/+ flies to exhibit shortened and broadened wings whose longitudinal veins fail to reach the margin (Mortin et al.). RpII215Ubl in heterozygous combination with deficien- cies for either ct or sno is lethal and with lethal alleles of ct produces a strong cut phenotype; produces a mutant pheno- type of allele specific severity in heterozygous combination with deficiencies for or lethal alleles of br, N, dm, slc, bi, oc, m, sd, and sw; interacts with heterozygotes for mutant alleles of oc, sno, and sw, but not the others; no interaction with dor, sn, ras, or g deficiencies. Influence of the mater- nal genotype apparent since patroclinous RpII215Ubl/Y and RpII215Ubl/0 males from non mutant mothers survive at 20% the expected rate; they are phenotypically normal but are sterile (Voelker et al.). #*rs: rose location: 3-35.0. phenotype: Eye color translucent purplish pink and ocelli colorless immediately after hatching; darken with age becoming sepia like, at least in the case of rs66j. Further, rs66j displays markedly decreased xanthopterin levels, reduced dro- sopterins, and higher than normal levels of sepiapterin and biopterin (Thorig and Scharloo, 1971, DIS 46: 40). rs very clear when combined with v (Akam), also interacts strongly with ltd (Silva and Mensua, 1985, DIS 51: 156). Larval Mal- pighian tubes pale yellow (Brehme and Demerec, 1942, Growth 6: 351-56). alleles: allele origin discoverer ref ( comments ____________________________________________________________ *rs1 spont Bridges, 23c10 1 male sterile; RK2 rs2 spont Bridges, 35d5 fertile; RK1 rs66j spont 2 heat sensitive ( 1 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 234; 2 = Thorig and Scharloo, 1971, DIS 40: 46. cytology: Placed 67F3-68A3 on the basis of its inclusion in Df(3L)vi2 = Df(3L)67F2-3;68D6 but not Df(3L)vi5 = Df(3L)68A3;69A1-2 (Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215-26). #*rsc: reduplicated sex combs location: 1- (between y and cv). origin: X ray induced. discoverer: Yanders, 56f6. references: 1957, DIS 31: 85. phenotype: Sex combs present on all six legs of males. Over- laps wild type in crowded cultures. Wings droop. Male fer- tile; viability only 15% wild type. Female lethal. RK2. other information: Possible allele of ph. # rsd: raised location: 3-95.4 (Ives); location in Act88F8 rsd stocks more proximal (Mahaffey et al., 1985). origin: Spontaneous. discoverer: Ives, 40i5. synonym: mod: modification. references: 1945, DIS 19: 46. 1947, DIS 21: 69. Lang, Wyss, and Eppenberger, 1981, Nature (London) 291: 506- 08. Mahaffey, Coutu, Fyrberg, and Inwood, 1985, Cell 40: 101-10. phenotype: Wings held straight up, nearly meeting over thorax. Appears to interfere with processing of certain muscle pro- teins (Mahaffey et al.). rsd strains analyzed in recent years also carry Act88F8. Viability and fertility normal. RK1. other information: Act88F8 rsd referred to as Act88F8 mod = rsd by Mahaffey et al. # rsi: reduced size location: 1-0.28 (no crossovers with br in 1038 flies). origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1954. references: 1959, DIS 33: 89. phenotype: Body small; eclosion delayed; viability reduced. RK3. cytology: Not in Df(1)RA19 = Df(1)1E3-4;2B9-10 or Df(1)sta = Df(1)1D3-E1;2A (Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbetova, Kramers, and Zhimulev, 1982, DIS 58: 184-90). other information: One allele each induced by CB. 1506 and CB. 3026. # Rsp: Responder location: 2-56.61 (based on 122 pr-cn recombinants). synonym: Ac-SD: Activator of SD (Hiraizumi and