#*rt: rotated abdomen location: 3-37 (based on location of rt2). discoverer: Bridges, 18g28. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 190 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 54 (fig.). phenotype: Abdomen twisted clockwise through 60 to 90, as viewed from behind. Both sexes sterile. Viability low. RK2. cytology: Placed in 68C8-11 based on inclusion in Df(3L)vin7 = Df(3L)68C8-11;69B4-5 but not Df(3L)vin6 = Df(3L)68C8-11;69A4-5 (Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215- 25). # rt2 origin: Spontaneous. discoverer: Bridges, 25l14. phenotype: Abdomen twisted, as is rt. Viability erratic, usu- ally about 50% wild type. Male fertile; female not tested. RK2. #*rtW: rotated abdomen of Wallbrunn origin: / ray induced. discoverer: Wallbrunn, 61i26. references: 1964, DIS 39: 59. phenotype: Like rt. RK2. #*rta: reduced tarsi location: 1-4.5. origin: Induced by methyl methanesulfonate (CB. 1540). discoverer: Fahmy, 1956. references: 1959, DIS 33: 89. phenotype: Tarsi short and sometimes deformed. Body small. Eyes and wings small and abnormal. Bristles often waved or bent; postscutellars often held upright. Male sterile. RK2. # rtv: retroactive location: 1-38. origin: Induced by ethyl-methanesulfonate. references: Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. phenotype: Recessive embryonic lethal; mouth parts darkly sclerotized. Embryo sometimes reversed in egg case (due to hyperactivity at late stages?). Zygotes from homozygous germ-line clones in females develop normally (Wieschaus and Noell, 1986, Roux's Arch. Dev. Biol. 195: 63-73). alleles: Allelism with Lefevre lethals reported by Perrimon, Engstrom, and Mahowald, 1989, Genetics 21: 333-52. allele origin discoverer synonym ref ( comments _____________________________________________________________________ rtv1 X ray Lefevre l(1)L1 3 rtv2 X ray Lefevre l(1)HC236 4 rtv3 X ray Lefevre l(1)JA10 4 rtv4 X ray Lefevre l(1)JC65 4 rtv5 EMS Lefevre l(1)VE701 5 rtv6 EMS Lefevre l(1)VE745 5 embryonic lethal; no maternal effect rtv7 EMS Lefevre l(1)VE800 5 rtv8 EMS l(1)v24 2 rtv8 EMS l(1)v68 2 rtv9 EMS l(1)v152 2 rtv10 MR Eeken l(1)D40 1 rtv11 EMS l(1)YA 6 rtv12 EMS 6 rtv13 EMS 6 ( 1 = Eeken, Sobels, Hyland, and Schalet, 1985, Mutat. Res. 150: 261-75; 2 = Geer, Lischwe, and Murphy, 1983, J. Exp. Zool. 225: 107-18; 3 = Lefevre, 1971, Genetics 67: 497- 513; 4 = Lefevre, l981, Genetics 99: 461-80; 5 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 6 = Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. cytology: Placed in 10A6-B1 based on its inclusion in Df(1)RA37 = Df(1)10A6;10B15-17 but not Df(1)GA112 = Df(1)10A11-B1;10C2. # ru: roughoid location: 3-0.0 [actually 2.57 units to the right of the end of the chromosome, based on recombination with y+ of T(1;3)scJ4) in a sample of 9106 flies (Strommer and Falk, 1981, DIS 56: 196)]. references: Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29. phenotype: Eyes small and rough, have irregular facets and hairs, and have black specks from erupted facets. Expression variable; sometimes overlaps wild type. SEM study by Stumm- Tegethoff and Dick (1974, Theor. Appl. Genet. 44: 262-65). alleles: allele origin discoverer ref ( comments ______________________________________________________________________ ru1 Sturtevant, 19b14 1, 3, 5 may overlap wild type *ru40k spont Steinberg, 40k 4 *ru100.392 X ray Alexander 6 Df(3L)61E;62A10-B1 *ru100.393 X ray Alexander 6 Df(3L)61F;62A4-6 *ru300.234 X ray Alexander 6 Df(3L)61E;62A2-4 rug spont Glass 2 RK1 ( 1 = Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 212 (fig); 2 = Glass, 1934, DIS 2: 8; 3 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 215 (fig.), 234; 4 = Steinberg, 1942, DIS 16: 54; 5 = Strong, 1920, Biol. Bull. 38: 33-37; 6 = Ward and Alexander, 1957, Genetics 42: 42-54. cytology: Placed in 61F5-62A3 on the basis of its inclusion in Df(3L)ru-K2 = Df(3L)61F4-5;61A10-B1 (Krivshenko, 1958, DIS 31: 81) and Df(3L)ru1300.234 = Df(3L)61E;62A2-4 (Ward and Alexander, 1957, Genetics 42: 42-54). # rub: rubroad location: 2-5.0 (to the right of dppd-ho). origin: Spontaneous. discoverer: Mohr, 31k20. phenotype: Eyes rough and kidney shaped. Wings broad and some- what arclike. Abdomen short and bloated; tergites irregular. External genitalia of male rotated in varying degrees. Over- laps wild type. RK3. rub: rubroad Edith M. Wallace, unpublished. #*rub48d origin: Spontaneous. discoverer: Chute, 48d. references: Sturtevant, 1948, DIS 22: 56. phenotype: Like rub; wings also show slight network of extra veins and thickening between L3 and L4. RK3. # rubb: rubbish (T. Schupbach) location: 2-89. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal effect lethal; embryos from homozygous mothers form a fragmanted cuticle with variable holes and head defects. alleles: One: rubbQD = rubb1. # rubroad: see rub # ruby: see rb # rud: ruddle location: 1-3.3. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 74. phenotype: Eye color dull reddish brown. Classification best in newly eclosed flies. Good viability and fertility. RK2. other information: One allele each induced by CB. 1528, CB. 3026, and X rays. # rudimentary: see r # rudimentary-like: see r-l # rue: ruffed eye location: 3- {47}. origin: Induced by ethyl methanesulfonate. discoverer: Kaufman. references: Lewis, Kaufman, Denell, and Tellerico, 1980, Genet- ics 95: 367-81. Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23. phenotype: Roughened eyes and fine bristles at 25; lethal at 28. cytology: Placed in 84C1-6 based on its inclusion in Df(3R)dsx2M = Df(3R)84C1-2;84E1 and Df(3R)Antp-X2 = Df(3R)84B6-C1;84C5-6. # rugose: see rg # rumpled: see rmp # run: runt location: 1- {65.8}. synonym: leg: legless. references: Nusslein-Volhard and Wieschaus, 1980, Nature (Lon- don) 287: 795-801 (fig.). Gergen and Wieschaus, 1986, Cell 45: 289-99 (fig.). Gergen, 1987, Genetics 117: 477-85 (fig.). Gergen and Butler, 1988, Genes Dev. 2: 1179-93. phenotype: A pair-rule embryonic lethal; causes deletions of the dentical belts of the mesothoracic and the first, third, fifth, and seventh abdominal segments, extending through the more anterior naked cuticle and into the denticle belts of the next most anterior segments. Deleted regions appear to be replaced by mirror image duplications of the remaining more anterior pattern elements. Deleted regions exceed duplica- tions in size, resulting in shorter embryos. The amount of material deleted varies among segments, alleles, and among animals with the same alleles. Hypomorphic alleles do not remove as much tissue as amorphs, and weak hypomorphic alleles produce occasional survivors missing methathoracic legs or halteres or both and are frequently missing one or more abdom- inal tergites. run31, among the weakest alleles, survives to adulthood. Deficiencies for run have discernable dominant effects on embryonic development; extra doses of run+ produce anti-runt phenotype, i.e., 30% of males with two doses of run+ display deletions of portions of the dentical belts of A6 and less frequently of A2 and A8; males with three run+ alleles more severely affected with 70% penetrance. run+ postulated to repress eve function and positively regulate ftz; run mutants show expansion of stripes of eve expression and prema- ture disappearance of stripes of ftz expression in the embryo (Frasch and Levine, 1987, Genes Dev. 1: 981-95). ftz+ expression in cellular blastoderm reduced in four anterior stripes; A5-A7 expression abnormal, possibly reflecting pat- tern duplication; nuclear shape abnormal [Carroll and Scott, 1986, Cell 45: 113-26 (fig.)]