# rd: reduced location: 2-51.2. origin: Spontaneous. discoverer: Bridges, 17g15. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 233-35. phenotype: Bristles reduced in length and thickness, sometimes twisted; best seen on sternopleurals; male more extreme than female (rd1); female may have abnormal abdominal banding (rds). Males fertile, but females may be sterile (rd1) (Lynch, 1919, Genetics 4: 501-33). alleles: allele origin discoverer ref ( comments ___________________________________________________________ rd1 spont Bridges, 17g15 2 rd4 / ray 1 on Sco rd7 / ray 1 on Sco rd9 / ray 1 on Sco | rds spont Bridges, 18j2 2 reduced-scraggly ( 1 = Angel, Ashburner, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186; 2 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 233-35. | rd9 is lethal in combination with Df(2L)osp18 and Df(2L)TE35BC-3 but not with Df(2L)nNXF1 or Df(2L)A72; com- plemented by all known lethal mutants in the region. cytology: Placed in 35C2-5 based on its inclusion in Df(2L)osp18 = Df(2L)35B1-2;35C4-5 but not Df(2L)el81i1 = Df(2L)34E1-2;35C2-3; also claimed to lie within deficiencies that include bands from 35B but not 35C [Df(2LA215; Df(2L)A400, Df(2L)Sco-1]. rds: reduced-scraggly Edith M. Wallace, unpublished. # RD(1): Recovery Disrupter (1) location: 1-62.9 [10% of the distance between car and su(f)]. origin: Found in a chronically irradiated population obtained from B. Wallace. discoverer: Hanks, 1957. references: Novitski and Hanks, 1961, Nature 190: 989-90. Erickson and Hanks, 1961, Am. Naturalist 95: 247-50. Hanks, 1964, Genetics 50: 123-30. phenotype: Males containing this factor, RD(2), and certain other factors produce approximately 67% female and 33% male progeny. The effect is not produced by zygotic mortality but by a mechanism that operates during meiosis, leading to frag- mentation of the Y chromosome and production of fewer than 64 sperm heads per sperm bundle (Erickson, 1965, Genetics 51: 555-71). The effect is maximal at 25 and less pronounced at both 18 and 27. Viability good but fertility reduced in both sexes. RK3. # RD(2) location: 2- (not located). origin: Found in a chronically irradiated population obtained from B. Wallace. discoverer: Hanks, 1960. references: Novitski and Hanks, 1961, Nature 190: 989-90. phenotype: Males with this factor, RD(1), and certain other factors produce about 67% female progeny. RK3. #*rdb: reddish brown location: 1-21.7. origin: Induced by methyl methanesulfonate (CB. 1540). discoverer: Fahmy, 1956. references: 1959, DIS 33: 89. phenotype: Eye color deep reddish brown. Wings frequently curve slightly upward at tips. Body somewhat small. Male sterile. Viability about 30% wild type. RK3. # rde: reduced eye location: 1-20 (inferred from Fig. 1 of Homyk and Sheppard and the known map position of hypoB). origin: Induced by ethyl methanesulfonate. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. Homyk, 1977, Genetics 87: 105-28. phenotype: Selected on basis of reduced ability to fly; other behavioral traits normal; also exhibits reduced eye size and frequently missing palpi. # rdgA: retinal degeneration A (J.C. Hall) location: 1-26.3. origin: Induced by ethyl methanesulfonate. synonym: receptor degeneration-I (Hotta and Benzer, 1970); x35 (Pak). references: Hotta and Benzer, 1970, Proc. Nat. Acad. Sci. USA 67: 1156-63. Harris and Stark, 1977, J. Gen. Physiol. 69: 261-91. Johnson, Frayer, and Stark, 1982, J. Insect Physiol. 28: 23- 42. Stark and Carlson, 1985, Int. J. Insect Morphol. Embryol. 14: 243-54. phenotype: Photoreceptors degenerate during first week of adult life, although electroretinogram is small at time of eclosion when photoreceptors are morphologically normal; exception: rdg1 which is already aberrant then (Stark and Carlson, 1985); degeneration of outer photoreceptors (R1-6) in each eye facet is more severe (i.e., is essentially complete) than that of inner two cells (R7,8), with the most severe central-cell degeneration caused by rdgA1 and rdgA2, rdgA4 being less severe, and rdg3 still less (Harris and Stark, 1977); the ocelli degenerate, too, with rdgA1 causing particularly severe effect (Johnson et al., 1982); degeneration of compound eye photoreceptors is not light- or temperature-dependent (Harris and Stark, 1977); such degeneration is photoreceptor- autonomous in mosaics (Hotta and Benzer, 1970; Harris and Stark, 1977); degenerating photoreceptor axon terminals, espe- cially those projecting from R1-6 into the lamina optic gan- glion, are phagocytosed by glia in that optic lobe (Stark and Carlson, 1985); in general, though, the gross and internal structure of the lamina seems quite normal, even after pho- toreceptor degeneration caused by most severe rdgA alleles is complete (Meyerowitz and Kankel, 1978, Dev. Biol. 62: 112-42; Johnson et al., 1982; Stark and Carlson, 1985); two polypep- tide spots in 2-d gel analysis of eye-specific proteins are reduced in intensity under influence of rdgA4 [Hotta, 1979, Mechanisms of Cell Change (Ebert and Okada, eds.). John Wiley, New York, pp. 169-82]; rdgA mutations said to cause hypoactive behavior, and one of them also leads to shaking on exposure to ether plus premature death after exposure to 29 (Homyk, Pye and Pak, 1981, Genetics 97: s50). cytology: Placed in 8A4-C6 based on its inclusion in Df(1)KA14 = Df(1)7F1-2;8C6 but not Df(1)RA2 = Df(1)7D10;8A4-5. alleles: allele origin discoverer synonym ref ( comments ______________________________________________________ rdgA1 EMS rdgABS12 4 rdgA2 EMS rdgAKO14 4 rdgA3 EMS rdgAPC47 4 rdgA4 EMS rdgAKS199 1 rdgA5 EMS Benzer rdgA6 EMS rdgAP35 3 rdgA7 EMS rdgAP36 3 rdgA8 EMS rdgAP38 3 rdgA9 EMS rdgAP59 3 rdgA10 EMS rdgAP63 3 rdgA11 EMS rdgAP65 3 rdgA12 EMS Heisenberg opm3 2 rdgA13 EMS Heisenberg opm4 2 rdgA14 EMS Heisenberg opm5 2 rdgA15 EMS Heisenberg opm9 2 rdgA16 EMS Heisenberg opm10 2 rdgA17 EMS Heisenberg opm14 2 rdgA18 EMS Heisenberg rdgA19 EMS Heisenberg rdgA20 EMS Heisenberg rdgA21 P Hardy ( 1 = Harris and Stark, 1977, J. Gen. Physiol. 69: 261-91; 2 = Heisenberg, 1971, DIS 46: 68; 3 = Homyk, Pye, and Pak, 1981, Genetics 97: s50; 4 = Hotta and Benzer, 1970, Proc. Nat. Acad. Sci. USA 67: 1156-63. # rdgB (J.C. Hall) location: 1-42.7. origin: Induced by ethyl methanesulfonate. synonym: receptor degeneration II (Hotta and Benzer, 1970); x36 (Pak). references: Hotta and Benzer, 1970, Proc. Nat. Acad. Sci. USA 67: 1156-63. Harris and Stark, 1977, J. Gen. Physiol. 69: 261-91. Stark and Carlson, 1982, Cell Tissue Res. 225: 11-22. Stark, Chen, Johnson, and Frayer, 1983, J. Insect Physiol. 29: 123-31. Stark and Carlson, 1985, DIS 61: 162-64. phenotype: Photoreceptors in each facet of compound eye show light-induced degeneration; morphology is essentially normal on eclosion, but maintenance of mutant adults on diurnal light regime causes severe degeneration within approximately one week (Harris and Stark, 1977); the cell bodies and axons of photoreceptors begin to look ultrastructurally abnormal after three days (Stark and Carlson, 1982); the various rdgB muta- tions tend to cause the outer photoreceptors (R1-6) in each facet to degenerate more than the inner two cells (R7,8), such that rdgB9 and rdgB1 have R7,8 preserved in nearly all omma- tidia, rdgB6 and rdgB8 retain most central cells, and rdgB7 plus rdgB5 show progressively worse degeneration of R7,8 with rdgB5 retaining these cells in only 10% of the facets accord- ing to Harris and Stark (1977); degeneration of R7,8 not con- firmed, however, by Stark et al. (1983). After R1-6 have degenerated and the central cells have or have not, depending on the allele, R7,8 retain at least quasi-normal function as indicated by electroretinograms (Stark, 1977, J. Comp. Phy- siol. 115: 47-59); degeneration is photoreceptor autonomous in mosaics (Hotta and Benzer, 1970; Harris and Stark, 1977); autonomous in mixed ommatidia at the electron-microscope level (Hofbauer and Campos-Ortega, 1976, Wilhelm Roux's Arch. Dev. Biol. 179: 275-89); ultrastructural details of