Nakazima). Dr: Director (Hartl). Receptor (Sandler and Carpenter). references: Hartl, 1974, Genetics 76: 477-86. Ganetzky, 1977, Genetics 86: 321-55. Brittnacher and Ganetzky, 1984, Genetics 107: 423-34. Wu, True, and Johnson, 1989, Nature (London) 341: 248-51. phenotype: The region of the chromosome upon which Sd acts to cause dysfunction of sperm that receive it; the sensitivity of Rsp is unaffected by its position in the genome, being equally responsive to Sd either in repulsion or coupling with Sd, or when located ectopically as in Dp(2;f)Rsp (Brittnacher and Ganetzky, 1989, Genetics 121: 739-50) or in Dp(2;Y)Rsp (Lyt- tle and Ault, 1985, Genetics 110: s23; Lyttle, 1989, Genetics 121: 751-63). alleles: Both sensitive and insensitive alleles occur, and evi- dence of their existence appeared in the earliest articles on Sd. By monitoring the relative recoveries of homologous second chromosomes from males carrying Dp(2;Y)B10-4 = Dp(2;Y)YL;36D2-3;40F, in which Sd and E(Sd) are transposed from the base of 2L into YL, Lyttle, Brittnacher, and Ganetzky (1986, Genetics 114: 183-202) were able to assign relative sensitivities to the Rsp alleles carried by different labora- tory chromosomes; Hiraizumi and Martin had made similar asses- ments based on the different degrees of distortion in response to heterozygosity to an SD chromosome. The degree of distor- tion as seen in genotypic ratios among the progeny of Sd/+ males depends on the sensitivity differential of Rsp on the two homologues. alleles: allele synonym ref ( comments ____________________________________________________________ Rspi Rsp, Rspins insensitive Rspi16 | 2 Rspi32 | 2 Rsps Rsp+, Rsps2 3, 4 sensitive Rspsi Rsps3 3, 4 intermediate sensitivity Rspss Rsps1 1, 3, 4 super sensitive ( 1 = Brittnacher and Ganetzky, 1984, Genetics 197: 423-34; 2 = Ganetzky, 1977, Genetics 86: 321-55; 3 = Hiriazumi, Martin, and Eckstrand, 1980, Genetics 95: 693-706; 4 = Lyt- tle, Brittnacher and Ganetzky, 1986, Genetics 114: 183-202. | X-ray-induced derivatives of Rsps (Ganetzky). cytology: Placed in 41A proximal to Df(2R)M41, Df(2R)B, and Df(2R)A' based on the observation that these deficiencies, all of which include the most proximal known lethally mutable locus on 2R, distort in Df/Sd males. Other proximal deficien- cies have lost sensitivity to Sd [Df(2R)A''] (Ganetzky; Sharp, Hilliker, and Holm, 1985, Genetics 110: 671-88). X-ray- induced deficiencies for Rsp delete the most proximal 2R lethal loci (Ganetzky). Insensitive chromosomes are charac- terized by the absence of 2R heterochromatic region h39; there is also one fewer n-band brought about by fusion of n bands in h38 and h40; supersensitive Responders are characterized by a duplication of h39 and a wholly heterochromatic pericentric inversion (Pimpinelli and Dimitri, 1989, Genetics 121: 765- 72). molecular biology: Responder activity correlated with the dosage of a tandemly arrayed 120-base-pair, AT-rich repeat that maps to the base of 2R and is transposed to the Y in Yrsps chromosomes of Lyttle. In one case in which reduced sensitivity is transposed to the Y leaving residual activity on 2R, repeated sequences are found on both elements of the transposition (Wu, Lyttle, Wu and Lin, 1988, Cell 54: 179- 89). other information: In flies without SD, deletion of the Rsp region results in flies (both male and female) that are less fit than Rsp+ flies (Wu et al., 1989). # rss: reduced scutellars and sternitals location: 1-17.4. origin: Spontaneous in a selection line for reduced bristle number. references: Sheldon and Evans, 1984, Aust. J. Biol. Sci. 37: 277-301. phenotype: Shows specific reduction in the number of scutellar bristles without appreciable effect on other microchaetae. Also shows a reduction in the number of sternital microchae- tae. # rst: roughest location: 1-2.2 (based on 132 w-spl recombinants). phenotype: Eyes rough and bulging; facets irregular in size and arrangement. alleles: X-ray-induced rst mutations associated with chromosome rearrangements; those induced by ethyl methanesulfonate appear to be point mutations, although some also affect vt; rst6 appears to be a point mutation that does not affect vt, is not rearranged and has normal viability in both sexes. allele origin discoverer synonym ref ( comments ____________________________________________________________________ rst1 X ray Bell, 32b25 T(1;3)rst; reduced viability rst3 X ray Gruneberg, 4, 5, 6, In(1)3C3-5;h28 33116 7, 8 rst4 EMS rst68i19 9 vt effect rst5 EMS rst68i25 9 vt effect rst6 EMS E. B. Lewis rst16172.646 9 no vt effect rstCT rst7 X ray Demerec, 38d rst264-57 2 In(1)N264-57; not variegated rst8 X ray Demerec, 39i rst265-86 1, 3, 10 In(1)N264-86 ( 1 = Demerec, 1940, Genetics 25: 618-27; 2 = Demerec, 1941, Proc. Intern. Congr. Genet., 7th, pp. 99-102; 3 = Demerec and Sutton, 1940, Proc. Nat. Acad. Sci. USA 26: 532-36; 4 = Emmens, 1937, J. Genet. 34: 191-202; 5 = Gruneberg, 1935, DIS 3: 27; 6 = Gruneberg, 1935, J. Genet. 31: 163- 84; 7 = Gruneberg, 1937, J. Genet. 34: 169-89; 8 = Kaufman, 1942, Genetics 27: 537-49; 9 = Lefevre and Green, 1972, Chromosoma 36: 391-412; 10 = Sutton, 1940, Genetics 25: 534-40. cytology: Placed in 3C5 by Lefevre and Green (1972, Chromosoma 36: 391-412); formerly placed in 3C4, which apparently does not exist. # Rst: Resistance A term used to denote genes that confer resistance to the killing effects of insecticides and other noxious agents. The symbol Rst is followed by parenthetical designation of the chromosomal location of the gene and then by an indication of the insecticide. Both dominant and recessive genes for insec- ticide resistance are conceivable. Several investigators have exposed populations to insecticides for numerous generations and selected resistant lines. In most cases, the genetic basis of resistance is multigenic, and unless a major factor has been identified, these strains are not included in this list. # Rst(1)JH: Resistance (1) Juvenile Hormone location: 1-35.4. origin: Induced by ethyl methanesulfonate. synonym: Met: Methoprene tolerant. references: Arking and Vlach, 1970, J. Insect Physiol. 22: 1143-51. Wilson, 1985, Genetics 100: s84. Wilson and Fabian, 1986, Dev. Biol. 118: 190-201. phenotype: Semidominant mutation conferring 50-100 fold increase in resistance to juvenile hormone III or its analogue methoprene over that of wild type. Also resistant to methoprene-induced tumors and abnormalities in adult cuticle; action of Rst(1)JH autonomous in gynandromorphs. Authors speculate that gene may affect juveline-hormone receptor. alleles: Six ethyl-methanesulfonate-induced, X-linked mutations resistant to juvenile hormone reported by Arking and Vlach (now lost); resistance factors varied from 1.4 to 21.5 by their methods. Presumed to be alleles of the mutation described by Wilson and Fabian. cytology: Placed in 10C2-D4 based on increased survival of flies raised on methoprene food when Rst(1)JH combined with Df(1)M259-4 = Df(1)10C2;10E2 and Df(1)N71 = Df(1)10B5;10D4, compared to Rst(1)JH/+. # Rst(1)mth: Resistance (1) malathion location: Thought to be polygenic. references: Sing and Morton, 1981, Can J. Genet. Cytol. 