# bi: bifid location: 1-6.9. discoverer: Morgan, 11k. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 28 (fig.). phenotype: Longitudinal veins fused at base of wing into bifid stalk. L3 delta-like at tip; L4 often incomplete at tip. Wing margins often excised at tip of L4. Wings spread in pro- portion to their shortness. High temperature enhances and low temperature produces overlapping of wild type. Stronger in male than in female. Hypomorphic allele; females heterozygous for bi and a deficiency for bi have outspread, crumpled, and very flimsy wings with an extreme bifid fusion of the basal regions of the longitudinal wing veins (Craymer and Roy, 1980, DIS 55: 204). Enhances Bx alleles as well as sd, cp, and vgnp (Waletzky). RK1. alleles: *bi35 (CP627). cytology: Placed in 4C5-6 based on its inclusion in Df(1)rb13 = Df(1)4C5-6;4D3-E1 but not in Df(1)GA56 = Df(1)4C5-6;4D1, as well as the bi phenotype of T(1;2)biD2 = T(1;2)4C5-6;46B5-7 and T(1;3)biD1 = T(1;3)4C5-6;65C3-5. (Banga, Bloomquist, Brod- berg, Pye, Larrivee, Mason, Boyd, and Pak, 1986, Chromosoma 93: 341-46). # bib: big brain location: 2-34.7. references: Lehmann, Dietrich, Jimenez, and Campos-Ortega, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 226-29. Lehmann, Jimenez, Dietrich, and Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 62-74. phenotype: Recessive embryonic lethal, a neurogenic mutant. Homozygotes fail to form ventral, lateral, and most of the cephalic epidermis. Central nervous system hypertrophied by recruitment of presumptive epidermal cells, but exhibiting considerable architectural normality. Most epidermal sense organs can be recognized in electron microscope preparations; chordotonal organs prevalent but with abnormal structures, perhaps owing to disrupted attachment. Supernumerary peri- pheral elements formed by recruitment of presumptive epidermal cells [Hartenstein and Campos-Ortega, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 210-21 (fig.). Cuticular clones of cells homozygous for bib1 or bib6 exhibit normal development (Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32). Effects on central nervous system intermediate with respect to mutations at other neurogenic loci. Insensitive to changes in dosage of other neurogenic genes (de la Concha, Dietrich, Weigel, and Campos-Ortega, 1988, Genetics 118: 499-508). alleles: Eight alleles with similar phenotypes. allele origin discoverer synonym ref ( _________________________________________________________________ bib1 EMS Nusslein-Volhard bibID05 1, 2, 3 and Wieschaus bib2 EMS Nusslein-Volhard bibIJ66 3 and Wieschaus bib3 EMS Nusslein-Volhard bibIIP39 3 and Wieschaus bib4 EMS Nusslein-Volhard bibIIV46 3 and Wieschaus bib5 EMS Nusslein-Volhard bibIIID118 3 and Wieschaus bib6 EMS Nusslein-Volhard bib6N37 3 and Wieschaus bib7 X ray Campos-Ortega bibFX1 3 bib8 | X ray Lehmann bibC7A 3 ( 1 = Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32; 2 = Hartenstein and Campos-Ortega, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 210-21 (fig.); 3 = Lehmann, Jimenez, Dietrich and Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 190: 226-29. | Associated with In(2L)30A9;30F. cytology: Placed in region 27D-31E based on the lethal pheno- type of the deficient segregant from T(Y;2)B231 in combination with bib. In(2L)bib8 = In(2L)30A9;30F further restricts posi- tion to 30A9-F (Campos-Ortega). molecular biology: Gene cloned and sequenced; conceptual amino-acid sequence indicates a gene product with 700 amino acids. The predicted bib product shows significant sequence similarity to a family of transmembrane proteins, some of which form channels permeable to small molecules (Rao, Jan, and Jan, 1990, Nature 345: 163-67). # bic: bicaudal location: 2-67.0 (inferred from cytological position; maps to 68 with respect to Bl and L, but penetrance problems introduce uncertainty). origin: Spontaneous. references: Bull, 1966, J. Exp. Zool. 161: 221-42 (fig.). Nusslein-Volhard, 1977, Wilhelm Roux's Arch. Dev. Biol. 183: 249-68 (fig.). 