degeneration include electron-dense cytoplasm with liposomes, lysosome-like bodies, myeloid bodies and vacuoles, and electron-dense reti- culum and degenerate mitochondria, electron opaque photorecep- tor axons lacking synaptic vesicles and containing seemingly none of the typical presynaptic structures (Stark and Carlson, 1982). Degenerating photoreceptors are associated with degen- eration in the first order optic ganglion (the lamina), though the second order medulla is spared (Stark et al., 1983); high temperature treatments accelerate degeneration, whereas homoz- ygosity for an Acph-1-null mutation delays it slightly (Harris and Stark, 1977). After rearing of rdgB animals in room light, the R1-6 cells are physiologically non-functional at eclosion (revealed by ERGs), in spite of apparently normal cellular structure (Harris and Stark, 1977). Prolonged depo- larizing afterpotentials (induced by strong blue light) are abnormally short-lived and cannot be reversed by orange light, unlike the response of wild-type (Harris and Stark, 1977); degeneration of the photoreceptors is dramatically retarded by rearing in the dark followed by maintenance of adults under this condition (Harris and Stark, 1977); the same retardation of the mutations' effects occur when an rdgB mutation is linked to an ERG-minus norpA mutation (Harris and Stark, 1977), although degeneration does eventually occur in the dou- ble mutants (Stark et al., 1983); three norpA mutations were induced based on their inhibition of rdgB-induced degeneration (Harris and Stark, 1977), with two of the new mutations lead- ing to very small ERGs but the third, norpAsuII, allowing for apparently normal retinal physiology (also see Stark et al., 1983); this mutation revealed as a norpA allele, based on uncoverage of its degeneration-suppressing effects by an ERG- minus norpA mutation (Harris and Stark, 1977); norpA56's suppressing effects are allele-specific, to the extent that rdgB9-induced degeneration is retarded (and this was the rdgB allele used to isolate this suppressor), but the effects of another allele, rdgB1, are not (Harris and Stark, 1977); ort1 ninaE1 (formerly oraJK84), an opsin-deficient genotype, also blocks light induced degeneration of receptor cells in rdgB9 (Stark and Carlson, 1985, DIS 61: 162-64). Two rdgB alleles (unspecified) are associated with premature death of adults exposed to 29 (Homyk, Pye and Pak, 1981, Genetics 97: s50); further indications of pleiotropic action of this gene come from isolation of a hypoactive rdgB allele [originally hypoF (Homyk, Szidonya and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65)]; this mutation (mapping between v and f, as does rdgB) was shown to be an rdgB allele by Homyk and is now called rdgB23; it causes adults to be somewhat inactive in their general movements and their jumping ability to be weak; there are no light-on or light-off transient spikes in the ERG, and optomotor responses are eliminated; two polypeptide spots observed in two-dimensional gel analysis of eye-specific proteins are reduced in intensity in an rdgB mutant -- the same spots as affected by rdgA [(Hotta, 1979, Mechanisms of Cell Change (Ebert and Okada, eds.). John Wiley, New York, pp. 169-82]. cytology: Placed in 12A6-D3 based on its inclusion in Df(1)HA92 = Df(1)12A6-7;12D3 (Deak, Bellamy, Bienz, Dubuis, Fenner, Gol- lin, Rahmni, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81). alleles: allele origin discoverer synonym ref ( comments ______________________________________________________ rdgB1 EMS rdgBKO45 5 rdgB2 EMS Benzer rdgB3 EMS Benzer rdgB4 EMS Benzer rdgB5 EMS rdgBEE170 1 rdgB6 EMS rdgBKS16 1 rdgB7 EMS rdgBKS100 1 rdgB8 EMS rdgBKS200 1 rdgB9 EMS rdgBKS222 1 rdgB10 EMS rdgBP6 3 rdgB11 EMS 3 rdgB12 EMS 3 rdgB13 EMS 3 rdgB14 EMS Heisenberg rdgBH6 rdgB15 EMS Heisenberg rdgBH11 rdgB16 EMS Heisenberg rdgBH12 rdgB17 EMS Heisenberg rdgB18 EMS Heisenberg rdgB19 EMS Heisenberg rdgB20 EMS Heisenberg rdgB21 EMS Heisenberg rdgB22 EMS Heisenberg rdgB23 EMS rdgB101 4 hypoF rdgB24 EMS Gerresheim rdgBa31 2 ( 1 = Harris and Stark, 1977, J. Gen. Physiol. 69: 261-91; 2 = Gerresheim, 1988, Behav. Genet. 18: 222-46; 3 = Homyk, Pye, and Pak, 1981, Genetics 97: s50; 4 = Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65; 5 = Hotta and Benzer, 1970, Proc. Nat. Acad. Sci. USA 67: 1156-63. other information: rdgB mutations, especially those causing R1-6-specific degeneration (notably rdgB9), frequently used in experiments aimed at assessing behavioral and physiological significance of light input through central photoreceptors only; hence, phototaxis mediated by R7,8 (Jacob, Willmund, Folkers, Fischbach and Spatz, 1977, J. Comp. Physiol. 118: 261-71; Broda and Willmund, J. Insect Physiol. 27: 789-92; Hu and Stark, 1980, J. Comp. Physiol. 135: 85- 95; Miller, Hansen and Stark, 1981, J. Insect Physiol 27: 813-19); optomotor responses eliminated by degeneration of R1-6 (Heisenberg and Buchner, 1977, J. Comp. Physiol. 117: 127-62); visual learning not impaired; intensity discrimination less acute than in wild type; no positive indi- cation of color discrimination (Bicker and Reichert, 1978, J. Comp. Physiol. 127: 29-38). Visual pigment specific to outer photoreceptors (Harris, Stark and Walker, 1976, J. Physiol. 256: 415-39); absence of physiological effects of rdgB on ocelli (Hu, Reichert and Stark, J. Comp. Physiol. 126: 15- 24); and physiological effects of a trp mutation on the cen- tral photoreceptors (Chen and Stark, 1983, J. Insect Physiol. 29: 133-40). #*rdm: reduced macros location: 1-59.8. origin: Induced by 2-fluoroethyl methanesulfonate (CB. 1522). discoverer: Fahmy, 1957. references: 1959, DIS 33: 89. phenotype: Most bristles thin and short. Eye shape slightly abnormal. Body short; wings short, broad, and frequently pleated. Male fertile. Viability about 10% wild type. RK3. # rdo: reduced ocelli location: 2-53. origin: Spontaneous. discoverer: E. M. Wallace, 37l13. phenotype: Ocelli small and colorless, often missing, leaving top of head smooth and sometimes pigmented. Hairs between ocelli fewer than wild type. Eye surface irregular. RK2. alleles: rdo2, spontaneous, Bridges, 38b10. cytology: Placed in 36E4-F1 based on its inclusion in the region of overlap of Df(2L)TW203 = Df(2L)36E4-F1;37B9-C1 and Df(2L)H20 = Df(2L)36A8-9;36E4-F1 (Wright). #*rdp: reduplicated location: 1-34.7. discoverer: Hoge-Richards, 12k. references: Hoge, 1915, J. Exp. Zool. 18: 241-97. phenotype: At low temperatures, most flies have malformed or branched legs, often with mirror image reduplication. At 25, most flies normal. RK3. #*rdt: reduced thorax location: 1-54.4. origin: Induced by p-N,N-di-(2-chloroethyl)amino- phenylethylamine (CB. 3034). discoverer: Fahmy, 1955. references: 1959, DIS 33: 89. phenotype: Head and thorax disproportionately small compared to abdomen. Wings short, reaching only to tip of abdomen; fre- quently incompletely expanded or misheld. Male shows reduced viability and usually sterile. RK3. # re: reduced eyes location: 3- (not located). origin: Spontaneous. discoverer: Rapoport. references: 1940, Dokl. Acad. Nauk SSSR 27: 1030-32. phenotype: Eye size reduced from the normal 750 to about 180 facets. Reduction more extreme in combination with B; some flies have no facets and are sterile. RK2. # re: see rey #*re-b: reduced eyes-b location: 3-45. origin: Spontaneous. discoverer: Whittinghill, 53g. references: Schacht, 1954, DIS 28: 78. phenotype: Eyes reduced in 80% of homozygotes. Expression varies independently in each eye from absence of facets to wild type. RK2. other information: Possibly allelic to re. # rea: rearranged tergites location: 1-25.4. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 73. phenotype: Tergites highly abnormal, partly missing, and have different segments united. Expression variable. Viability and fertility inversely related to tergite abnormality. RK2. other information: One allele induced by CB. 3025. # rec: recombination defective (R.F. Grell) location: 3-58 (between 57.0 and 58.2). references: Grell, 1978, Proc. Nat. Acad. Sci. USA 75: 3351- 54. Grell and Generoso, 1980, Chromosoma 81: 339-48. Grell, 1984, Genetics 108: 425-33. Grell, 1985, Aneuploidy (Dellarco, Voytek, and Hollaender, eds.). Plenum Press, New York and London, pp. 317-36. phenotype: Recombination in homozygous females drastically reduced; total cross over between y and f in the X chromosome reduced from 56% to 2% with distal recombination being more severely affected than proximal. X nondisjunction increased from virtually 0 to 27%. In rec1/rec2, females show a similar reduction for ten regions between al and sp, where crossing over decreases to 9.1%, corresponding to 9% of normal. The number of progeny per homozygous female is reduced 75%; attri- buted to lethality of nondisjunctional products arising from distributive pairing between noncrossover heterologues. Phenotype of rec/+ is the same as wild-type; rec1 and rec2 homozygotes and hemizygotes have equivalent effects on recom- bination. alleles: allele origin discoverer synonym comments _______________________________________________________________________ rec1 EMS R.F. Grell & rec-16 null allele E.E. Generoso, 72k rec2 EMS R.F. Grell & rec-116 null allele E.E. Generoso, 74d rec3 EMS R.F. Grell & rec-126 temperature sensitive allele ( E.E. Generoso, 74i ( See below for description. cytology: Placed in 88F9-89B4 based on its inclusion in Df(3R)sbd105 = Df(3R)88F9-89A1;89B9-10 (Lewis, 1948, DIS 22: 72-73) but not Df(3R)sbd45 = Df(3R)89B3-4;89B10-11 (Grell, 1984, Genetics 108: 425-43). other information: Not allelic to c(3)G, since rec and c(3)G fully complement, also unlike c(3)G, rec has no discernable effect on the synaptonemal complex. # rec3 phenotype: At 17 recombination in rec3/+, rec3/rec3, and rec3/Df(3R)sbd105 is elevated. At 25, the homozygote and the heterozygote display normal values, but recombination in the hemizygote is significantly reduced. At 31, rec3/+ remains normal but rec3/rec3 recombination is drastically reduced. The hemizygote is sterile above 28. In rec2/rec3 females which show the most extreme temperature responses, application of the restrictive temperature at sequential days during development at 25 shows control value activity to be reduced only with treatment on days six and seven, and more precisely during a 36-hour period beginning at the time of pro-oocyte formation between 126 and 132 hours and terminating at 162 hours. This 36-hour period coincides with the boundaries of the S period as well as those of the heat-sensitive period for enhancing recombination in the normal genotype [Grell and Day, 1974, Mechanisms in Recombination (R. F. Grell, ed.). Plenum Press, New York and London, pp. 327-49]. Activity of the rec gene product in the range of 17 to 31 shows a sharp decline between 28 and 31 typical of a protein denaturation curve. If denaturation of a rec protein by the restrictive temperature marks its active phase, then recombination must terminate at the end of S, when the restrictive temperature becomes inef- fective. Electron microscopy of serially sectioned oocyte nuclei from rec2/rec3 females maintained at the restrictive or at the permissive temperature reveals synaptonemal complexes indistinguishable in length and fine structure, implicating recombination and not synapsis as the target of the rec gene product. # Receptor: see Rsp # receptor degeneration: see rdg # recombination defective: see rec # Recovery Disrupter: see RD # red: red Malpighian tubules location: 3-53.6. origin: Spontaneous. discoverer: Muller, 49a. synonym: bw-l: brown-like. references: Oster, 1954, DIS 28: 77-78. Aslaksen and Hadorn, 1957, Arch. Julius Klaus-Stift. Verer- bungsforsch. Sozialanthropol. Rassenhyg. 32: 464-69. phenotype: Malpighian tubes of larva and adult rusty red. Eye color brown, darkening with age. kar2, red flies have orange eyes (Henikoff, 1979, Genetics 93: 105-15); cn; red colorless (Paton and Sullivan, 1975, Genetics 80: s63). Malpighian tubes of v; red and cn; red are colorless and tubes of bw; red are red; therefore, pigment an ommochrome. Eyes contain less drosopterin and isoxanthopterin and more of the other pteri- dines than normal. Eye color autonomous in red eye disks transplanted into wild-type host. Wild-type Malpighian tubes acquire some red pigment after transplantation into red hosts. RK1. cytology: Placed in 88B1-3 based on its inclusion in Df(3R)red21 = Df(3R)88B1-2;88B2-3 (Spillman and Nothiger, 1978, DIS 53: 163). # red blood cells: see rc # red cells: see rc # red Malpighian tubules: see red # red wine: see rwi # reddish brown: see rdb # reduced: see rd # reduced bristle: see rbl # reduced eye: see rde # reduced eyes: see re # reduced macros: see rdm # reduced mushroom body: see mbmB # reduced ocelli: see rdo # reduced optic lobes: see rol # reduced pigment: see rgt # reduced size: see rsi # reduced tarsi: see rta # reduced thorax: see rdt # reduplicated: see rdp # reduplicated sex combs: see rsc # ref: refractaire Mutants at several loci that interfere with the normal mul- tiplication of some strains of sigma virus, as indicated by delayed acquisition of CO2 sensitivity following viral injec- tion. They are designated ref followed by parenthetical indi- cation of the chromosome on which they reside and then a locus designating letter; the permissive or normal allele is desig- nated by superscript o indicating standard allele from Oregon-R; restrictive alleles are superscripted with a letter indicating origin: b = Belinga; e = ebony stocks; h = Hikone; m = Moire stock; n = Nagasaki; p = Paris. Except for the case of ref(3)O, in which the restrictive allele is dominant, per- missive and restrictive alleles are codominant. genetic restrictive locus location allele ref ( comments | ______________________________________________________________ ref(1)H 1-14 ref(1)Hh 1, 2 viral replication ref(1)Hb ref(2)M 2-40 ref(2)Mm 1, 2 viral replication ref(2)P 2-54.0 ref(2)Pp 1, 2, 4 viral replication ref(2)Pn ref(3)D 3-90 ref(3)Dp 1, 2 viral replication ref(3)O 3-69.8 ref(3)Oe 1, 2, 3 viral maturation ref(3)V 3-96.7 ref(3)Vp 1, 2 viral replication in male germ line ( 1 = Brun and Plus, 1980, Genetics and Biology of Drosophila (Ashburner and Wright, eds.). Academic Press, London, New York, San Francisco, Vol. 2d, pp. 625-702; 2 = Gay, 1978, Mol. Gen. Genet, 159: 269-83; 3 = Herforth, 1978, Genetics 88: 505-13; 4 = Ohanessian-Guillemain, 1953, DIS 27: 59. | Mechanism inferred to be affected. # ref: see rfr # ref(2)P synonym: ref. phenotype: ref(2)Pp is the first refractaire mutant found and the most thoroughly studied. Allele frequency about 0.2 in Paris population and approaches the same incidence in caged populations with or without the presence of sigma virus (Fleu- riet, 1980, Genetics 95: 459-65; 1981, Genetics 97: 415-25). Refractaire phenotype expressed in cultured cells (Richard- Molard, 1975, Arch. Virol. 47: 139-46) and in imaginal disks transplanted into stably infected hosts (Bernard, 1968, Exp. Cell Res. 50: 117-26). Inhibition of viral multiplication increases with increased doses of ref(2)Pp, with added doses of ref(2)Po having an antagonistic effect (Nakamura, 1978, Mol. Gen. Genet. 