. For expression pattern later in development see Kania, Bonner, Duffy, and Gergen (1990, Genes Dev. 4: 1701-13). run is autonomous in gynandropmorphs both for missing and for mirror-image duplicated phenotypes, suggesting that the duplication does not result from proli- feration following cell death (Gergen and Wieschaus, 1985, Dev. Biol. 109: 321-35). Also, the earliest embryonic pheno- types are dosage compensated (Gergen, 1987). run embryos produced by homozygous ovarian clones not different from those produced by heterozygous mothers (Wieschaus and Noell, 1986, Roux's Arch. Dev. Biol. 195: 63-73). alleles: allele origin discoverer synonym ref ( comments _____________________________________________________________________________________________________________________________ run1 Novitski l(1)152 run2 EMS Lifschytz l(1)AA33 3, 8, 11 weak hypomorph run3 mit C Baldwin l(1)LB5 3, 9 amorph run4 EMS Baldwin l(1)LB19 9 run5 EMS Lifschytz l(1)P235 3, 8 intermediate hypomorph run6 EMS Lifschytz l(1)P425 8 run7 EMS Lifschytz l(1)P515 8 run8 EMS Lifschytz l(1)W1 3, 8 amorph; also unc8 run9 EMS Lifschytz l(1)W3a 7 also mutant for unc run10 X ray Lefevre l(1)HA14 5 T(1;3)19E;80 run11 X ray Lefevre l(1)RF45 5 T(1;2)19E-20F;52A run12 EMS Lefevre l(1)DC839 run13 EMS Lefevre l(1)EA14 3, 6 intermediate hypomorph run14 EMS Lefevre l(1)EF535 run15 EMS Lefevre l(1)VE726 3, 6 strong hypomorph run16 EMS Lefevre l(1)VE751A 3, 6 amorph run17 spont Schalet l(1)16-137 run18 neutron Munos l(1)17-26 3-10 amorph; deletion with one breakpoint at -5.4 and extends in + direction run19 neutron Munos l(1)17-169 3, 9, 10 weak hypomorph; breakpoint between -7.9 and -6.4 also vao mutant run20 HMS Kramers l(1)HM48 4 run21 HMS Kramers l(1)HM449 4 run22 EMS Wieschaus l(1)XA06 3, 10 amorph run23 EMS Wieschaus l(1)XD106 3, 10 amorph run24 EMS Wieschaus l(1)XK52 1, 3, 10 intermediate hypomorph run25 EMS Wieschaus l(1)YC28 2, 3, 10 intermediate hypomorph run26 EMS Wieschaus l(1)YC47 3, 10 strong hypomorph run27 EMS Wieschaus l(1)YD24 3, 10 intermediate hypomorph run28 EMS Wieschaus l(1)YE96 1, 3, 10 strong hypomorph run29 EMS Wieschaus l(1)YP17 3, 10 intermediate hypomorph temperature sensitive run30 P Gergen l(1)34A 3, 11 intermediate hypomorph; breakpoint near -0.9 run31 P Gergen l(1)50-2 3, 11 weak hypomorph; P-insert site defined as coordinate 0 run32 P Gergen l(1)PV1 3, 11 amorph; 5 kb deletion between -6.5 and 8.7 ( 1 = Carroll and Scott, 1986, Cell 45: 113-26 (fig.); 2 = Gergen, 1987, Genetics 117: 477-85; 3 = Gergen and Wieschaus, 1986, Cell 45: 289-99; 4 = Kramers, Schalet, Paradi, and Huiser-Hoogteyling, 1983, Mut. Res. 107: 187- 201; 5 = Lefevre, 1981, Genetics 99: 461-80; 6 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 7 = Lifschytz and Falk, 1968, Mut. Res. 6: 235-44; 8 = Lifschytz and Falk, 1969, Mut. Res. 8: 147-55; 9 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902; 10 = Wieschaus, Nusslein- Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307; 11 = Zusman, Coulter, and Gergen, 1985, DIS 61: 217-18. cytology: Placed in 19E1-3 on the basis of its inclusion in the region of overlap of Df(1)16.3.35 = Df(1)19D2-D3;E3 and Df(1)B57 = Df(1)19E1-2;19F1 (Miklos, Kelly, Coombe, Leeds, and Lefevre, 1987, J. Neurogenet. 4: 1-19). molecular biology: Gene cloned by transposon tagging; 50 kb cloned. Mutational lesions define a segment of at least 8.5 kb required for run function; transposition of a 14.5 kb seg- ment that includes the 8.5 kb sequence elicits partial rescue of run mutants. Genomic sequences identify a 2.6 kb poly- adenylated mRNA on northern blots. Transcript uniformly dis- tributed in early embryo; most abundant during blastoderm when it is expressed in the seven stripes characteristic of other pair-rule genes; switching to every-segment expression during gastrulation and showing expression in the head and proctodeal primordium at that time [Gergen and Butler, 1988, Genes Dev. 2: 1179-93 (fig.)]. # runt: see run # rut: rutabaga (J.C. Hall) location: 1- {46}. references: Duerr and Quinn, 1982, Proc. Nat. Acad. Sci. USA 79: 3646-50. Dudai, Uzzan, and Zvi, 1983, Neurosci. Lett. 42: 207-12. Tempel, Bonini, Dawson, and Quinn, 1983, Proc. Nat. Acad. Sci. USA 80: 1482-86. Gailey, Jackson, and Siegel, 1984, Genetics 106: 613-23. Kyriacou and Hall, 1984, Nature (London) 308: 62-65. Livingstone, Sziber, and Quinn, 1984, Cell 37: 205-15. Livingstone, 1985, Proc. Nat. Acad. Sci. USA 82: 5992-96. Tully and Quinn, 1985, J. Comp. Physiol. 157: 263-77. Mariath, 1985, J. Insect Physiol. 31: 779-87. phenotype: Mutant males and homozygous females impaired in several types of learning and memory; associative conditioning defective in tests using either reward (Tempel et al., 1983) or aversive unconditioned stimuli (e.g. Dudai, 1983, Proc. Nat. Acad. Sci. USA 80: 5445-48; Dudai, Svi, and Segel, 1984, J. Comp. Physiol. 155: 569-76; Livingstone et al.), including tests of "classical" (e.g. Tully and Quinn, 1985) and "operant" conditioning (Mariath, 1985); able to learn in asso- ciative conditioning tests involving visual cues, but at sub- normal levels (Folkers, 1982, J. Insect. Physiol. 