1979, Symp. Soc. Dev. Biol. 37: 185-211 (fig.). phenotype: Homozygous bic females produce variable numbers of eggs that fail to hatch (e.g., 25-50%). bic/Df(2R)vgB females produce higher embryonic mortality. Males of either genotype are normal. A wide array of developmental anomolies observed among arrested embryos. Many fail to show outward signs of initiation of development, although in at least some zygotes nuclear divisions can be demonstrated. Others show replace- ment of anterior embryonic segments by a mirror-image set of posterior segments. The majority of these bicaudal embryos are symmetrical with opposing sets of the two to five posterior-most segments; mirror-imaged structures include den- ticle belts, posterior spiracles, Malpighian tubules, genital disc, and posterior midgut invagination. Polar cells form at the original but not the duplicated posterior end. Asymmetri- cal bicaudal embryos such as 3/6 or 3/7 have fewer duplicated than original posterior segments. Other embryos have the head replaced by posterior abdominal structures or show abnormal development of the cephalopharyngeal apparatus. Finally, some embryos are foreshortened and seem to lack internal segments. Maximum production of bicaudal embryos occurs in the first eggs produced by females developing at 28-29. The incidence of bicaudal embryos falls rapidly during the first 60 hr after eclosion. Incidence of bicaudal embryos and nondeveloping eggs depends on genotype: bic/Df(2R)vgB > bic/Df(2R)vgD > Df(2R)vgB/+ > bic/bic > bic/+ = 0. alleles: bic44 (Basel). cytology: Placed between 49D3 and 49E6 based on the absence of normal allele in Df(2R)vgB = Df(2R)49D3-4;50A and Df(2R)vgD = Df(2R)49C1-2;49E2-6. # BicC: Bicaudal C location: 2-52.0. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Jurgens, 1982, Verh. Dtsch. Zool. Ges. 91-104. Mohler and Wieschaus, 1986, Genetics 112: 803-22. phenotype: A maternal-effect semilethal; the majority of embryos produced by BicC/+ mothers given rise to normal larvae a minority fail to hatch and vary in phenotype. Double- abdomen embryos have a normal posterior end and the anterior end replaced by mirror image series of posterior segments, e.g. A8-A4|A4-A8 to A8-A6|A6-A8; they need not have the same number of segments on either side of the reversal of polarity, the duplicated portion having fewer segments; generally more segments seen ventrally than dorsally. Less severely affected embryros may be headless, or with reduced mouth parts, or even normal appearing but failing to hatch. The incidence and severity of abnormal embryos vary with genetic background and temperature, the incidence being highest at 25 and decreasing at lower and higher temperatures. The majority of the embryos produced by BicC/BicD trans heterozygotes are abnormal. Homozygotes are abnormal. Homozygous BicC females sterile, germ-cell differentiation blocked at the beginning of vitello- genesis. Follicle cells do not invade between oocyte and nurse cells; they do synthesize a chorion which remains open ended like a chalice or a cup; such eggs never fertilized. alleles: Five ethyl-methanesulfonate-induced alles; BicC3 and BicC5 more severe than the others. allele discoverer synonym ref ( ______________________________________________________ BicC1 BicCIIF34 1, 2 BicC2 Nusslein-Volhard BicCC96 1 BicC3 Schupbach BicCRU35 1 BicC4 Schupbach BicCWC45 1 BicC5 BicCYC33 1, 2 ( 1 = Mohler and Wieschaus, 1986, Genetics 112: 803-22; 2 = Nusslein-Volhard, Wieschaus, and Jurgens, 1982, Verh. Dtsch. Zool. Ges. 