159: 285-92). Strains of sigma virus capa- ble of multiplication in restrictive strains can be selected; P+ virus strains multiply in ref(2)Pp hosts, whereas P- strains do not; no such distinction in ref(2)Po hosts. Also 5-FU-induced host-adapted strains of virus (haP) capable of replication in ref(2)Pp; many are temperature sensitive, sug- gesting that ref(2)Pp interacts with a viral protein (Coulon and Contamine, 1982, Virology 123: 381-92). Males homozygous for null alleles sterile; elongating spermatids display degen- eration of axonemes (Dezelee, Bras, Contamine, Lopez-Ferber, Segretain, and Teninges, 1989, EMBO J. 8: 3437-46). alleles: In addition to naturally occurring ref(2)Pp and ref(s)Po, X-ray-induced (Nakamura) and three hybrid- dysgenesis-induced null alleles, ref(2)Phd1, ref(2)Phd2, and ref(2)Phd3 (Contamine, Petijean, and Ashburner, 1989, Genetics 123: 525-33). cytology: Placed in 37E2-F4 based on its being localized between Df(2L)TW158 = Df(2L)37B2-8;37E2-F4 and Df(2L)TW12 = Df(2L)37E2-F4;39D1-2. molecular biology: ref(2)P cloned (Contamine, Petitjean and Ashburner, 1989, Genetics 123: 525-33). Genomic DNA isolated by transposon tagging; sequencing indicates a structural gene with three exons and conceptual amino-acid sequence of 599 residues containing internal PEST repeats and interesting structural motifs, such as zinc fingers and amphiphilic hel- ices; no homology with known proteins (Dezelee, Bras, Contam- ine, Lopez-Ferber, Segretain, and Teninges, 1989, EMBO J. 8: 3437-46). # refringent: see rfr # regulator of (glycerol phosphate dehydrogenase: see r((GPDH) # Regulator of bithorax: see trx # Regulator of post bithorax: see hb # rem: see mbmB # rem: remnants (T. Schupbach) location: 2-32. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal effect lethal; eggs laid by females homozy- gous for rem1 show no visible sign of development when observed under transmitted light in stereomicroscope; eggs derived from rem2 often allow embryonic development; those embryos form fragmented cuticle with variable holes and head defects. alleles: rem1 and rem2 recovered as A and HG. cytology: Located in 30A-C since included in Df(2L)30A;C. # Resistance ( ): see Rst( ) # Responder: see Rsp # ret: reticent (T. Schupbach) location: 2-62. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Maternal effect lethal; embryos from homozygous mothers develop into larvae with no visible cuticular abnor- malities, but do not hatch out of the egg case. alleles: retPK = ret1. #*ret: reticulated location: 1- (rearrangement). origin: Induced by L-p-N,N-(2-chloroethyl)aminophenyl-alanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 73. phenotype: Wing veins increased to anastomosing reticulated areas. Wings shortened, deformed, and blistered. Eyes large and rough. Postvertical bristles usually absent. Male sterile; viability about 20% wild type. RK2A. cytology: Associated with T(1;2)ret = T(1;2)20A5-B2;2R. # reticent: see ret # reticulated: see *ret # retina aberrant in pattern: see rap # retinal degeneration: see rdg # retroactive: see rtv # Rev: Revolute location: 2- (rearrangement). origin: X ray induced. discoverer: Dobzhansky, 31b5. phenotype: Wings of heterozygote spread at 45 from midline; edges curled, giving spoon shape. Sense organs along veins enlarged. Eyes mottled in Rev/lt. Homozygote viable and fer- tile, somewhat more abnormal than heterozygote. Phenotype suppressed by extra Y's, probably a variegated position effect. RK2A. cytology: Associated with In(2LR)Rev = In(2LR)40F;52D10-E1 [Bridges and Li, in Morgan, Bridges, and Schultz (1936, Year Book - Carnegie Inst. Washington 35: 293)]. # RevB: Revolute of Bridges origin: Spontaneous as a single homozygous female in a culture with no heterozygote. discoverer: Bridges, 36e22. synonym: Rvd: Revolutoid. references: Morgan, Bridges, and Schultz, 1936, Year Book - Carnegie Inst. Washington 35: 293. phenotype: Wings spread and curved. A variegated position effect based on enhanced phenotype by rearing at low tempera- ture and Y suppressibility (Wargent, 1972, DIS 49: 50-51). Expression suppressed by In(1)mK, and variegation of mK enhanced by In(2LR)RevB (Wargent and Hartmann-Goldstein, 1974, Heredity 33: 317-26); incidence of chromosomes heterochroma- tinized in vicinity of breakpoints shows parallel interactions (Hartmann-Goldstein and Wargent, 1975, Chromosoma 52: 349- 62). Homozygous lethal; Rev/RevB viable (E. B. Lewis). RK2A. cytology: Associated with In(2LR)RevB = In(2LR)40F;52D5 (War- gent). # Revolute: see Rev # Revolutoid: see RevB # rex: rapid exhaustion (J.C. Hall) location: 1-17.0. origin: Induced by ethyl methanesulfonate. references: Grigliatti, Hall, Rosenbluth and Suzuki, 1973, Mol. Gen. Genet. 120: 107-14. Homyk, Sinclair and Suzuki, 1979, Genetics 91: s49-50. phenotype: Adults briefly paralyzed after movement, especially when they are induced to move rapidly; recovery occurs within one min, followed by uncoordinated movements and a period refractory to induction of further paralysis of at least one hr (Grigliatti et al., 1973); rex is temperature sensitive for lethality, i.e., as induced by holding adults about ten days at 29 (Homyk et al., 1979); also there are semi-lethal effects on development [i.e., ca. 50% viability after rearing at 29 (Homyk, Sinclair, Wong, and Grigliatti, 1986, Genetics 113: 367-89)]. rex also hypersensitive to killing effects of caffeine (Homyk et al., 1979). Causes an abnormally slow recovery from blue-light induction of prolonged depolarizing afterpotential (PDA) of photoreceptors; recovery induced rapidly by orange light (Homyk and Pye). Mosaic analysis of leg paralysis induced by rex suggests mesodermal (possibly muscle) foci, separate focus for each leg (Homyk et al., 1986). cytology: Placed in 7C1-4 based on its inclusion in Df(1)ct4b1 = Df(1)7B2-4;7C3-4 but not in Df(1)ct268-42 = Df(1)7A5-6;7B8- C1 or Df(1)ct-J4 = Df(1)7A2-3;7C1 (Homyk). alleles: One mutant allele, sometimes called rexts (Homyk et al., 1979). # Rex: Ribosomal exchange (L. Robbins) location: 1-66 [proximal to su(f) (Rasooly)]. origin: Spontaneous? Discovered in Df(1)wrJl bearing chromo- some. references: Robbins, 1981, Genetics 99: 443-59. Swanson, 1984, Ph.D. dissertation, Michigan State University. Swanson, 1987, Genetics 115: 271-76. phenotype: Semi-dominant, maternal-effect locus which causes an early mitotic exchange between blocks of rDNA in 1 to 10% of the offspring of Rex-bearing females. Rex affects chromosomes with two separated, complete or partial ribosomal-DNA regions, such as YSX.YL or In(1)scS1Lsc4R. Chromosomes having separated blocks of heterochromatin that do not both include ribosomal genes, such as In(1)wm4, are insensitive. Affected chromosomes may pair in either spiral or hairpin configura- tions; the former results in loss of the intervening material (e.g., YbbRex, Dp(1;f)scS1Lsc4R, Dp(1;f)wm51bLwm4R), the latter in the inversion of that material (Dp(1;1)scS1Lsc4R, Dp(1;1)wm51bLwm4R) (Robbins and Swanson, 1988, Genetics 120: 1053-59). Exchanges usually occur early enough to yield whole-body recombinant genotypes, but a minority of events yield half-half mosaics. The exchange event generally results in partial deletion of rDNA (Robbins). #*rey: rough eye location: 1-0.6 (from combined measurements on rey, rey2, and rey3). phenotype: Eyes extremely small and rough in male, less extreme in female. Areas of thorax often underdeveloped, sometimes hemithoracic. (rey2). Homozygous female viable and infertile (rey3). alleles: Complementation tests not performed; allelism inferred from similarity of phenotype and map position. allele origin discoverer synonym ref ( ___________________________________________________________ *rey1 spont Neel, 41g7 re 2 *rey2 spont Sturtevant, 1948 rey 3 rey3 CB 3025 Fahmy, 1953 re2; 1 rougheye-like rey4 CB 3007 Fahmy 1 ( 1 = Fahmy, 1958, DIS 32: 73; 2 = Neel, 1942, DIS 16: 52; 3 = Sturtevant, 1948, DIS 22: 55-56. cytology: Outside of region 1E1-2B9 based on complementation of rey3 by both Df(1)sta = Df(1)1D3-E1;2A and Df(1)RA19 = Df(1)1E3-4;2B9-10 (Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbetova, Kramers, and Zhimulev, 1982, DIS 58: 184-90). other information: Not recognized as such in recent studies of polytene region 2 by Lefevre or by Perrimon. #*rf: roof wings location: 2-81. discoverer: Bridges, 1921. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 233. phenotype: Wings rotated on long axis so that inner margins are raised and costal margins lowered. Overlaps wild type. RK3. # rf2 origin: Spontaneous. discoverer: Redfield, 1926. references: Franke, 1933, Ph.D. Thesis, Univ. Berlin. phenotype: Like rf. RK3. # Rf: Roof location: 3-59. origin: Spontaneous. discoverer: Waddington, 38a. references: 1939, DIS 12: 48-49. phenotype: Wing position normal at eclosion, becomes rooflike in 12-hr imagos. RK1. cytology: Tentatively placed in 89C-90E based on the observa- tion that a third chromosome deficiency combining the left portion of T(Y;3)L142 = T(Y;3)89C and the right portion of T(Y;3)B116 = T(Y;3)90E has a Rf-like phenotype (Rendel, 1977, DIS 52: 86). #*Rf-c: Roof-c location: 3- (to the left of se). discoverer: Bridges, 20a1. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 228 (fig.). phenotype: Wings slanted at roof-like angle. RK3. # rfd: see sas # rfr: refringent location: 1- 67.9[to the left of ot at 1-65.7, since it is not covered by y+Ymal106 which does cover ot (Schalet, 1972, DIS 49: 36)]. origin: Induced by D-p-N,N-di-(2-chloroethyl)aminophenyl- alanine (CB. 3026). discoverer: Fahmy, 1955. synonym: ref (preoccupied). references: 1959, DIS 33: 89. phenotype: Wing surface yellowish and iridescent; occasionally, one or both wings held out; inner margins may be incised. Expression more extreme in male than in female. Male viable and fertile; female has reduced viability and is sterile. RK2. alleles: One allele each induced by CB. 3026 and CB. 3034. # rg: rugose location: 1-11.0. references: Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29. phenotype: Eyes variably rough depending on strength of allele; stronger alleles display reduced viability. Additional traits include wings thin, curled upward (rgP), margins somewhat frayed (rg1); eclosion delayed (rg7); body pale (rgP). alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________ *rg1 Bridges, 21c roughish 5 rg2 Demerec, 28f23 rough-64 *rg3 spont 4 *rg4 Ives, 33g22 rg33g 6, 7 *rg5 spont Bridges, 38c9 4 *rg6 spont Bridges rox 4 *rg7 X ray Cantor, 46d20 rgc 3 In(1)4E;7A (Valencia) *rgP 32P Bateman, 1950 1, 2 In()1)3C;4E (Darby) ( 1 = Bateman, 1950, DIS 24: 54; 2 = Bateman, 1951, DIS 25: 77-78; 3 = Cantor, 1946, DIS 20: 64; 4 = CP552; 5 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 234; 6 = Plough, 1934, DIS 2: 34; 7 = Plough and Ives, 1935, Genetics 20: 42-69. cytology: Locus at 4E1-3 (Demerec, Kaufmann, Fano, Sutton, and Sansome, 1942, Year Book - Carnegie Inst. Wash. 41: 191). Placed in 4E2 based on its inclusion in Df(1)ovo6 = Df(1)4C5- 6;4E2-3 and Df(1)bi-DL3 = Df(1)3C7-12;4E1-2 but not Df(1)bi- DL5 = Df(1)3C7-12;4E1-2 (Oliver). # Rg-bx: see trx # Rg-pbx: see hb #*rgt: reduced pigment location: 1-11.5. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1954. references: 1959, DIS 33: 89. phenotype: Characteristic pigmentation of fifth tergite reduced or absent in male. Body color yellowish. Eyes bright red. Male sterile. RK2. # rh: roughish location: 2- 54.7[on 2R based on its recovery in newly gen- erated C(2R) chromosomes and placed distal to ap (2-55.2) on the basis of its being complemented by Df(2R)M41A4 (Hilliker, Gibson, Yeomans, and Holm, 1977, DIS 52: 32)]. origin: Spontaneous. discoverer: Bridges, 21a3. phenotype: Eyes moderately rough. At 19, bristles slightly wavy and wings broad. RK2. # rh: see gl3 # Rh1: see ninaE # Rh2: Rhodopsin 2 location: 3- {65}. references: Cowman, Zuker, and Rubin, 1986, Cell 44: 705-10. phenotype: Encodes the opsin moiety of the rhodopsin specific to the ocelli. Not expressed in the eye nor is it expressed in Bolwig's organ, the larval photoreceptor [Pollock and Benzer, 1988, Nature (London) 333: 779-82)]. Rh2 under the control of the ninaE promotor in a ninaE background functions in R1-6 cells (Zuker, Mismer, Hardy, and Rubin, 1988, Cell 55: 475-82) but with different spectral characteristics and physiology (Feiler, Harris, Kirschfield, Wehrkan, and Zuker, 1988, Nature (London) 333: 737-41). RH2 is a 381-amino-acid protein that is 67% homologous to the opsin found in R1-6 encoded by ninaE, but only 35% homologous to RH3 and RH4. cytology: Located in 91D1-2 by in situ hybridization. molecular biology: Genomic clone isolated by cross homology with a clone containing the ninaE gene. Sequence analysis indicates the presence of three introns, the position of the second of which is shared with that of the fourth intron of ninaE; positions of the other introns are not conserved. The conceptual amino-acid sequence reveals many features that characterize opsins: seven hydrophobic domains separated by hydrophylic sequences, a putative retinal-binding site in the seventh transmembrane domain, a glycosylation site in the extra cytoplasmic face, and a series of potential phosphoryla- tion sites in the C-terminal region. Head specific transcrip- tion depends on elements between -183 and -112 (Mismer, Michael, Laverty, and Rubin, 1988, Genetics 120: 173-80); contains an eleven-base-pair sequence common to ninaC and ninaE (Mismer et al.). # Rh3 location: 3- {70}. references: Zuker, Montell, Jones, Laverty, and Rubin, 1987, J. Neurosci. 7: 1550-57. phenotype: Encodes the opsin moiety of a rhodopsin specific to the rhabdomere of the seventh photoreceptor cell. Also expressed in Bolwig's organ [Pollock and Benzer, 1988, Nature (London) 333: 779-82)]. Transcript first appears during the last 48 hr of the pupal stage and is found in newly eclosed adult heads. RH3 is a 383 amino acid protein that is 35% homologous to the opsins found in R1-6 encoded by ninaE and in ocelli encoded by Rh2 but 72% homologous to the Rh4-encoded protein. cytology: Located in 92D1 by in situ hybridization. molecular biology: Genomic clone isolated by hybridization to oligonucleotide probes containing sequences highly conserved between ninaE and Rh2. The gene contains no introns. The conceptual amino-acid sequence reveals features characteristic of opsin molecules (see Rh2). # Rh4 location: 3- {45}. references: Montell, Jones, Zuker, and Rubin, 1987, J. Neu- rosci. 7: 1558-66. phenotype: Encodes the opsin moiety of a rhodopsin specific to the rhabdomere of the seventh photoreceptor cell; Rh3 and Rh4 are expressed in nonoverlapping subsets of ommatidia; the dis- tribution of the two types of R7 cells within the eye is irregular. Transcript first appears during the last 48 hr of the pupal stage and is found in newly eclosed adult heads. Also expressed in Bolwig's organ [Pollock and Benzer, 1988, Nature (London) 333: 779-82)]. RH4 is a 378 amino acid pro- tein that is 35% homologous to the opsins found in R1-6 encoded by ninaE and in the ocelli, encoded by Rh2, but 72% homologous to the Rh3-encoded protein. cytology: Located in 73D3-5 by in situ hybridization. molecular biology: Genomic clone isolated by hybridization to the Rh3 gene. Sequence analysis reveals the presence of a single 9.0 kb intron, which subdivides the gene into exons of 676 and 719 nucleotides. The conceptual amino-acid sequence reveals features characteristic of opsin molecules (see Rh2). # RH11: see eas # rho: see ve # Rho: see Lcp10 # Rhodopsin: see Rh # rhomboid: see ve ri: radius incompletus From Edith M. Wallace, unpublished. # ri: radius incompletus location: 3-46.8. (Arajarvi and Hannah-Alava, 1969, DIS 44: 73). phenotype: Vein L2 interrupted. Wings slightly warped and blunt. Acts during contraction period in D. simulans, inhi- biting fusion of small spaces into a vein (Waddington, 1940, J. Genet. 41: 75-139). RK1. alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________ ri1 spont Tshetverikov, 1926 *ri2 Nordenskiold, 1935 3 *ri51k spont Meyer, 51k 1 ri53j spont Meyer, 53j 2 ( 1 = Meyer, 1952, DIS 26: 67; 2 = Meyer, 1953, DIS 27: 58; 3 = Nordenskiold, 1937, DIS 7: 18. cytology: Tentatively placed in salivary region 77E-F (Arajarvi and Hannah-Alava, 1969, DIS 44: 73). # RIDDT: see Rst(2)DDT # RIII: see Rst(2)DDT # rib: ribbon location: 2-88. 