23: 355-69. phenotype: Both larvae and adults show resistance to malathion. # Rst(1)str: Resistance (1) streptomycin location: 1- (not mapped). synonym: str-R. references: Lambertsson and Rasmuson, 1971, Hereditas 69: 299. phenotype: Dominant; ribosomes from homozygotes and hemizygotes bind about one-tenth the amount of streptomycin bound by wild-type ribosomes. Resistant flies appear to lack one ribo- somal protein found in wild type. # Rst(2)amd: Resistance (2) alpha methyl dopa location: 2- (not mapped). references: Sparrow and Wright, 1974, Mol. Gen. Genet. 130: 127-41. Sherald and Wright, 1974, Mol. Gen. Genet. 133: 35-36. phenotype: Partially dominant; resistant to levels of alpha methyl dopa in the medium that are lethal to wild type. # Rst(2)DDT: Resistance (2) DDT location: 2-65 (64.5-66). origin: Naturally occurring allele. discoverer: Tsukamoto and Ogaki, 1953. synonym: RIDDT: Resistance to Insecticide-DDT; RIII: Resistance to Insecticide on chromosome 2. references: 1954, Botyu-Kagaku 19: 25. Tsukamoto, 1958, DIS 32: 87. Kikkawa, 1961, Ann. Rept. Sci. Works, Fac. Sci., Osaka Univ. 9: 1-20. Ogaki, Nakashima-Tanaka, and Murakami, 1967, Jpn. J. Genet. 42: 387-94. phenotype: Rst(2)DDT is a major dominant gene responsible for the phenotype of a line selectd for resistance to DDT. Median lethal dose of DDT for Rst(2)DDT lines is about 4000 ug/cc of medium; that for sensitive lines is 50-100 ug/cc. Also resis- tant to BHC (benzene hexachloride) and organophosphorus insec- ticides such as parathion and malathion. Median lethal dose of parathion is 2 ppm for resistant line and 0.08 ppm for sen- sitive. Sensitive to phenylthiourea (Ogita, 1958, Botyu- Kagaku 2: 188-204) and phenylthiocarbamide (Dauring and Sunner, 1971, Hereditas 68: 115-22). Shows maternal effect in that progeny of Rst(2)DDT/+ female crossed to +/+ male are more resistant that those of reciprocal cross. Larva more resistant than adult. RK3. other information: Possible to select new resistant alleles by growing the offspring of irradited wild-type flies on parathion (Kikkawa, 1968, DIS 43: 161). # Rst(3)amd: Resistance (3) alpha methyl dopa location: 3- (between h at 25.6 and th at 43.2). origin: Induced by ethyl methanesulfonate. references: Bishop and Sherald, 1981, DIS 56: 21-22. phenotype: Homozygous lethal. LD50 concentration of ( methyl dopa for heterozygotes more than three times that of wild type. alleles: Two alleles (PR40 and PR45) exhibiting weak complemen- tation for lethality. # Rst(Eth): see Eth # Rst(3)FU: Resistance (3) Fluorouracil location: 3- (not mapped). origin: Spontaneous. references: Duke and Glassman, 1968, Nature (London) 220: 588-89. phenotype: Partially dominant; homozygote survives 0.003% fluorouracil, whereas 0.0008% lethal to most strains. #*Rst(3)ns: Resistance (3) nicotine sulfate location: 3-49.5. origin: Spontaneous. discoverer: Tsukamoto, 1954. references: 1955, Botyu-Kagaku 20: 73. 1956, Botyu-Kagaku 21: 71. 1958, DIS 32: 87. phenotype: Median lethal dose to homozygote is 600 ppm of nicotine sulfate added to culture medium (from first instar larva through eclosion); to heterozygote, it is 300 ppm; to susceptible strains, 40 ppm. RK3. #*rstl: roughestlike location: 1- (rearrangement). origin: X ray induced. discoverer: Oliver, 29d3. synonym: lz-l: lozenge-like. references: 1935, DIS 3: 28. phenotype: Eyes rough; more extreme than lz. Viability low. RK2A. cytology: Associated with In(1)rstl; breakpoints unknown.