91-104. cytology: Placed in 35D4-E6 based on the sterility of females carrying BicC and heterozygous for Df(2L)osp29 = Df(2L)35B3;35E6 but not Df(2L)75c = Df(2L)35A1-2;35D4-7 (Mohler and Wieschaus). # BicD location: 2-52.91 (to the right of dl; based on an estimated four recombinants between dl and BicD out of 4,000 tests). references: Nusslein-Volhard, Wieschaus, and Jurgens, 1982, Verh. Dtsch. Zool. Ges. 91-104. Mohler and Wieschaus, 1986, Genetics 112: 803-22. Steward and Nusslein-Volhard, 1986, Genetics 113: 665-78. Suter, Romberg, and Steward, 1989, Genes Dev. 3: 1957-68. Wharton and Struhl, 1989, Cell 59: 881-92. phenotype: A maternal-effect semilethal; substantial numbers of embryos produced by BicD/+ mothers give rise to normal larvae; the remainder fail to hatch and vary in phenotype. The array of phenotypes encountered is the same as that produced by BicC/+ females. The incidence and severity of abnormal embryos vary with genetic background and temperature, the incidence being highest at 18, and decreasing at higher tem- peratures. BicD homozygotes, either homoallelic or heteroal- lelic, and BicC/BicD heterozygotes are female fertile, although producing eggs with fused or reduced chorionic appendages; the majority of their embryos are abnormal and the influence of temperature, if any, obscure. BicD/+/+ duplication-bearing females produce few if any abnormal embryos, whereas BicD/Df(2L)TW119 females produce more abnor- mal embryos than BicD/+, i.e., with respect to the severity of phenotype, BicD/0 > BicD/+ > BicD/+/+; however, simply a defi- ciency of BicD product does not account for the abnormal phenotype, since embryos produced by females carrying one dose of BicD+ over a deficiency develop normally. Embryos produced by homozygous BicD females display symmetrical patterns of cad+ polypeptide distribution during early development (Mlod- zik and Gehring, 1987, Cell 48: 465-78). Abnormal embryo production by BicD/+ females enhanced by the heterozygosity for the mutant allele of or deficiency for l(2)49; Mohler and Wieschaus speculate that l(2)49 is an allele of bic In addition, eg, stau, tor, and trk, maternal- effect mutants that affect early anterior but not posterior development, act as dominant enhancer of BicD; other maternal-effect mutants ineffective. Bicaudal embryos exhibit nanos protein at both anterior and posterior poles and the absence of hunchback protein in both ends of the embryo; embryos produced by BicD1/BicD2;osk/osk females do not express nos; display a burst of anterior, bcd- dependent hb expression not seen in bicaudal embryos, which is correlated with a dramatic expansion of kni expression (abdom- inal) and failure to express Kr (thorax and anterior abdomen). BicD expressed early in oogenesis; in wild type, protein first appears in the cytoplasm of all cells in 16-cell cysts in the middle of the germarium; upon entering the vitellarium, pro- tein begins to accumulate in the oocyte and continues to do so for as long as observations are possible. The early embryos produced by such females show uniform distribution of BicD protein, which becomes localized to the cortical cytoplasm at blastoderm formation; anterior-to-posterior distribution remains uniform. Protein disappears at gastrulation. In BicD1/BicD2 females protein accumulation in the oocyte is precocious and greater than normal and the adjacent nurse cells may become visibly depleted; in the embryo, the protein appears to be concentrated as a cap over the anterior third and uniformly less concentrated in the remainder of the embryo. BicDrv1 females display extreme concentration of pro- duct in the presumptive oocyte and virtually none in the nurse cells; however, the presumptive oocyte never develops as an oocyte but remains nurse-cell like until the cyst degenerates. alleles: allele origin synonym ref ( comments ______________________________________________________________________ BicD1 EMS BicD71.34 3 TTC -> ATC = lys224 -> glu BicD2 EMS BicDIIIE48 3 GAG -> AAG = ile684 -> phe BicDr BicDPA66 2 recessive female sterile allele BicDrv1 X ray BicD7134R26 1, 3 recessive female sterile; revertant of BicD1; deletion of residues 376-379 superimposed on BicD1 lesion ( 1 = Mohler and Wieschaus, 1986, Genetics 112: 803-22; 2 = Suter, Romberg, and Steward, 1989, Genes Dev. 3: 1957-68. 