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: 209-26. phenotype: Homozygous embryonic lethal; lateral extents of belts narrow; fusion of adjacent dentical bands in ventral midline; dorsal closure defective. alleles: Nine; rib1 recovered as IK and weak allele rib2 recovered as IIB; seven alleles discarded. # Ribosomal exchange: see Rex # Ribosomal protein 49: see M(3)99D # Ribosomal protein A1: see RpA1 # rickets: see rk # rimy: see rm # Ring magnifier: see Rm # rk: rickets (M. Ashburner) location: 2-48.8 (immediately to the right of j). phenotype: Strong alleles have legs, especially metathoracic ones, flattened and bent. Femora and tibiae bowed in middle; first two tarsal joints shortened, bent, and flattened; last three tarsal joints almost fused. Wings unexpanded, resem- bling those of pu. Posterior scutellar bristles erect and crossed. Viability may be reduced. Weak alleles do not show the leg phenotype, or they overlap wild type; may have par- tially expanded wings and normal posterior scutellar bristles. Even strong alleles more extreme when hemizygous with rk defi- ciencies. alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________________ rk1 UV Edmondson, 48h 2 strong allele rk2 UV Erickson, 50a 7 weak allele, stronger at 29 than 17 rk3 UV Meyer, 54d 4 strong allele, body small, bristles fine | rk4 spont Jackson, 54c cq: creeper 3, 5 | rk5 spont Mischaikow, 59a 8 weak allele | rk6 X ray Thomas, 60g 6 | rkcyl spont Stroher, 58 9 | rk76 EMS 1 intermediate allele; cytologically normal rk80l1 EMS Bodmer strong allele rk80l2 EMS Bodmer weak allele rk81f2 EMS Harrington strong allele, on In(2LR)O, induced with b81f2 rk1250 EMS Lindsley intermediate allele rkEMS EMS Grell on Dp(2;2)Adh3 ( 1 = Ashburner, Faithfull, Littlewood, Richards, Smith, Vel- issariou, and Woodruff, 1980, DIS 55: 193; 2 = Edmondson, 1948, DIS 22: 53; 3 = Jackson, 1954, DIS 28: 74; 4 = Meyer, 1955, DIS 29: 74; 5 = Meyer, 1958, DIS 32: 83; 6 = Meyer, 1963, DIS 37: 51; 7 = Meyer, Edmondson, Byers, and Erickson, 1950, DIS 24: 60; 8 = Mischaikow, 1959, DIS 33: 98; 9 = Mainx, 1958, DIS 32: 82. | Additional description below. cytology: Placed in 31E1-5 based on its inclusion in Df(2L)b-L = Df(2L)34D3;34E3-5 and Df(2L)el82f1 = Df(2L)34E1-2;35C3-5, but not Df(2L)b82a2 = Df(2L)34D1-2;34E1-2. # rk4 phenotype: Wings unexpanded, spread, and drooping. Posterior legs malformed. Both sexes fully viable and fertile. rk4 male mates with wild-type female only if wings removed from female. Viability 60% of wild type. # rk5 phenotype: Wings sometimes fully expanded and held out. # rk6 phenotype: Legs weak, wings unexpanded. Viability higher at higher temperature. # rkcyl phenotype: Abdomen cylindrical; terminal segments thickened; halteres small and melanotic; legs like those of bal, but less deformed. Viability low but fertility good. # rl: rolled location: 2-55.1 [between centromere and stw (Sturtevant); 0.03 unit to the left of stw (Tano, 1966, J. J. Genet. 41: 299- 308)]. phenotype: Most alleles lethal. The viable allele, rl1, has wing edges rolled downward; margins somewhat frayed; L4 inter- rupted distal to posterior crossvein. Eyes small, dark, and rough. Most extreme at 26, less extreme above and below that temperature (Lakovaara, 1963, Proc. Intern. Congr. Genet., 11th., Vol. 1: 175). Temperature sensitive period for eye phenotype during larval stages with most sensitive stage about 60 hr after hatching, i.e., at the beginning of the third- instar (Hackman and Lakovaara, 1966, DIS 41: 92). Effects of dosage of rl and rl+ on eye pigment deposition investigated by Lakovaara (1966, Hereditas 56: 1-19). rl1 lethal in combina- tion with all lethal alleles except rl6, with which it is fully viable and exhibits a rl phenotype. Hemizygotes for lethal alleles, except for rl6, die as third-instar larvae completely devoid of imaginal disks; when heterozygous for rl1 or rl6, the lethal alleles lead to pupal lethality (Hilliker, 1976, Genetics 83: 765-82). allele origin discoverer synonym ref ( comments _____________________________________________________________ rl1 spont Bridges, 22f23 4 viable, RK2 rl2 EMS Hilliker l(2)EMS34-29 3 L3 rl3 EMS Hilliker l(2)EMS43 3 L3 rl4 EMS Hilliker l(2)EMS45-32 3 L3 rl5 EMS Hilliker l(2)EMS45-39 3 L3 rl6 EMS Hilliker l(2)EMS45-52 3 P rl7 EMS Hilliker l(2)EMS45-54 3 L3 rl8 EMS Hilliker l(2)EMS45-95 3 L3 rl9 EMS Hilliker l(2)EMS64 3 L3 rl10 EMS Hilliker l(2)EMS698 3 L3 *rlG heat Goldschmidt, 1, 2 viable 1929 ( 1 = Goldschmidt, 1929, Biol. Zentralbl. 49: 437-48; 2 = Goldschmidt, 1939, Am. Nat. 73: 547-59; 3 = Hilliker, 1976, Genetics 83: 765-82; 4 = Morgan, Bridges, and Stur- tevant, 1925, Bibliog. Genet. 2: 233. cytology: Placed in 41A on the basis of its inclusion in Df(2R)M41A10 = Df(2R)41A (Morgan, Schultz, and Curry, 1941, Year Book - Carnegie Inst. Washington 40: 284). Further res- tricted to the middle of the proximal heterochromatin on the basis of its inclusion in Df(2R)A but not Df(2R)B (Hilliker, 1976, Genetics 93: 765-82). #*rlu: rolled up location: 1- (rearrangement). origin: Spontaneous in In(1)scS1+d1-49. discoverer: Reddi. references: 1963, DIS 37: 53. phenotype: Wings rolled. Good viability and fertility. RK2A. # rm: rimy location: 1-48.1. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1958, DIS 32: 74. phenotype: Eyes often dull brownish red with conspicuous white hairs between ommatidia. Wings longitudinally pleated. Via- bility and fertility good. RK2. other information: One allele each induced by CB. 1540 and CB. 1592. # rm: see rmp # Rm: Ring magnifier location: Autosomal; not mapped. origin: Spontaneous. references: Endow, Komma, and Atwood, 1984, Genetics 108: 969-83. phenotype: Existence of such a mutant inferred from the behavior of ring chromosomes in magnifying genotypes in dif- ferent autosomal backgrounds. In the absence of Rm, magnify- ing conditions cause the meiotic loss of bb-bearing ring chro- mosomes from R(1), bb/Ybb- males, as detected by both a shift in the sex ratio among the progeny and the production of offspring with no paternally inherited sex chromosome; some bbr (bobbed-reduced) offspring are observed, but there are no bbm (bobbed magnified) offspring. In the presence of Rm, the incidence of ring-chromosome loss is elevated and bbm offspr- ing occur. Postulated that sister-chromatid exchange outside of the ribosomal cistrons correlated with magnifying sister- chromatid exchanges within the ribosomal cistrons may occur in the presence of Rm but not Rm+. # Rm2: Ring magnifier on chromosome 2 location: 2-48. origin: Spontaneous. discoverer: Komma and Atwood. references: Endow, Komma, and Atwood, 1984, Genetics 108: 969-83. phenotype: Dominant mutant that permits recovery of magnified bb alleles in ring chromosomes. Also increases incidence of dicentric rings as seen in the primary spermatocyte division. Postulated to engender sister chromatid exchanges outside the ribosomal DNA. # Rm4 location: 4-. origin: Spontaneous. discoverer: Komma. phenotype: Similar to that of Rm2. #*rmp: rumpled location: 1-14.4. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1955. synonym: rm (preoccupied). references: 1959, DIS 33: 89. phenotype: Wings variably unexpanded. Bristles deranged; postverticals frequently crossed. Derangement of bristles correlated with degree of wing abnormality. Viability and fertility good in both sexes. RK2. # rn: rotund (S. Kerridge) location: 3-47.6 [from location of rn3 (Puro and Nygren, 1975, Hereditas 81: 237-48); distal to roe (Agnel et al.)]