28: 535- 39), and memory appears to be normal. Learning scores subnor- mal when measured immediately after certain types of training; then either scores decay rapidly with time (Tempel et al., 1983; Tully and Quinn, 1985) or there is no indication of memory (Mariath). Although defective in some aspects of learning, heterozygous females behave essentially normally in shock/odor tests (Dudai et al., 1983). Courtship also defec- tive; unlike wild-type males, rut males court inseminated and virgin females with equal vigor; they may be unable to distin- guish them (Gailey et al.). In tests of non-associative con- ditioning, rut shows aberrant habituation and sensitization to sugar stimuli (Duerr and Quinn); rut males subnormal in learn- ing to avoid courtship of immature males; and homozygous or hemizygous rut females defective in "priming" of mating behavior by prestimulations with artificial courtship songs; effects of such acoustical prestimulations decay more rapidly than normal (Kyriacou and Hall). In either the homozygous or heterozygous condition rut acts as a partial suppressor of the sterility of homozygous dnc females inversely related to degree of rescue, suggesting both a maternal and a zygotic role of rut (Bellen, Gregory, Olsson, and Kiger, 1987, Dev. Biol. 121: 432-44; Bellen and Kiger, 1988, Roux's Arch. Dev. Biol. 197: 258-68). Double mutant females mated to Canton-S males lay many eggs, but most of the eggs fail to hatch. Biochemically, rut influences adenylate cyclase activity (Dudai et al., Livingstone et al.); it seems to abolish a calcium or calmodulin stimulated component of adenylate cyclase activity (Livingstone, Dudai, and Zvi, 1984, Neurosci. Lett. 47: 119-24), while leaving intact a component of activity stimulated by guanyl nucleotides, fluoride, or monoamines, suggesting that rut may directly affect the cata- lytic subunit of the adenylate cyclase complex (Livingstone et al., Dudai et al., 1984); consistent with this hypothesis is the observation that cyclase activity in rut is lower than normal, even in the presence of forskolin (Dudai et al., 1984; Dudai, Sher, Segal, and Yovell, 1985, J. Neurogenet. 2: 365- 80). rut primarily affects total cyclase activity in the adult abdomen, with progressively milder effects on thoracic and head cyclase (Livingstone et al., Dudai and Svi, 1985, J. Neurochem. 45: 355-64); reduction of abdominal adenylate cyclase activity of rut1>rut2>rut3 (Bellen et al.); the major- ity of adenylate cyclase activity in wild type is in a parti- culate fraction, and rut lacks up to 35% of total particulate activity (Dudai and Zvi, 1985). That rut may in fact encode a component of the fly's adenylate cyclase catalytic subunit is suggested by altered Km of enzyme activity in mutant flies (e.g. Dudai et al., 1983, 1985) and by the fact that hypo- ploidy of rut+ in females leads to approximately half normal levels of that cyclase activity specifically affected by the rut mutations (Livingstone et al.), and hyperploidy for the normal allele leads to increased activity (Livingstone). The biochemical results suggest that rut1 could be a null muta- tion. alleles: Three alleles: rut2 and rut3 recovered as partial suppressors of the female sterility of homozygous dnc females. allele origin discoverer synonym ref ( comments ______________________________________________________________ rut1 EMS Sziber rut2 EMS Gregory BG2 1 partial suppressor of dnc rut3 EMS Gregory BG3 1 partial suppressor of dnc ( 1 = Bellen, Gregory, Olsson, and Kiger, 1987, Dev. Biol. 121: 4332-44. cytology: Placed in 12F5-13A1 based on its inclusion in the region of overlap of Df(1)KA9 = Df(1)12E2-3;12F5-13A1 and Df(1)RK4 = Df(1)12F5-6;13A9-B1. # rux: roughex location: 1-15.0. references: Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29. phenotype: Eyes smaller than wild type and uniformly rough. Male sterile. RK2. alleles: allele origin discoverer ref ( comments __________________________________________________________ rux1 Bridges, 33d24 1 male sterile rux2 Curry, 37l1 1 rux60d spont. Rolfes, 1960 1, 2, 3 60% viability ( 1 = CP627; 2 = Hollander, 1960, DIS 34: 50; 3 = Hollander and Festing, 1962, DIS 36: 79. cytology: Placed in 5C5-D6, possibly in 5D2-6 (Ashburner). # rv: raven location: 1-4.4. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1959, DIS 33: 89. phenotype: Body small and heavily melanized. Eye color dark. Wings short and frequently divergent or not fully expanded. Male fertile but viability reduced; female more inviable and infertile. RK2. # Rvd: see RevB # rw: raised wing location: 2-93.2. origin: Spontaneous. discoverer: Gomes, 55a. references: Burdick, 1955, DIS 29: 70. phenotype: Wings held vertically; venation normal. Legs mor- phologically normal, but fly has difficulty walking. Penetrance and expressivity good. Viability poor. RK2. # rw: see rwi #*Rw: Rough wing location: 2-56 [locus from crossing over in triploids (Schultz)]. discoverer: Harnly. phenotype: Wings notched and veins irregular. An occasional extra antenna. Rw/+/+ triploid female slightly fertile. Rw/+ female sterile. RK3. # rwg: see hdprwg # rwi: red wine location: 3-22.7. origin: Spontaneous. synonym: rw. references: Mostashfi and Kolianz, 1970, DIS 45: 34. phenotype: Eye color wine like. # ry: rosy (A. Chovick and colleagues) location: 3-52.0. phenotype: The structural gene for xanthine dehydrogenase [XDH (EC.1.2.1.37)]; it is a homodimer with subunit molecular weight estimated from its DNA sequence as 146,898 daltons (Keith, Riley, Kreitman, Lewontin, Curtis, and Chambers, 1987, Genetics 116: 67-73). Enzyme level responds to dose of ry+ alleles (Grell, 1962, Z. Indukt. Abstamm. Vererbungsl. 93: 371-77). XDH is a molybdenum hydroxylase and requires the activity of cin+, lxd+, mal+ for normal activity, though not for normal levels of CRM (Glassman, Shinoda, Duke, and Collins, 1968, Ann. N. Y. Acad. Sci. 151: 263-73). CRM (cross reacting material) contains bound molybdenum in the presence of mal; however, enzyme activity inhibited (Andres 1976, Eur. J. Biochem. 62: 591-600). Homozygotes for null alleles lack XDH activity (Forrest, Glassman, and Mitchell, 1956, Science 124: 725-26; Glassman and Mitchell, 1959, Genetics 44: 153-62; Hubby and Forrest, 1960, Genetics 45: 211-24) and have reddish brown eyes; accumulate enzyme's substrates, xanthine and 2-amino-4-hydroxypteridine as larvae plus hypoxanthine in the adult; precursors collect as solid granules in Malpighian tubules (Bonse, 1967, Z. Naturforsch. 