3 = Wharton and Struhl, 1989, Cell 59: 881-92. cytology: Placed in 36C2-D1 based on its inclusion in Df(2L)TW137 = Df(2L)36C2-4;37B9-C1, but not Df(2L)VA18 = Df(2L)36C4-D1;37C2-D1 (Steward and Nusslein-Volhard). molecular biology: The gene has been cloned and sequenced (Suter, Romberg, and Steward, 1989, Genes Dev. 3: 1957-68; Wharton and Struhl, 1989, Cell 59: 881-92); identified by transformation rescue of BicDrv1 female sterility. Two tran- scripts found in early embryos of 3.6 and 4.0 kb (Wharton and Struhl; 3.8 and 4.4 kb according to Suter et al.), which differ only in their 3 untranslated regions; transcription occurs from right to left. Gene contains at least eight exons; encodes a polypeptide of 782 amino acids and ~89 kd molecular mass; pI = 4.93. Sequence similar to that of the C-terminal half of myosin-heavy-chain polypeptides, and simi- lar coiled-coil molecules, which contain long ( helices that form double- or triple-chain coils. These species contain an underlying heptad amino-acid repeat in which residues one and four are generally hydrophobic; about half of the BicD protein comprises such heptad repeats. other information: Mohler and Wieschaus describe a polygenic strain, designated YC67 that parallels the behavior of BicD in all respects except that it is unmappable. # BicF location: 3- (unmapped). references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Dominant maternal effect giving bicaudal embryos in some genetic backgrounds (e.g., with In(2LR)O, Cy l(2)DTS513. High temperatures and short egg shape may enhance this effect. Homozygous phenotype is probably collapsed eggs. # bie: bientot (T. Schupbach) location: 2-97. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect female-strile mutant; homozygous females lay eggs which show no visible signs of development when observed under transmitted light in a stereo microscope. These eggs are defective in fertilization or very early embryonic development. biePV sometimes gives rise to embryos which form irregular blastoderms and develop abnormally, pro- ducing fragmented pieces of cuticle. alleles: Three, bie1 - bie3 isolated as RD, PV, and SD, respec- tively. # bifid: see bi # big brain: see bib # Billa: see Fs(2)Sz2 # bip: bipolar oocyte location: 3-10. origin: Induced by ethyl methanesulfonate. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Female sterile; no eggs laid. Oocytes often have nurse-cell clusters at both ends (15 nurse cells altogether). Mature oocytes can have micropiles at both ends, no dorsal appendages and no polarity. # bis: bistre location: 1-21+ (T. K. Johnson). origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 67. phenotype: Very dark brown eye color; ocelli also dark. Wings frequently unexpanded. Males sterile, but homozygous females fertile (T. Johnson). Viability varies from less than 10% to 70% wild type. RK2A. cytology: Placed between 7B5 and 9 by Lefevre. #*Bit: Bitten location: 3- (not located; crossing over between ru and th almost completely suppressed). origin: X ray induced. discoverer: Lefevre, 48g5. references: 1949, DIS 23: 58. phenotype: Inner margin of wing indented. Wings, normally folded, appear to have had a bite taken out of the back. Mar- ginal hairs present