. references: Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23. Kerridge and Thomas-Cavallin, 1988, Roux's Arch. Dev. Biol. 197: 19-26. Agnel, Kerridge, Vola, and Griffin-Shea, 1989, Genes Dev. 3: 85-95. phenotype: All alleles are viable as homozygotes. Both males and females are sterile; sterility is not germ line dependent. Two transcripts from the rotund region of Drosophila show similar positional specificities in imaginal disc tissues. Adult defects are restricted to homologous distal parts of the appendages, i.e., the antennae, legs, wings, halteres, and proboscis. In the antenna the basal capsule is missing and the third antennal segment is reduced in size; all other antennal and eye disc derivatives are normal. In all three pairs of legs abnormalities caused by the lack of rn+ product are localized specifically in the tarsus; instead of five individual tarsal segments, a single tarsus-like segment dif- ferentiates. The distal claw and proximal leg articulations (tibia, femur, trochanter, and coxa) are unaffected. Incom- plete and duplicated joints seen at the presumptive positions of the tarsus 1-2 and 4-5 joints; intermediate joints virtu- ally absent (Held, Duarte, and Derakhshanian, 1986, Wilhelm Roux's Arch. Dev Biol. 195: 145-57). Of the wing disc derivatives, the medial and distal costa are fused and the corresponding region in the posterior wing, the alula, is smaller, making the wing as a whole appear shorter; distal wing and mesonotum are formed as in wild type. Vein L5 and to a lesser extent L2 interrupted (rn3). Specific and localized deficiencies of labial and haltere disc derivatives are also evident. Genital and abdominal patterns are indistinguishable from wild-type patterns; however, seminal receptacles shorter than in wild-type females. Examination of the imaginal discs from third-instar rn larvae shows localized cell death in regions determined from fate maps to give rise to distal appendage parts (Cavallin). alleles: No interallelic complementation detectable. allele origin discoverer synonym ref ( comments _________________________________________________________________________ rn1 X ray Glass, 1929 1, 3 T(2;3)40-41;80-81; 84D3-4 *rn2 spont Carlson 2 rn3 X ray Hannah-Alava 1, 5 cytology normal rn4 EMS Kaufman 1 roe- scr- rn5 / ray Williams 1 aberration at 84D3-4 rn6 X ray Kerridge 1 rn7 EMS Ait-Ahmed 1 roe- rn8 EMS Kerridge 1 roe- rn10 EMS Kerridge 1 roe- rn11 EMS Kerridge 1 lesion in 20.5 to 22.8 rn14 EMS Kerridge 1 rn15 EMS Kerridge 1 rn16 DEB Kerridge 1 1 kb deletion between -6.5 and -2.1 kb; roe- rn18 DEB Kerridge 1 roe- rn19 DEB Kerridge 1 sequences distal to 12.3 deleted rn20 DEB Kerridge 1 all cloned sequences missing roe- rn21 DEB Kerridge 1 roe- rn23 DEB Kerridge 1 roe- rnD X ray Kerridge Dipr 1, 4 In(3R)84D3-4; 84F6-11 | rnFC8 X ray Lehman 1 Tp(3;1)84D3-4;85 rnX49 X ray Jurgens rnroeX49 1 roe- rnX130 X ray Jurgens rnXT130 1 In(3R)81;84D9-10 ( 1 = Agnel, Kerridge, Vola, and Griffin-Shea, 1989, Genes Dev. 3: 85-95; 2 = Carlson, 1956, DIS 30: 70, 109; 3 = Glass, 1934, DIS 2: 8; 4 = Kerridge, 1981, Mol. Gen. Genet. 184: 519-25; 5 = Puro and Nygren, 1975, Hereditas 81: 237-48. | More detailed description below. cytology: Placed in 84D3 on the basis of its inclusion in the region of overlap between Df(3R)dsx10M = Df(3R)84D3;84F1 and Df(3R)Scx4 = Df(3R)84B1-2;84D3-4. The heterozygote between the two deficiencies survives and is rotund in phenotype. molecular biology: Gene localized within a 70 kb walk on the basis of the clustering of restriction-fragment-length differ- ences associated with rn mutations. Mutational lesions are arrayed over a 50 kb region from -6.5 to +44 kb. 0 is defined as the distal breakpoint of Df(3R)Scx4, positive values extending to the right. Two transcripts identified from the region, a 5.3 kb transcript hybridizing to a genomic fragment from 23.8 to 34.4 kb which accumulates steadily from the embryonic stage until the end of pupation and a 1.7 kb tran- script between coordinates 6.3 and 12.0 kb, which appears dur- ing the third larval instar and peaks during the first two days of pupation. Both sequences are transcribed from left to right. Spatial distribution of expression of the two sequences in white prepupae highly concordant. Found in the distal-forming regions of the wing, haltere, leg, and labial discs. Adepithelial cells of the wing discs thought to con- tribute to thoracic masculature also exhibit expression as does a narrow strip of tissue in the genital disc destined to give rise to the internal ducts. # rnD: rotund-Dominant synonym: Dipr: Distal into proximal. phenotype: Dominant mutation with complete penetrance and high expressivity. In Dipr/+ flies the distal wing blade reduced to two-thirds normal length; triple row replaced by two to three rows of irregularly sized bristles resembling those found on costa; occasionally these bristles may be bracted as are those of proximal costa. Posterior row of marginal bris- tles absent distally. Venation in proximal portion of wing irregular and crowded but more nearly normal distally. Tri- chomes of wing blade organized into whorls. Capitellum of haltere covered with small adventitious bristles and sometimes pedicellar-like sensilla. Pleura, coxa, trochanter, femur, tibia, and fifth tarsal segment unaffected; other tarsal seg- ments reduced; tarsal segments two to four variably fused; ectopic sex combs form on second tarsal segment in 70-90% of forelegs. Basal cylinder of antenna reduced or missing; replaced by bristle elements at third-segment-arista junction resembling those on third segment. Proboscis contains five to seven rows of pseudotracheae rather than normal twelve; replaced by bristles laterally. Kerridge suggests transforma- tion of distal into more proximal appendage elements. Homozy- gotes survive and are more extreme. other information: Probably a hypermorphic allele of rn. X- ray-induced revertants designated Dipr+R1-Dipr+R9 (lacking +R3 and +R6); the three that are visibly deleted are deficient for the more distal inversion realignment of chromosome segments. rn: rotund From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 159. # RNA: Genes described below: # RNA polymerase: see RpII # rRNA5s: see min # rRNA5.8s: see bb # rRNA18s: see bb # rRNA28s: see bb # snRNA: small nuclear RNA RNA molecules ranging in size from about 100 to 300 nucleo- tides, which in association with polypeptides comprise a fam- ily of nuclear ribonucleoprotein (snRNP) complexes. The polypeptides are recognized by antibodies produced by patients with systemic lupus erythematosus; in Drosophila such sera recognize a 26 kd polypeptide, which is conserved between flies and mammals, as well as an 18 kd polypeptide (Wooley, Cone, Tartof, and Chung, 1982, Proc. Nat. Acad. Sci. USA 79: 6762-66). Significant sequence homology is found between Drosophila snRNA molecules and those isolated from mammals. Some snRNA genes have been cloned and sequenced, but as yet not localized by in situ hybridization; in other cases, the RNA's have been isolated and complementary genomic sequences located by hybridization to polytene chromosomes. Where in situ hybridizations have been carried out, single snRNA species hybridize to a fixed number of specific sites, and with the exception of 39B no two hybridize to the same site. locus location synonym ref ( comments ______________________________________________________________ snRNA1 2 homologous to mammalian U1; cloned and sequenced; ca 164 nucleotides snRNA2 39B snRNA1 1, 3, 4 3 copies; homologous 40A-B to mammalian U2; cloned and sequenced; ca 186 nucleotides snRNA3 22A snRNA2 1, 3 7 copies; homologous 82E to mammalian U3 95C snRNA4 14B snRNA3 3 7 copies; homologous 23D to mammalian U4 34A 35E-F 39B 63A snRNA6 96A snRNA4 3 1-3 copies; homologous to mammalian U6 ( 1 = Alonso, Jorcano, Beck, and Spiess, 1983, J. Mol. Biol. 169: 691-705; 2 = Mount and Steitz, 1981, Nucl. Acids Res. 9: 6351-68; 3 = Saluz, Schmidt, Dudler, Altwegg, Stumm, Zollinger, Kubli, and Chen, 1983, Nucl. Acids Res. 11: 77- 90; 4 = Wooley, Cone, Tartof, and Chung, 1982, Proc. Nat. Acad. Sci. USA 79: 6762-66. other information: Since the numerical designations applied by Saluz et al. are generally offset from those of the mammalian numbering system, we here reconcile the two systems by renumbering the Drosophila snRNA species. # tRNA: transfer RNA As many as 90 different tRNA sequences have been identified in the Drosophila melanogaster genome, each being present in from eight to twelve copies. tRNA species have been differen- tiated and designated according to the chromatographic mobil- ity of their amino-acylated derivatives and without regard to their anticodon content (White, Tener, Holden, and Suzuki, 1973, Dev. Biol. 33: 185-95). The number of isoacceptor forms resolvable by column chromatography varies from two for histidine to eleven for asparagine. Several forms show evi- dence of