22B: 1027-29); lack enzyme products uric acid and isox- anthopterin (Mitchell, Glassman, and Hadorn, 1959, Science 129: 268-69). Mutant homozygotes are also sensitive to administration of purine to the medium (Glassman, 1965, Fed. Proc. 24: 1243-51); survival on purine supplemented medium can be used to select for rare ry+ recombinants (Chovnick, Ballantyne, Baillie, and Holm, 1970, Genetics 66: 315-29) and unequal crossovers producing tandem duplications (Gelbart and Chovnick, 1979, Genetics 92: 849-59). Hypomorphic alleles that have normal eye color are also sensitive to appropriate levels of purine supplementation; furthermore, both wild types and hypomorphs can be made to display mutant eye color by administration of appropriate levels of the XDH inhibitor, HPP (allopurinol) [4-hydroxypyrazolo-(3,4-d) pyrimidine] (Glass- man, 1965, Fed. Proc. 24: 1243-51; Boni, DeLerma, and Parisi, 1967, Experientia 23: 186-87; McCarron and Chovnick, 1981, Genetics 97: s70-71); in vitro and in vivo complementation between mal and ry products was demonstrated by Glassman (1952, Proc. Nat. Acad. Sci. USA 48: 1491-97; Glassman and McLean, 1962, Proc. Nat. Acad. Sci. USA 48: 1712-18). Pigmen- tation is nonautonomous in ry eye disks trans- planted into wild-type hosts (Hadorn and Schwink, 1956, Nature 177: 940-41). Enzyme levels climb from low levels in the zygote to a peak at puparium formation; the level then falls but increases again to a maximum a few days after eclosion (Chovnick, McCarron, Hilliker, O'Donnell, Gelbart, and Clark, 1978, Cold Spring Harbor Symp. Quant. Biol. 42: 1011-21). Enzyme derived from the paternal genome appears during gastru- lation; activity at time zero is low in ry+ zygotes produced by ry/+ females but undetectable in those produced by ry females (Sayles, Browder, and Williamson, 1973, Dev. Biol. 33: 213-17). Enzyme activity present in larval and adult fat bodies, larval and adult Malpighian tubules, and, in smaller amounts, in various regions of the larval and adult gut [Ursprung and Hadorn, 1961, Experientia 17: 230-31; Munz, 1964, Z. Indukt. Abstamm. Vererbungsl. 95: 195-210; Reaume, Clark, and Chovnick, 1989, Genetics 123: 503-09; Reaume (unpublished observations)]. XDH is not synthesized in the adult eye, but is transported there [Reaume et al., 1989]. alleles: ry alleles have been detected by several criteria, including electrophoretic mobility of XDH, purine sensitivity, and rosy eye color, either in the absence or presence of allo- purinol. Alleles are presented in two tables; the first table includes the wild-type variants, and the second the mutant alleles. Chovnick and his colleagues (Chovnick, Gelbart, and McCarron, 1980, Cell 11: 1-10) identify at least seven dif- ferent electromorphs in laboratory stocks; using a highly discriminating series of gel conditions, Buchanan and Johnson (1983, Genetics 104: 301-15) identified, among 62 wild-type chromosomes isolated from nature, fourteen electromorphs, two of which corresponded to those contained among the earlier seven. Both induced mutations and natural variable sites are designated by the number of the + progenitor followed by specific derivative numbers, e.g. ry102 is the second mutant derivative of ry+1. Not all mutants with allelic designations with values less than 100 are known to be derivatives of ry+0; however, those numbered from 3a to 54 (excepting 17, 20, and 21) are known to be so derived. However, those mutations discovered by Girton, Green, Daniels, Lewis, Spradling and Rubin do not use this system of nomenclature. Also, those alleles marked with an asterisk are no longer available. Finally, Chovnick's laboratory maintains several hundred mutants not reported here, including a group generated on a ry+11 background. rosy molecular map Data of Chovnick and colleagues. Table I seq. data rel. tentative origin allele( avail.| mob. constitution/ ref` of line ___________________________________________________________________________ ry+0 + 1.00 0 0/0 0 0 1, 3-7, 9, 10 cu kar stock- ry+1d - 1.02 0 0/0 0 - 3, 4, 7, 9, 10 conversion of Oregon-R ry ry+2 + 1.03 0 0/- 0 0 1, 3-5, 7, 9, 10 Oregon-R iso-3 ry+3 - 1.05 0 0/- 0 - 3, 4, 7, 9, 10 Amherst iso-3 ry+4 + 1.02 0 +/0 0 - 2-7, 9, 10 Pacific iso-3 ry+5 + 1.05 0 0/- 0 - 3-5, 7-9, 10 zeste; ry+ iso-3 ry+6 + 1.00 0 0/0 0 0 3-7, 9, 10 Hikone iso-3 ry+10 + 0.97 - 0/0 + 0 2-8, 10 Bethulie iso-3 ry+11 + 1.02 0 0/0 0 - 3-5, 7, 10 kar2 ry+ stock ry+12d - 0.90 0 0/0 + 0 3, 4, 10 conversion of ry16608.19 (Lewis) against ry8 ry+13d - 0.90 0 0/0 + 0 3, 4, 10 (see ry+12d) ry+14d - 0.94 0 0/0 + - 3, 4, 10 (see ry+12d) ry+15 + 1.02 0 0/0 0 - 5 Kalahari iso-3 ry+16 - 1.02 0 0/0 0 - 10 Kalahari iso-3 ry+19d - 1.00 0 0/0 0 0 4 conversion of Weymouth ry against ry8 ry+21d - 1.03 0 0/- 0 0 4 conversion of ry2101(copia) ry+31 + 1.00 0 0/0 0 0 5 Okanogon iso-3 ( ry+ allele designation refers to the entire rosy DNA sequence. Electrophoretic markers and control variants characteristic of a given allele represent only a few of the bp polymorphisms distinguishing one ry+ allele from another. ry+ alleles originated as iso-3 stocks from wild popula- tions, with the exception of those marked (derivative) which are conversions to wild type of an unique rosy mutant allele. These may carry bp polymorphisms within the conver- sion segment not common to the original rosy mutant. | Sequence data have been submitted to the EMBL/Gen Bank Data Libraries under the accession number Y 00307 and Y 00308. Data on other wild-type sequence are available (5, 6). / Polymorphic sites segregating in wild type alleles; the digits to the left of the slash bar represent the phenotype with respect to the 5' cis-acting control elements, 1005 and 409, with "0" indicating the CRM levels of ry+0, "+" representing higher CRM, and "-" indicating lower CRM. The remaining digits designate the electrophoretic charge rela- tive to that of XDH produced by ry+0 attributable to the amino-acid residues inferred to correspond to the three sites inferred from mapping and sequencing results; the sites are indicated in order and are located at +736, +1551, and +3557 in the gene sequence (5): "0" indicates the rela- tive charge at the three sites of ry+0; "-" indicates a more negative charge, i.e. less anodically migrating; and "+" a more positive charge. ` 1 = Buchanan and Johnson, 1983, Genetics 104: 301-15; 2 = Clark, Daniels, Rushlow, Hilliker, and Chovnick, 1984, Genetics 108: 953-68; 3 = Chovnick, Gelbart, and McCarron, 1980, Cell 11: 1-10; 4 = Cote, Bender, Chovnick, 1986, Genetics 112: 769-83; 5 = Curtis, personal communication; 6 = Curtis, Clark, Chovnick, and Bender, 1989, Genetics 122: 653-61; 7 = Gelbart, McCarron, Pandey, and Chovnick, 1974, Genetics 78: 869-86; 8 = Lee, Curtis, McCarron, Love, Gray, Bender, and Chovnick, 1987, Genetics 116: 55-66; 9 = McCarron, Gelbart, and Chovnick, 1974, Genetics 76: 289-99; 10 = McCarron, O'Donnell, Chovnick, Bhullar, Hewitt, and Candido, 1979, Genetics 91: 275-93. - The only extant non-derivative ry+0 sequence is carried in the multiple break rearrangement In(3LR)UbxA. Table II allele origin discoverer synonym ref( characterization| ___________________________________________________________________________________________________________________________________________ ry1 spont Bridges 2, 3, 8, 14, 0.1 kb deletion including SstI site at +0.95 kb; 17, 20, 22, non-complementing allele; null 24 ry2 spont Hadorn & 3, 5, 6, B104 insertion at +3.2 kb; Schwinck 8, 14, 19, complementing allele; null 20, 24 ry3 spont Hubby 7, 8, 20, B104 insertion at +2.2 kb; leaky 22, 24 ry3a X ray Schalet 2, 3, 14, Non-complementing allele; null 21, 24 ry4 X ray Schalet 2, 3, 8, 14, Apparent point; non-complementing allele; null 15, 24, 29 ry5 X ray Schalet 2, 3, 8, 14, 19 bp deletion from +294 to +312; frameshift; 18, 20, 24, missing SstI site at -1.0 kb; 29 non-complementing allele; null ry6 X ray Schalet 2, 8, 14, Apparent point; non-complementing allele; null 20, 24, 29 ry7 X ray Schalet 2, 8, 14, 0.6 kb deletion between +2.9 and +4.2 kb; 24, 29 non-complementing allele; null ry8 X ray Schalet 1-3, 8, 14, 17 bp deletion from +1283 to +1299; 15, 18, 20, frameshift; null 24, 29 ry9 X ray Schalet 2, 3, 8, 14, Apparent point; non-complementing allele; null 24, 29 *ry10 X ray Schalet 24, 29 Null *ry11 X ray Schalet 24, 29 Null *ry12 X ray Schalet 24, 29 Null *ry13 X ray Schalet 24, 29 Null *ry14 X ray Schalet 24, 29 Null *ry15 X ray Schalet 24, 29 Null *ry16 X ray Schalet 24, 29 Null ry17 X ray Schalet 8, 14, 24, Apparent point; non-complementing allele; null 29 *ry18 X ray Schalet 14, 24, 29 Non-complementing allele; null *ry19 X ray Schalet 14, 24, 29 Non-complementing allele; null ry20 X ray Schalet 8, 14, 24, Apparent point; non-complementing allele; null 29 ry21 X ray Schalet 8, 14, 24, Apparent point; non-complementing allele; null 29 *ry22 X ray Schalet 24, 29 Null ry23 X ray Schalet 2, 3, 8, 14, Apparent point; non-complementing allele; null 24, 29 ry24 X ray Schalet 2, 3, 8, 14, Apparent point; non-complementing allele; null 24, 29 *ry25 X ray Schalet 2, 24, 29 Null ry26 X ray Schalet 2, 3, 8, 14, GG->T (frameshift, Amber) 18, 20, 24, at +2804-5; non-complementing 29 allele; null *ry37 X ray Schalet 24, 29 Null *ry38 X ray Schalet 24, 29 Null ry40 X ray Schalet 8, 14, 24, Apparent point; non-complementing allele; null 29 ry41 X ray Schalet 2, 8, 9,14, Apparent point; non-complementing allele; null 15, 20, 24, 29 ry42 X ray Schalet 2, 14, 18, Complementing allele; null; 16 bp 20, 24, 29 deletion and insertion of 7 bp of non-rosy DNA at +2030, yielding a net 9 bp "in frame" deletion *ry43 X ray Schalet 24, 29 Null *ry44 X ray Schalet 24, 29 Null ry45 X ray Schalet 14, 24, 29 Non-complementing allele; null *ry46 X ray Schalet 24, 29 Null *ry47 X ray Schalet 24, 29 Null ry48 X ray Schalet 8, 14, 24, Apparent point; non-complementing allele; null 29 *ry49 X ray Schalet 24, 29 Null *ry50 X ray Schalet 24, 29 Null *ry53 X ray Schalet 24, 29 Null ry54 X ray Schalet 8, 24, 29 In(3R)81;87D8-12; break between +1.9 and +2.6 kb; null *ry55 X ray Kernaghan 24, 29 Null ry56 X ray Kernaghan 8, 14, 24, Apparent point; non-complementing allele; null 29 ry57 X ray Kernaghan 8, 14, 24, Apparent point; non-complementing allele; null 29 ry58 X ray Kernaghan 8,14,24, Apparent point; non-complementing allele; null 29 ry59 X ray Kernaghan 8, 14, 24, Apparent point; non-complementing allele; null 29 ry60 X ray Kernaghan 7, 8, 14, 20, 1.1 kb deletion between +0.95 and +2.6 kb; 24,29 complementing allele; null ry61 X ray Kernaghan 14, 24, 29 Non-complementing allele; null ry62 X ray Kernaghan 8, 14, 24, Apparent point; missing Sst I site at +0.5 kb; 29 non-complementing allele; null ry63 X ray Kernaghan 14, 24, 29 Non-complementing allele; null ry64 X ray Kernaghan 8, 14, 24, In(3LR)64E;87D; breakpoint in +1.5 to +3.6; 29 1.9 to 3.0 kb deleted; non-complementing allele; null *ry65 X ray Kernaghan 24, 29 Null *ry67 X ray Kernaghan 24, 29 Null *ry68 X ray Kernaghan 24, 29 Null *ry69 X ray Kernaghan 24, 29 Null *ry71 X ray Kernaghan 24, 29 Null *ry72 X ray Kernaghan 24, 29 Null *ry73 X ray Kernaghan 24, 29 Null ry77y6 P Green 8 5 kb insertion (copia ?) between +1.9 and +2.6 kb; null ry102 / ray Chovnick 8, 14, 15, Apparent point; non-complementing allele; null 20, 26 ry103 / ray Chovnick 8, 14, 15, Apparent point; non-complementing allele; null 20, 26 ry105 / ray Chovnick 8 Apparent point; null ry106 / ray Chovnick 8, 14, 15, 5 kb insertion between +1.3 and +2.6 kb; 20, 26 non-complementing allele; null ry110 / ray Chovnick 8, 14, 15, Apparent point; non-complementing allele; null 20, 26 ry111 spont McCarron rye111 9, 15, 26 Electrophoretic variant at 3' end, probably at +3557 ry201 / ray Gelbart 8, 14, 15, Frameshift insert TT at +737; non-complementing 18, 20 allele; null ry203 / ray Gelbart 8, 14, 15, Apparent point; non-complementing allele; null 20 ry204 / ray Gelbart 8, 14, 15, Frameshift deletion of GCC -> GC at +685; 18, 20 non-complementing allele; null ry205 / ray Gelbart 8, 14, 15, Apparent point; non-complementing allele; null 20 ry206 EMS Gelbart 8, 14 Apparent point; non-complementing allele; null ry207 EMS Gelbart 8, 14, 20 Apparent point; complementing allele; null ry208 EMS Gelbart 8, 14 Apparent point; non-complementing allele; null ry209 EMS Gelbart 8, 14 Apparent point; non-complementing allele; null ry210 EMS Gelbart 8, 14 Apparent point; non-complementing allele; null ry211 EMS Gelbart 8 Apparent point; leaky - ry213 EMS Gelbart 8 Apparent point; leaky ry214 EMS Gelbart ryps214 1, 8, 14, Apparent point; leaky; XDH activity 24% normal 20 ry217 spont McCarron rye217 9, 14, 15, Electrophoretic variant at +736 20 ry218 EMS Gelbart ryps218 5, 8, 20 Apparent point; leaky ry219 EMS Gelbart ryps219 8, 20 Apparent point; leaky ry220 EMS Gelbart 8 Apparent point; null ry222 EMS Gelbart ryps222 8 Apparent point; 2% XDH activity; resistant to HPP and purine ry223 EMS Gelbart ryps223 5, 8, 20 Apparent point; leaky ry224 EMS Gelbart 8 Apparent point; leaky ry225 EMS Gelbart 8 Apparent point; leaky ry226 EMS Gelbart 8 Apparent point; leaky ry227 EMS Gelbart 8 Apparent point; leaky ry228 EMS Gelbart ryps228 5, 8 Apparent point; leaky ry230 spont McCarron rye230 9 Electrophoretic variant at +3557 ry301 EMS Gelbart 6-8, 14, 7.6 kb insertion (calypso) at +0.5 kb; 15, 20 non-complementing allele; null ry302 spont McCarron rye302 9, 15 Electrophoretic variant at +3557 ry303 spont McCarron rye303 15 Electrophoretic variant at +736 ry402 / ray Gelbart 1, 8, 15, 20 Apparent point; null ry404 EMS Gelbart 14 Non-complementing allele; null ry405 EMS Gelbart 1, 8, 14, Apparent point; non-complementing allele; null 20 ry406 EMS Gelbart 1, 7, 14, Complementing allele: G -> A at +451; null 27 ry407 EMS Gelbart ryps407 8 Apparent point; leaky ry408 spont McCarron rye408 9, 15 Electrophoretic