unlike N and ct. Flight is impeded, although little wing area lost. Homozygous lethal. RK1A. cytology: Associated with In(3L)Bit; breakpoints not deter- mined. # bithorax: see bx under BXC # Bithoraxlike: see Ubx under BXC # bithoraxoid: see bxd under BXC # Bitten: see Bit #*bk: buckled location: 1-59.8. origin: Induced by p-N,N-di-(2-chloroethyl)amino- phenylethylamine (CB. 3034). discoverer: Fahmy, 1955. references: 1959, DIS 33: 83. phenotype: Wings slightly altered in shape and frequently divergent; membranes warped between longitudinal veins. Veins slightly thickened at wing margins. Eye shape slightly altered. Scutellar bristles frequently abnormal, either inserted in base atypically, bent, or duplicated. Males viable and fertile. RK3. alleles: *bk2 (CP627). # Bkd: Blackoid location: 2-65 (Braun). origin: Spontaneous. discoverer: Goldschmidt, 1938. phenotype: Body color black in homozygote, distinctly darker than wild type in heterozygote. RK2. alleles: *Bkd1 (spontaneous, Goldschmidt, 1938); BkdM (induced by ethyl methanesulfonate + formaldehyde, Marsh and Mack, 1985, DIS 61: 214); allelism of BkdM inferred from phenotype and position between cn and c. #*bkl: buckledlike location: 1-59.9. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1955. references: 1959, DIS 33: 83. phenotype: Wings slightly divergent with membranes warped between longitudinal veins, which themselves are often slightly thickened. Abnormally-shaped eyes, frequently compressed dorsoventrally. Both sexes viable and fertile. RK3. other information: Probably a complementing allele of bk. One X-ray-induced allele. # Bl: Bristle location: 2-54.8 (crossing over may be reduced). origin: Spontaneous. discoverer: R. L. King, 25d11. references: 1927, Biol. Bull. 53: 465-68. phenotype: Bristles one-half to two-thirds normal length, blunt, thicker, and beaded in outline. Posterior scutellars often cross and adhere to body. Eyes somewhat larger and rougher. Overlaps wild type when reared at 20 (Ashburner). Probably affects nature of bristle secretion, particularly outer layer [Lees and Waddington, 1942, DIS 16: 70; Lees and Picken, 1945, Proc. Roy. Soc. (London), Ser. B 132: 396-423 (fig.)]. Viability of heterozygote is good but erratic; homozygotes usually lethal; survivors female sterile with roughish eye character. RK1 as dominant. alleles: *Bl30 and *Bl31 (Plough and Ives, 1935, Genetics 20: 42-69). cytology: Between 38A6 and 38E9 based on inclusion within Df(2L)TW2 = Df(2L)37D2-E1;38E6-9 but not Df(2L)TW9 = Df(2L)37E2-F4;38A6-C1 or Df(2L)TW158 = Df(2L)37B2-8;37E2-F4 (Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85). #*bla: bladderwing location: 1-43.2. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 67-68. phenotype: Wings grossly deformed, small, and normally full of fluid. Eyes slightly abnormal in shape. Males fertile; females sterile. Viability about 50% wild type. RK3. # Bla: see nwB # black: see b # Black cells: see Bc # black leg: see bleg # Blackoid: see Bkd # bladderwing: see bla # Blastoderm-specific gene: see Bsg # blc: blocked (T. Schupbach) location: 2-43. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female-sterile; homozygous females often have under- developed ovaries which seem to lack germ cells altogether. In some females a small number of developing egg chambers is found; may contain abnormal numbers of nurse cells, and never develop beyond the first few stages of oogenesis. alleles.: blcWE = blc1, blcHM. # bld: bald location: 3-48.1 (in 3R to the left of Ki). origin: Induced by ethyl methanesulfonate; detected by the presence of X-ray-induced somatic spots in the progeny of treated males. references: Garcia-Bellido and Dapena, 1974, DIS 50: 179. 1974, Molec. Gen. Genet. 