post-transcriptional modification in that an earlier form (`) decreases during development while a form that elutes from the column at reduced ionic strength (/) displays a con- committant increase (White, Tener, Holden, and Suzuki, 1973, J. Mol. Biol. 74: 635-51). The several copies of a particular isoform need not occur together on the chromosome, although numerous cases of clustering of copies of the same isoform as well as of different tRNA's have been recorded. In cases of clustered tRNA genes, transcription may take place in both directions. Dosage compensation has been observed for tRNA- Ser4 (Birchler, Owenby, and Jacobson, 1982, Genetics 102: 525-37) as well as in the case of tRNA-Val3b in hetero- zygotes for Df(3R)Antp17 = Df(3R)84A6;84D13-14 [Tener, Hayashi, Dunn, Delaney, Gillam, Grigliatti, Kaufman, and Suzuki, 1980, Transfer RNA (Abelson, Schimmel, and Soll, eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, pp. 295-307]; however, these observations are based on specific amino acylation activity and need not reflect increased transcription from 12D-E or 84D alone. In the table below, each of the isoforms is listed and, where available, the cytological locations, as determined by in situ hybridiza- tion with purified samples or cloned sequences, are indicated; where localizations do not specify isoform, a numerical desig- nation is omitted. In only a few cases has crossreaction in in situ hybridizations been ruled out by competition experi- ments. Where the numbers of copies are indicated, these are minimum estimates based on cloned segments from the regions involved; other indications of copy number are available from grain counts in autoradiograms; for example the grain-number ratio in 84D:90B-C:92D for tRNA-Val3b is 6:3:1 (or 5:4:1) and in 42A:42E:50B:62A:63B for tRNA-Lys2 is 5:3:1:1:1 (Tener et al., 1980). Sequencing, where indicated, has been performed either on purified tRNA samples or on cloned DNA sequences. locus location ref ( comments _____________________________________________________________________ tRNA-Ala 63A 9, 24 90C 9, 24 tRNA-Ala1 tRNA-Ala2 tRNA-Ala3 tRNA-Ala4 tRNA-Ala5 tRNA-Arg1 tRNA-Arg2 42A 9, 12, 18, 24, 8 copies; sequenced 29, 30, 33 (CGU binding) 56E-F 12 84E-F 7, 9, 12, 24 5 copies; cloned tRNA-Arg3 tRNA-Arg4 tRNA-Arg5 tRNA-Asn1 tRNA-Asn2 ` and / forms tRNA-Asn3 ` and / forms tRNA-Asn4 ` and / forms tRNA-Asn5 42A 9, 12, 18, 24, ` and / forms; 30, 32 (AAC binding) cloned and sequenced 59F 24 60C 24 84F 7, 9, 12, 24 3 copies; cloned tRNA-Asn6 tRNA-Asn7 tRNA-Asp1 tRNA-Asp2 25D 12, 26 29D-E 9, 12, 26, 25, 30 ` and / forms 70A 7, 9, 25 cloned and sequenced 96A 12 96B 12 tRNA-Asp3 tRNA-Asp4 tRNA-Cys1 tRNA-Cys2 tRNA-Cys3 tRNA-Cys4 tRNA-Gln1 tRNA-Gln2 tRNA-Gln3 tRNA-Gln4 tRNA-Gln5 tRNA-Glu1 tRNA-Glu2 tRNA-Glu3 tRNA-Glu4 52F 9, 20 (GAA binding) 56E-F 9, 19, 20, 30 3 copies, cloned and sequenced 62A 4, 9, 16, 20 5 copies; cloned and sequenced tRNA-Glu5 tRNA-Glu6 tRNA-Gly1 tRNA-Gly2 58A 13 (GGA binding) 84C 13 90E 13 tRNA-Gly3 22B-C 12, 23 (GGC binding) 28D? 12 35B-C 9, 12 53E? 12 55E? 12 56E-F 9, 11, 15, 20, 2 copies; cloned 30 and sequenced 57B-C 12 tRNA-His1 48F 4, 7, 9, 24 ` and / forms; (CAC binding) cloned and sequenced 56F 24 tRNA-Ile 42A 9, 12, 17, 18, 1 copy 24, 30, 33 (AUU binding) 50A-B 22 5 copies; cloned and sequenced tRNA-Ile1 tRNA-Ile2 tRNA-Ile3 tRNA-Ile4 tRNA-Leu1 tRNA-Leu2 44F 13, 14 50A? 13 66B5-8 9, 12, 13, 14, 30 70A? 13 79F 13 95A 13 tRNA-Leu3 50A-B 22 2 copies, cloned and sequenced; both have introns tRNA-Lys1 tRNA-Lys2 42A 9, 10, 12, 18, 5 copies; cloned 24, 27, 30, 32, and (AAG binding) 33 sequenced 42E1-2 9, 10, 11, 12, 30 4 copies 44E 13 50B5-8 9, 12, 30 56E-f 11, 12 62A1-2 9, 12, 16, 20 63B1-2 12, 30 66B5-8 13 79F 13 tRNA-Lys3 tRNA-Lys4 tRNA-Lys5 29A 5, 6, 12 may not be transcribed (AAA binding) 84A-B 5, 6, 9, 12, 30 cloned and sequenced 85B 12 87B 12 tRNA-Lys6 tRNA-Met1 tRNA-Met2 48B5-7 9, 12, 30 2 copies 63A? 9, 12, 24 72F1-2 9, 12, 30 2 copies 83F3-84A2 9, 12, 30 tRNA-Met3 19-20 12 tRNA-Met3 is the initiator sequence; (AUG binding) 42A? 9 cloned and sequenced 42E? 9 46A1-2 12, 30 56E-F 12 61D1-2 9, 12, 28, 30 70F1-2 9, 12, 30 tRNA-Phe1 tRNA-Phe2 56F 3, 9, 20, 30 four (UCC binding) postranscriptionally modified forms 89B-C 1 cloned and sequenced tRNA-Phe3 tRNA-Pro1 tRNA-Pro2 tRNA-Pro3 tRNA-Ser1 tRNA-Ser2b 86A 13, 14, 31 88A9-12 13, 14 94A6-8 13, 14 tRNA-Ser3 tRNA-Ser4 12D-E 8, 9, 12, 31 cloned 23E 8, 9, 12 cloned 56D 12 64D 12 tRNA-Ser5 tRNA-Ser6 tRNA-Ser7 12D-E 8, 9, 12, 31 cloned 23E 8, 9, 12 cloned 56D 12 64D 12 tRNA-Thr1 tRNA-Thr2 tRNA-Thr3 47F 13, 14 87B 13, 14 tRNA-Thr4 93A1-2 13, 14 tRNA-Thr5 tRNA-Thr6 56E-F 14 61F 14 tRNA-Thr7 tRNA-Thr8 tRNA-Trp1 tRNA-Trp2 tRNA-Trp3 tRNA-Tyr1 19F 13, 14 ` and / forms 22F-23A 13, 14 28C 13 41 13 42A 9, 12, 18, 24, 30, 33 42E 9, 30 50C1-4 13, 14 polymorphic 85A 13, 14 tRNA-Tyr2 tRNA-Tyr3 tRNA-Val1 tRNA-Val2 tRNA-Val3a 64D1-2 2, 9, 12, 30 cloned and sequenced (GUA binding) tRNA-Val3b 84D3-4 2, 8, 9, 12, 5 copies; cloned 21, 30 and sequenced 90B-C 8, 9, 13, 24, 30 cloned 92B1-11 9, 12, 30 4 copies tRNA-Val4 56D3-7 9, 12, 30 70B-C 1, 8, 9, 12, 30 cloned and sequenced 89B 1, 8, 9, 30 cloned and sequenced 90B-C 1, 13, 21 cloned and sequenced tRNA-Val5 tRNA-Val6 tRNA-Val7 ( 1 = Addison, Astell, Delaney, Gillam, Hayashi, Miller, Rajpur, Smith, Taylor, and Tener, 1982, J. Biol. Chem 257: 670-73; 2 = Addison, Gillam, Hayashi, and Tener, 1985, Canadian J. Biochem. and Cell Biol. 63: 176-82; 3 = Altweg and Kubli, 1979, Nucl. Acids Res. 7: 93-105; 4 = Altweg and Kubli, 1980, Nucl. Acids Res. 8: 215-23; 5 = Cribbs, Gil- lam, and Tener, 1982, Nucl. Acids Res. 10: 6393-6400; 6 = DeFranco, Burke, Hayashi, Tener, Miller, and Soll, 1982, Nucl. Acids Res. 10: 5799-5808; 7 = Dudler, Egg, Kubli, Artavanis-Tsakonas, Gehring, Steward, and Schedl, 1980, Nucl. Acids Res. 8: 2921-27; 8 = Dunn, Delaney, Gillam, Hayashi, Tener, Grigliatti, Misra, Spurr, Taylor, and Miller, 1979, Gene 7: 199-215; 9 = Elder, Szabo, and Uhlen- beck, 1980, J. Mol. Biol. 142: 1-17; 10 = Gergen, Loewen- berg, and Wensink, 1981, J. Mol. Biol. 147: 475-99; 11 = Hayashi, Addison, Gillam, Grigliatti, and Tener, 1981, Chromosoma 82: 385-97; 12 = Hayashi, Gillam, Delaney, Dunn, Tener, Grigliatti, and Suzuki, 1980, Chromosoma 76: 65-84; 13 = Hayashi, Gillam, Grigliatti, and Tener, 1982, Chromo- soma 86: 279-92; 14 = Hayashi, Gillam, Tener, Grigliatti, and Suzuki, 1980, Genetics 94: s42; 15 = Hershey and David- son, 1980, Nucl. Acids Res. 8: 4899-4910; 16 = Hosbach, Silberklang, and McCarthy, 1980, Cell 21: 169-78; 17 = Hovemann, Schmidt, Yamada, Silverman, Mao, DeFranco, and Soll, 1980, Transfer RNA (Abelson, Schimmel, and Soll, eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, pp. 325-38; 18 = Hovemann Sharp, Yamada, and Soll, 1980, Cell 19: 889-95; 19 = Indik and Tartof, 1982, Nucl. Acids Res. 10: 4159-72; 20 = Kubli and Schmidt, 1978, Nucl. Acid Res. 5: 1465-78; 21 = Miller, Tener, Bradley, and Scraba, 1981, Gene 15: 361-64; 22 = Robinson and Davidson, 1981, Cell 23: 251-59; 23 = Schedl and Donelson, 1978, Biochim. Biophys. Acta 520: 539-54; 24 = Schmidt and Kubli, 1980, Chromosoma 80: 277-87; 25 = Schmidt, Egg, and Kubli, 1978, Mol. Gen. Genet. 164: 249-54; 26 = Schmidt, Mao, Silverman, Hovemann, and Soll, 1978, Proc. Nat. Acad. Sci. USA 75: 4819-23; 27 = Silverman, Gillam, Tener, and Soll, 1979, Nucl. Acids Res. 6: 435-42; 28 = Silverman, Heckman, Cowling, Delaney, Dunn, Gillam, Tener, Soll, and Ray, 1979, Nucl. Acids Res. 6: 421-33; 29 = Silverman, Schmidt, Soll, and Hovemann, 1979, J. Biol. Chem. 254: 10290-94; 30 = Tener, Hayashi, Dunn, Delaney, Gillam, Grigliatti, Kaufman, and Suzuki, 1980, Transfer RNA (Abelson, Schimmel, and Soll, eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, pp. 295-307; 31 = White, Dunn, Gillam, Tener, Armstrong, Skoog, Frihart, and Leonard, 1975, J. Biol. Chem. 251: 515-21; 32 = Yen and Davidson, 1980, Cell 19: 889-95; 33 = Yen, Sodja, Cohen, Conrad, Wu, Davidson, and Ilgen, 1977, Cell 11: 763-77.