variant at +3557 ry409H / spont McCarron ryi409 1, 4, 10, cis-acting control element site in intron 1 at -1145; 27 normal -> fatbody specific overproduction ry501 / ray Gelbart 8, 14, 15, Apparent point; complements ry606; null 20 ry502 / ray Gelbart 8, 14, 15, 3 bp deletion from +683 to +685 and insertion of an "A"; frameshift; non-complementing allele; null 18, 20 ry503 / ray Gelbart 8 Apparent point; null ry506 / ray Gelbart 7, 8, 14, 3.4 kb deletion between +1.1 and +5.0 kb; null 15, 20 ry507 spont McCarron 9, 14, 15, Electrophoretic variant at +736 20 ry508 spont McCarron rye508 9, 15 Electrophoretic variant at +3557 ry509 HN2 McCarron 18 Deletion of bases +626 through +698; frameshift; non-complementing allele; null ry516 ENU McCarron 18, 25 C -> T (Amber) at +1521; non-complementing allele; null ry523 ENU McCarron 23, 25 G -> A in 3' splice dinucleotide of intron 1 at -551; non-complementing allele; null ry531 DEB McCarron 18 G -> A at +3312; complements ry606; null ry537 ENU McCarron 7, 25 Deletion of 200-250 bp in Pvu II 2.55 kb fragment; non-complementing allele; null ry538 DEB McCarron 23 Deletion of 56 bp at -168 to -111; non-complementing allele; null ry544 ENU McCarron G1011 -> E 18, 25 G -> A at +2721; 75% CRM; non-complementing allele; null ry545 ENU McCarron 23, 25 G -> A in 3' splice dinucleotide of intron 1; non-complementing allele; null ry549 ENU McCarron 18, 25 T -> C at +3498; non-complementing allele; null ry553 ENU McCarron 18, 25 C -> T (Opal) at +816; non-complementing allele; null ry554 ENU McCarron 18, 25 G -> A (Amber) at +109; non-complementing allele; null ry556 TEM McCarron Non-complementing allele; null ry561 ENU McCarron 18, 25 T -> C at +846; non-complementing allele; null ry564 ENU McCarron 18, 25 C -> T (Amber) at +75; non-complementing allele; null ry569 ENU McCarron 25 85% CRM; non-complementing allele; null ry573 ENU McCarron 18, 25 G -> A at +3179; complements ry606; null ry601 EMS Gelbart 8, 14 Apparent point; null ry602 EMS Gelbart S357 -> F 8, 14, 18, C -> T at +478; complementing allele; leaky 20 ry603 EMS Gelbart 14 Non-complementing allele; null ry604 EMS Gelbart 8, 14 Apparent point; null ry605 EMS Gelbart 8, 14 Apparent point; new Sst I site at +1.7 or +4.1; null ry606 EMS Gelbart 1, 5, 7, G -> A at -468; complementing allele; null 8, 10, 14, 18, 20 ry607 EMS Gelbart 8, 14 Apparent point; null ry608 EMS Gelbart 8, 14 Apparent point; null ry609 EMS Gelbart 8, 14, 18, G -> A at +3506; complementing allele; null 20 ry610 EMS Gelbart 8 Apparent point; leaky ry611 EMS Gelbart ryps611 8, 14 Apparent point; leaky; XDH activity 1% normal ry612 EMS Gelbart ryps612 5, 8, 14, Apparent point; leaky; XDH activity 5% normal 20 ry613 EMS Gelbart 8 Apparent point; leaky ry621 spont McCarron rye621 9 Electrophoretic variant at +736 ry1001 EMS Gelbart 14 Non-complementing allele; null ry1002 EMS Gelbart 8, 14 Apparent point; null ry1003 EMS Gelbart 8, 14, 27 Apparent point; complementing allele; null ry1004 spont McCarron rye1004 9, 27 Electrophoretic variant at +1551 ry1005 / spont McCarron ryi1005 4, 10, 27 T -> C at -1701; normal -> underproducer; cis-acting control element ry1009 X ray O'Donnell 8 1.0 deletion between 0.95 and 2.6 kb; null ry1012 X ray O'Donnell 8 Apparent point; null ry1202 / ray Gelbart 8 Apparent point; null ry1302 / ray Gelbart 8 Apparent point; null ry1401 EMS Gelbart 8, 20 Apparent point; null ry1404 spont McCarron rye1404 Electrophoretic variant; slower than ry+10 ry1407 spont McCarron rye1407 9 Electrophoretic variant at +3557 ry1901 spont McCarron 8 Apparent point; null ry2101 P Chovnick 7, 8 copia insert at +0.3 kb; null ry5102 ENU McCarron 18, 25 G -> A at -1365; splice donor mutation; non- complementing allele; null ry5105 ENU McCarron 18, 25 G -> A (Opal) at +2683; non-complementing allele; null ry5106 ENU McCarron 25 20% CRM; non-complementing allele; null ry5107 ENU McCarron 25 80% CRM; non-complementing allele; null ry5115 ENU McCarron 18, 25 G -> A (Opal) at +110; non-complementing allele; null ry5117 ENU McCarron 18, 25 T -> C at -1364; splice donor mutation; non- complementing allele; null ry5122 ENU McCarron 18, 25 Deletion of 500-700 in 602 region plus 300 bp insertion of unknown material; non-complementing allele; null ry5135 ENU McCarron 18, 25 G -> A (Opal) at +2683; non-complementing allele; null ry5144 ENU McCarron 18, 25 C -> T (Opal) at +816; non-complementing allele; null ry5148 ENU McCarron 18, 25 C -> T (Amber) at +2573; non-complementing allele; null ry5163 ENU McCarron 18, 25, 28 C -> T (Amber) at +3626; 23 amino acids from 3' end; temperature sensitive; leaky ry5182 ENU McCarron 9, 23, 25 G -> A (new start) at -1435; 35% CRM; leaky ry5184 ENU McCarron 18, 25 C -> T at +3513; leaky ry5185 ENU McCarron 18, 25 G -> A at +466; 100% CRM; leaky ry5187 ENU McCarron 18, 25 G -> A at +3524; leaky ry5192 ENU McCarron 18, 25 A -> G at +213 (altered mobility 1.07); complementing allele; leaky ry5198 ENU McCarron 23, 25 C -> T at -225; 40% CRM; leaky ry5204 ENU McCarron 23, 25 T -> C at -1388 and a frameshift deletion of a T at -1386; leaky ry5205 ENU McCarron ryps5205 5, 18, 25 G -> A at +3486; 25% CRM; complementing allele; leaky ry5207 ENU McCarron 23, 25 rearrangement breakpoint near -1200 ry5208 ENU McCarron 23, 25 G -> A at -1366 (alters splice efficiency at exon 1/intron 1 junction); leaky ry5214 ENU McCarron 18, 25 T -> C at +3850 (mRNA processing?); 100% CRM; leaky ry5215 ENU McCarron 18, 25 C -> A at +43; about 35% CRM ry5220 ENU McCarron 18, 25 T -> C at -226; 15% CRM; leaky ry5231 ENU McCarron E89 -> K 18, 25 G -> A at -328; altered mobility -- slower than ry+5; 50% CRM; leaky ry5235 ENU McCarron 18, 25, 28 T -> C at +1539; 10% CRM; temperature sensitive; leaky ry5241 ENU McCarron 18, 25, 28 C -> T (Amber) at +1772; temperature sensitive; null` ry5252 ENU McCarron 18, 25 T -> C at -123; leaky ry5256 ENU McCarron 18, 25 C -> T (Amber) at +3221; null` ry5262 ENU McCarron 18, 25, 28 C -> T (Amber) at +3626 (23 amino acids from 3' end); 5% CRM; temperature sensitive; leaky ry5264 ENU McCarron 18, 25 G -> A at +1807; 10% CRM; leaky ry5281 ENU McCarron 18, 25 C -> T at -214; 50% CRM; leaky ry5322 ENU McCarron 18, 25 G -> A at +180; about 100% CRM; leaky ry5331 ENU McCarron 18, 25 G -> A (new start) at -1435; 40% CRM; leaky rya1 EMS Girton 16 Null rya2 EMS Girton 16 Null rya3 EMS Girton 16 Complementing allele; null rya4 EMS Girton 16 Complementing allele; null rya5 EMS Girton 16 Complementing allele; null rya6 EMS Girton 16 Null rya7 EMS Girton 16 Null rya8 EMS Girton 16 Complementing allele; null rya9 EMS Girton 16 Complementing allele; null