128: 117-30. phenotype: Homozygous lethal (lethal may be independently induced); not cell lethal. In homozygous cuticular spots, chetae, trichomes and cuticle appear depigmented and transparent; trichomes long, thin, and wooly. RK1 as a marker for cuticular clones. # Bld: Blond location: 1- or 2- (associated with rearrangement). origin: Spontaneous in chromosome containing In(2R)Cy. discoverer: Burkart, 1930. references: 1931, Rev. Fac. Agron. Vet. Univ. Buenos Aires 7: 393-491. Burkart and Stern, 1933, Z. Indukt. Abstamm. Vererbungsl. 64: 310-25 (fig.). phenotype: Bristles of heterozygote are gleaming yellow at tips and for varying lengths of more basal regions. Hairs not much paler and bristles of abdomen only slightly affected. Larval mouth parts wild type. No overlap. ERG normal [Hotta and Benzer, 1969, Nature (London) 222: 354-56]. Viability and fertility excellent. Most available T(1;2)Bld chromosomes carry a lethal in 2R; lethal easily separated from translocation by recombination in T(1;2)Bld/In(2R)Cy females. cytology: Associated with T(1;2)Bld = T(1;2)1B13-C1;60B12-13 (Lefevre). other information: Bld phenotype associated with the 2RDXP ele- ment of the translocation. # Ble: Barlike eye location: 3-94. origin: X ray induced. discoverer: Crowell, 57i. references: Meyer, 1958, DIS 33: 97. phenotype: Eye shape indistinguishable from Bar. Expression of Ble/+ varies, best at 26. Excellent expression in homozygote at all temperatures. Ble/Ble in combination with B results in an extremely narrow eye. RK1. other information: If Ble represents a transposition of the Bar locus to chromosome 3, the flanking loci of f+ and od+ have not been transposed. Also against transposition is absence of sexual dimorphism that dosage compensation of B should produce in such a case. #*bleg: black leg location: 3- (near p). discoverer: Bridges, 16b23. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 158. phenotype: Legs black; body color pallid; wings flimsy. RK3. # blistered: see bs # Blisterlike: see Bsl # blistery: see by # blo: bloated location: 2-58.5. origin: Recovered among descendants of heat-treated flies. discoverer: Ives, 33f26. synonym: Originally referred to as ba2: balloon and ba33f26. references: Plough and Ives, 1934, DIS 1: 33. 1934, DIS 2: 10. 1935, DIS 3: 6. Bridges, Skoog, and Li, 1936, Genetics 21: 788-95. phenotype: Wings spread, crumpled, and vesiculated; wing shows irregular plexus of extra veins. In extreme cases, wings unexpanded. Occasional hooked or wavy bristles. Developmen- tal studies by Waddington [1939, Proc. Nat. Acad. Sci. USA 25: 299-307 and 1940, J. Genet. 41: 75-139 (fig.)] show intervein material spongy and veins swollen with inadequate contraction after inflated stage of pupal wing. Droplets of hemolymph often become clothed with cells liberated from epithelium and remain along basal processes. Does not overlap wild type but has poor viability and hatches later. RK2. cytology: Not included within and does not recombine with (0/1098) Df(2R)Np = Df(2R)44F1-2;45E1-2 (Bridges, Skoog, and Li, 1936). # blocked: see blc # Blond: see Bld # blot: see apblt #*blt: ballet location: 1- (not located). origin: X ray induced. discoverer: Iyengar. references: 1962, DIS 36: 38. phenotype: Wings one-third the normal length, stretched outward and slightly upward; wing tip broadened; venation markedly altered as in fused. Male viability impaired; females almost completely lethal. RK2. # blt: see apblt #*blu: blunt location: 3- (near ru). origin: Spontaneous. discoverer: Walbrunn, 46j23. references: 1947, DIS 21: 71. phenotype: Wings slightly shorter and broader than normal, giv- ing a squared appearance. Sometimes difficult to classify. RK3. # Blunt short bristle: see Bsb # bly: bellyache location: 1-28.3. origin: Induced by ethyl methanesulfonate. references: Eberl and Hilliker, 1988, Genetics 118: 109-20. phenotype: Recessive lethal. Dispersed or poorly formed Mal- pighian tissue and often a yolk plug; cuticle appears normal. alleles: Two putative alleles, bly1 and bly2; isolated as l(1)EH290 and l(1)EH740a. #*bn: band location: 3-72. origin: Spontaneous. discoverer: Morgan, 12g. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 79 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 215 (fig.), 218. phenotype: Trident pattern and scutellum darker with dark transverse band across anterior portion of mesonotum. Thorax vacuolated; hairs on thorax sparse and directed medially in bowed lines. RK2. # bo: bordeaux location: 1-12.5. discoverer: Nazarenko. phenotype: Eye color dark wine; not completely separable from wild type. Transplantation indicates bo may be nonautonomous (Ephrussi and Beadle, 1937, Genetics 22: 65-75). Larval Mal- pighian tubules bright yellow (Beadle, 1937, Genetics 22: 587-611). RK3. other information: CalTech stock, bo v, contains w alleles. Schalet thinks bo is a dark allele of w; bo/wa looks like dark allele of w series. # bobbed: see bb # bobbed on the Y chromosome: see bbY # bod: bowed location: 3-48.3. origin: Spontaneous. discoverer: Nichols-Skoog, 35b20. references: 1937, DIS 7: 6. phenotype: Wings bowed downward over abdomen with curvature along both axes; curvature occasionally reversed. Wings some- what smaller than wild type. Whole fly smaller and humpy; eyes slightly bulged. Overlaps wild type slightly. Viability 75% wild type. RK3. # Bojla: see Fs(3)Sz5 #*bord: bordered location: 1-70. origin: Spontaneous. discoverer: Bridges, 1916. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 220. phenotype: Wings smaller and slightly extended; venation ragged; veins bordered by darker bands. Viability poor; clas- sification unreliable. RK3. # bordeaux: see bo # bordered: see bord #*bos: bordosteril location: 3-0.0. origin: Spontaneous. discoverer: Fabian, 1941. references: 1948, Arch. Julius Klaus-Stift. Vererbungsforsch. Sozialanthropol. Rassenhyg. 23: 512-17. phenotype: Eye color dark brownish red, darkens with age. Mal- pighian tubules and testis sheaths colorless. Male fertile; female sterile. RK2. other information: Possibly an allele of she. # boss: bride of sevenless location: 3.90.5 (just proximal to Pr). references: Reinke and Zipursky, 1988, Cell 55: 321-30. phenotype: Homozygotes lack photoreceptor cell R7; phenotype indistinguishable from that of sev. Mosaic studies demonstrate that boss+ activity required in R8 and in no other photorecep- tor cell for the normal development of the R7 cell in the same ommatidium. boss+ R8 cell cannot rescue R7 development in adjacent ommatidia. alleles: Sixteen alleles induced by X rays, ethyl methanesul- fonate, and hybrid dysgenesis. cytology: Placed in 96F5-14 by deficiency mapping. # bot: botch (T. Schupbach) location: 2-20. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect female-sterile mutant; embryos from homozygous mothers do not hatch and show irregular segmenta- tion, variable segment fusions, and holes in cuticle. alleles: botQ1 = bot1. # Botond: see Fs(3)Sz6 #*bow: bow wings location: 1- (not located). discoverer: Bridges, 12h15. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 46 (fig.). phenotype: Wings curved downward over abdomen and also side- ways, like bowl of a spoon. Overlaps wild type. RK3. # Bow: Bowed (M. Ashburner) location: 2-55.1. origin: Induced with ethyl methanesulfonate. discoverer: Detwiler. phenotype: Wings of heterozygotes at 45 to body axis; macro- chaetae, especially scutellars, with hooked tips. cytology: Cytologically normal (Ashburner). # bow-legged: see bwl # bowed: see bod # Bowed: see Bow # bp: see bulbp # br: see BRC #*Br: Bridged location: 1- (right half; crossing