rya10 EMS Girton 16 Complementing allele; null rya11 EMS Girton 16 Null ryL.12 EMS E. B. Lewis L.16608.12 14 non-complementing allele; null ryL.14 EMS E. B. Lewis L.16608.14 14 non-complementing allele; null ryL.18 EMS E. B. Lewis L.16608.18 14 non-complementing allele; null ryL.19 EMS E. B. Lewis L.16608.19 7, 14, 20 G -> A at +3332; complementing allele; null [ry+i4-1a] P Daniels 12, 13 ry+ P-element transposition to 57F; very reduced expression [ry+i4-1a-4] P Daniels 12, 13 ry+ P-element transposition to 68A; near normal expression [ry+72-1] P Daniels 12, 13 ry+ P-element transposition to 100D; reduced expression [ry+i77-1] P Daniels 12, 13 ry+ P-element transposition to 16D; reduced expression [ry+201-4] P Daniels 12, 13 ry+ P-element transposition to 43EF; elevated expression [ry+241-8] P Daniels 12, 13 ry+ P-element transposition to 76F; normal expression [ry+401.1] P Spradling 12, 13, 30 ry+ P-element transposition to 101; and Rubin variegated expression [ry+403.1] P Spradling 12, 13, 30 ry+ P-element transposition to 7D; and Rubin normal expression [ry+2216] P Daniels 11, 12, 13 ry+ P-element transposition to sd at 13F; normal expression [ry+2216-547] P McCarron 9, 11, 13 deletion internal to intron 1 from -1263 to -809; reduced fat body activity; leaky ( 1 = Chovnick, Gelbart, McCarron, Osmond, Candido, and Ballie, 1976, Genetics 84: 233-55; 2 = Chovnick, Schalet, Kernaghan, and Krauss, 1964, Genetics 50: 1245-59; 3 = Chovnick, Schalet, Kernaghan, and Talsma, 1962, Am. Nat. 96: 281-96; 4 = Clark, Daniels, Rushlow, Hilliker, and Chovnick, 1984, Genetics 108: 953-68; 5 = Clark, Hilliker, and Chovnick, 1986, Genet. Res. 47: 109-16; 6 = Clark, Hilliker, and Chov- nick, 1988, Genetics 118: 261-66; 7 = Clark, McCarron, Love, and Chovnick, 1986, Genetics 112: 755-67; 8 = Cote, Bender, Curtis, and Chovnick, 1986, Genetics 112: 769-83; 9 = Curtis and Bender (unpublished results); 10 = Curtis, Clark, Chov- nick, and Bender, 1989, Genetics 122: 653-61; 11 = Daniels, McCarron, Love, and Chovnick, 1985, Genetics 109: 95-117; 12 = Daniels, McCarron, Love, Clark, and Chovnick, 1986, Genetics 113: 265-85; 13 = Dutton and Chovnick, 1988, Dev. Biol. 5: 267-316; 14 = Gelbart, McCarron, and Chovnick, 1976, Genetics 84: 211-32; 15 = Gelbart, McCarron, Pandey, and Chovnick, 1974, Genetics 78: 869-86; 16 = Girton, Lo, and Bell, 1979, Can. J. Genet. Cytol. 21: 379-89; 17 = Glassman and Mitchell, 1959, Genetics 44: 153-62; 18 = Gray and Bender (unpublished results); 19 = Hadorn and Schwinck, 1956, Z. Indukt. Abstamm. Vererbungsl. 87: 528-53; 20 = Hilliker and Chovnick, 1981, Genet. Res. 38: 281-96; 21 = Hubby, 1961, DIS 35: 46; 22 = Hubby and Forrest, 1960, Genetics 45: 211-24; 23 = Lee, Curtis, McCarron, Love, Gray, Bender, and Chovnick, 1987, Genetics 116: 55-66; 24 = Lindsley and Grell, 1968, Carnegie Inst. Wash. Publ. No. 627; 25 = McCarron and Chov- nick, 1981, Genetics 97: s70-71; 26 = McCarron, Gelbart, and Chovnick, 1974, Genetics 76: 289-99; 27 = McCarron, O'Donnell, Chovnick, Bhullar, Hewitt, and Candido, 1979, Genetics 91: 275-93; 28 = Reaum and Chovnick (unpublished results); 29 = Schalet, 1964, DIS 39: 62-64; 30 = Spradling and Rubin, 1982, Science 218: 341-47. | +1 of the nucleotide sequence defined as the second base pair in an EcoRI site in the second exon; transcription from left to right. / Additional description below. ` Adult eye color is not the same as in most null mutants. Some residual XDH activity may be present. - Leaky = hypomorph. cytology: Placed in 87D8-12 based on Df(3R)ry74 = Df(3R)87D4;87D12 and in 87D11-12 based on in situ hybridiza- tion with radioactively-labelled ry DNA probe (Lefevre, 1971, DIS 46: 40; Spierer, Spierer, Bender, and Hogness, 1983, J. Mol. Biol. 168: 35-50) and with biotin labelled ry DNA probe [Duttaroy, 1988, (unpublished results)]. molecular biology: Gene sequence originally included in a 315- kb walk in region 87D-E (Bender, Spierer, and Hogness, 1983, J. Mol. Biol. 168: 17-33). Location of ry restricted to region between the right breaks of Df(3R)karIG27 between coor- dinates -191 and -187 kb and Df(3R)ry36 between -166 and -163.5 kb (Spierer, Spierer, Bender, and Hogness, 1983, J. Mol. Biol. 168: 35-50). A group of ry mutants with molecular lesions were confined to 4 kb between -171 and -167 kb; 0 on the nucleotide map is within an EcoRI restriction site at -171 kb (Clark, McCarron, Love, and Chovnick, 1986, Genetics 112: 755-67; and Cote, Bender, Curtis, and Chovnick, 1986, Genetics 112: 769-83). The genomic sequence has been cloned and sequenced (Lee, Curtis, McCarron, Love, Gray, Bender, and Chovnick, 1987, Genetics 116: 55-66; Keith, Riley, Kreitman, Lewontin, Curtis, and Chambers, 1987, Genetics 116: 67-73). The gene is transcribed from the centromere (proximal to distal) and comprises four exons and three introns; exon one is at least 179 bp in length; it contains the ATG codon and encodes the first fourteen amino acids. The codon for Lys14 is followed by an 815 bp intron (coordinates -1365 to -551). Exon 2 begins at nucleotide -550 with the codon for Val15 and extends for 2601 base pairs encoding 867 amino acids ending in Ser881. Intron 2 contains 281 base pairs from 2052 to 2332. Exon 3 is 1314 base pairs in length and encodes 438 amino acids from Val882 to Leu1319. Finally, intron 3 extends from base pair 3647 through 3711 and is followed by the 3' exon beginning with Leu1320 and ter- minating at the carboxyl end with Pro1335 at nucleotide 3759. Seven conservative nucleotide substitutions noted between the Canton-S genomic sequence and Oregon-R cDNA sequences. The molecular biology of ry alleles (listed according to their position on the DNA map of the locus) is summarized in the table on the next page. other information: The locus has been extensively mapped by reciprocal recombination and conversion studies (see appended maps). Seven different classes of complementing or partially complementing alleles described; complementation map circular (Gelbart, McCarron, and Chovnick, 1976, Genetics 84: 211-32). ry+ commonly used as a marker in P-element transformation experiments (Spradling and Rubin, 1982, Science 218: 341-47; Rubin and Spradling, 1982, Science 218: 348-53). allele position ( molecular biology | ______________________________________________________________________________ ry1005 -1701 TC; normal->underproducer; 50% CRM ry5331 -1435 G->A; GTG->ATG (new start); 40% CRM; leaky ry5182 -1435 G->A; GTG->ATG (new start); 35% CRM; leaky ry5204 (-1382/-1386) TTTTT->TTTT (frameshift deletion of and 1388 one base) and T->G; produces TGA stop in the new frame two codons downstream; leaky ry5208 -1366 G->A; AAG->AAA (no amino acid change); alters splice efficiency of exon 1/intron 1 junction; leaky ry5102 -1365 G->A; GT->AT (splice donor mutation); null ry5117 -1364 T->C; GT->GC (splice donor mutation); null ry[2216-547] -1263 deletion internal to intron 1 from -1263 1263 to -809; reduced fat body activity activity ry5207 rearrangement breakpoint near -1200 ry409 -1145 G->C; normal->overproducer; fat body specific ry545 -551 G->A; AG->AA (3' splice dinucleotide); null ry523 -551 G->A; AG->AA (3' splice dinucleotide); null ry606 -468 G->A; GGA->GAA (Gly->Glu); null; complementing allele ry5231 -328 G->A; GAG->AAG (Glu->Lys); electrophoretic variant; slower than ry+5; leaky ry5220 -226 T->C; TTC->CCC (Ser->Pro); 15% CRM; leaky ry5198 -225 C->T; TCC->TTC (Ser->Phe); 40% CRM; leaky ry5281 -214 C->T; CTT->TTT (Leu->Phe); 50% CRM; leaky ry538 -168 deletion through -111; frameshift; null ry5252 -123 T->C; CTC->CCC (Leu->Pro); leaky ry5215 +43 C->A; CCG->CAG (Pro-Gln); 35% CRM; leaky ry564 +75 C->T; CAG->TAG (Gln->Amber); null ry554 +109 G->A; TGG->TAG (Trp->Amber); null ry5115 +110 G->A; TGG->TGA (Trp->Opal); null ry5322 +180 G->A; GGC->AGC (Gly->Ser); 100% CRM; leaky ry5192 +213 A->G; AAG->GAG (Lys->Glu); electrophoretic variant; faster than ry+5; leaky ry5 +294 deletion through +312; frameshift yielding two downstream stop codons; null; non-complementing allele ry2101 copia insert at +0.3 kb; null ry406 +451 G->A; GGA->GAA (Gly->Glu); null; complementing allele ry5185 +466 G->A; GGC->GAC (Gly->Asp); 100% CRM; leaky ry602 +478 C->T; TCC->TTC (Ser->Phe); leaky ry5122 +500 deletion of 500-700 bp in 602 region, plus insertion of 300 bp of unknown material; null ry301 7.6 kb calypso insert at 0.5 kb; null; non-complementing allele ry62 apparent point mutation; missing SstI site at +508; null; non-complementing allele ry509 +626 deletion through +698; frameshift; null ry502 +683 deletion through +685 and A insertion yielding a net two base deletion frameshift; null; non-complementing allele ry204 +685 deletion of C; GCC->GC; frameshift; null ry507 +736 A; CAC (His); electrophoretic variant; faster than ry621 ry217 +736 electrophoretic variant, same mobility as ry507 ry303 +736 electrophoretic variant, same mobility as ry507 ry621 +736 A->G; CAC->CGC (His->Arg); electrophoretic variant; slower than ry507 ry201 +737 TT insertion; frameshift; null ry5144 +816 C->T; CGA->TGA (Arg->Opal); null ry553 +816 C->T; CGA->TGA (Arg->Opal); null ry561 +846 T->C; TGG->CGG (Trp->Arg); null ry1 deletion of 0.1 kb SstI site at +940 ry8 +1283 deletion through +1299; frameshift; null ry537 deletion of 200-250 bp in PvuII 2.55 kb fragment; null ry516 +1521 C->T; CAG->TAG (Gln->Amber); null ry5235 +1539 T->C; TCC->CCC (Ser->Pro); 10% CRM leaky; temperature sensitive ry1004 +1551 G->A; GAC->AAC (Asp->Asn); electrophoretic variant ry5241 +1722 C->T; CAG->TAG (Gln->Amber); null;/ temperature sensitive ry5264 +1807 G->A; GGA->GAA (Gly->Glu); 10% CRM; leaky ry42 +2030 deletion of 16 bp and insertion of 7 bp of non-rosy DNA yielding a net 9 bp "in frame" deletion; no CRM ; null; complementing allele ry3 B104 insert at 2.2 kb; leaky ry5148 +2573 C->T; CAG->TAG (Gln->Amber); null ry5105 +2683 G->A; TGG->TGA (Trp->Opal); null ry5135 +2683 G->A; TGG->TGA (Trp->Opal); null ry544 +2721 G->A; GGA->GAA (Gly->Glu); null ry26 +2804-5 GG->T; GGAG->TAG [Gly->(frameshift) Amber]; null ry41 +3095 deletion through +3097; Gly codon lost; null ry573 +3179 G->A; GGA->AGA (Gly->Arg); null ry2 B104 insert at +3.2 kb; null; complementing allele ry5256 +3221 C->T; CAG->TAG (Gln->Amber); null/ ry531 +3312 G->A; GGC->GAC (Gly->Asp); null; complementing allele ryL19 +3332 G->A; GAG->AAG (Glu->Lys); null; complementing allele ry5205 +3486 G->A; GGT->GAT (Gly->Asp); 25% CRM; leaky; complementing allele ry549 +3498 T->C; CTC->CCC (Leu->Pro); null ry609 +3506 G->A; GGA->AGA (Gly->Arg); null ry5184 +3513 C->T; TC->TTT (Ser->Phe); leaky ry5187 +3524 G->A; GCC->ACC (Ala->Thr); leaky ry508 +3557 G; GAT (Asp); electrophoretic variant; faster than ry230 ry302 +3557 electrophoretic variant; same mobility as ry508 ry408 +3557 electrophoretic variant; same mobility as ry508 ry1407 +3557 electrophoretic variant; same mobility as ry508 ry230 +3557 G->A; GAT->AAT (Asp->Asn); electrophoretic variant; slower than ry508 ry5163 +3626 C->T; CAG->TAG (Gln->Amber) 23 amino acids from 3' end; leaky ry5262 +3626 C->T; CAG->TAG (Gln->Amber) 23 amino acids from 3' end; 5% CRM; leaky; temperature sensitive ry5214 +3850 T->C; ATGTTTT->ATGCTTT; 100% CRM; leaky ( Positions are relative to the EcoRI site in exon 2. | The molecular biology was referenced from one or more of the following: Curtis and Bender (unpublished results); Curtis, Clark, Chovnick and Bender, 1989, Genetics 122: 653-61; Gray and Bender (unpublished results); Lee, Curtis, McCar- ron, Love, Gray, Bender, and Chovnick, 1987, Genetics 116: 55-66. / Adult eye color is not the same as in most null mutants. Some residual XDH activity might be present. # ry409 phenotype: Designation applied to the site at -1145 in ry+4 that is responsible for the higher than normal XDH CRM of that allele (i.e., ry409H vs. ry409N, the normal alternative; Curtis, Clark, Chovnick, and Bender, 1989, Genetics 122: 653-61). Enzyme activity two to three times that of other ry+ alleles (Chovnick, Gelbart, McCarron, Osmond, Can- dido, and Baillie, 1976, Genetics 84: 223-55); large tissue- specific increase in specific activity observed in late third-instar larval fat body, but not Malpighian tubules; mRNA levels 3.2 times higher than normal (Covington, Fleenor, and Devlin, 1976, Genetics 84: 211-32; see also Clark, Daniels, Rushlow, Hilliker, and Chovnick, 1984, Genetics 108: 953-68). Maps genetically to the right of ry1005 (Clark et al., 1984). # ry1005 phenotype: Designation applied to the site at -1701 in ry+10 that is responsible for the lower than normal XDH CRM of that allele (i.e., ry1005L vs. ry1005N, the normal alternative) (Curtis, Clark, Chovnick, and Bender, 1989, Genetics 122: 653-61). Enzyme levels 50% those of other normal alleles (McCarron, O'Donnell, Chovnick, Bhullar, Hewitt, and Candido, 1979, Genetics 91: 275-93); mRNA levels 52% normal (Coving- ton, Fleenor, and Devlin, 1976, Genetics 84: 211-32). Maps genetically to the left of ry409 (Clark, Daniels, Rushlow, Hilliker, and Chovnick, 1984, Genetics 108: 953-68). molecular biology: ry+10 sequenced from nucleotides -2105 to -260; 25 differences from the corresponding sequence of ry+5 noted; none could be associated with the difference in tran- scription levels (Lee et al, 1987).