over suppressed to the right of v). origin: X ray induced. discoverer: Muller, 27l3. references: 1935, DIS 3: 29. phenotype: Plexus-like wings with extra crossveins bridging longitudinals. L4 bent. Wings arched. Male lethal. RK3A. cytology: Associated with In(1)Br. # Br: see Sp # brachymacrochaetae: see brc # brahma: see brm # braille: see brl # bran: see aba # Bran: see aBa # branch: see bch # Branchlet: see Bt #*brb: broad abdomen location: 1-52.9. origin: Induced by styrylquinoline (CB. 3086). discoverer: Fahmy, 1956. references: 1959, DIS 33: 83. phenotype: Fly with broad abdomen and slightly shortened thorax and wings. Wings frequently slightly divergent. Eyes small and dull red with reflection spots. Bristles slightly shortened and lying flatter on thorax. Males and females viable and fertile. RK2. alleles: One allele induced by L-p-N,N-di-(2- chloroethyl)amino-phenylalanine. # brc: brachymacrochaetae location: 1-0.0 [no recombinants with sc among 6746 sons; placed between su(s) and tw by duplication analysis (Maddern, 1972, DIS 49: 40); placed just proximal to tw between l(1)1Da and l(1)1Dc, by Voelker, using terminal deficiencies]. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1952. references: 1958, DIS 32: 68. phenotype: One or more thoracic bristle much reduced in size; scutellars and dorsocentrals most frequently affected. Occa- sional bristles duplicated. Extra-bristle phenotype enhanced by duplications for the tip of X with breakpoint between su(s) and tw (Maddern, 1972, DIS 49: 40). Good viability and fer- tility in both sexes. brc6, a lethal allele, causes pupal death with substantial pupal histolysis, especially at ante- rior end (Eberl, Hilliker, and Voelker, 1988, DIS 67: 36). alleles: Majority of alleles are lethal. allele origin ( discoverer synonym ref | comments _____________________________________________________________________ brc1 TEM Fahmy, 1952 1 viable brc2 CB. 3025 Fahmy, 1952 1 viable brc3 X ray Fahmy, 1952 1 viable brc4 X ray Lefevre l(1)C93 2 brc5 EMS Lefevre l(1)VA23 3, 4 polyphenic; no maternal effect brc6 DCE Kramers l(1)DCE12 brc7 ENU Voelker l(1)B1 brc8 ENU Voelker l(1)B5 semilethal; brc phenotype brc9 ENU Voelker l(1)B20 semilethal; brc phenotype brc10 ENU Voelker l(1)B29 brc11 ENU Voelker l(1)B43 brc12 ENU Voelker l(1)B45 ( 1 = Fahmy, 1958, DIS 32: 68; 2 = Lefevre, l971, Genetics 67: 497-513; 3 = Lefevre and Watkins, l986, Genetics 113: 869-95; 4 = Perrimon, Engstrom, and Mahowald, 1984, Dev. Biol. 105: 404-14. # BRC: Broad Complex location: 1-0.28 (left of dor); mapped to 1-0.43 based on 15 crossovers between npr4 and y, 36 between npr4 and w, and 159 between npr4 and ec (Belyaeva et al.). synonym: o.c.c.: overlapping complementation complex; ecs: ecdysone sensitivity (Zhimulev, Belyaeva, Fomina, Protopopov, and Bolshakov, 1987, Chromosoma 94: 492-504). references: Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Bar- itcheva, Gorelova, and Zhimulev, 1980, Chromosoma 81: 281- 306. Belyaeva, Protopopov, Baritcheva, Semeshin, and Izquierdo, 1987, Chromosoma 95: 295-310. Kiss, Beaton, Tardiff, Fristrom, and Fristrom, 1988, Genetics 118: 249-57. genetics: The Broad Complex resides in the early ecdysone- induced puff at the left end of the X chromosome; it comprises a number of mutations with complicated phenotypic and comple- mentation characteristics. Russian investigators originally defined four mutually complementing, lethally mutable loci, which function in ecdysone-dependent induction of metamor- phosis: br = broad, rbp = reduced bristles on palpus, l(1)2Bc, and l(1)2Bd. Based on amorphic mutations, defined on the basis of having equivalent phenotypes in homozygous and hemiz- ygous females, Kiss et al. define two complementation groups: br [comprising br, rbp, and l(1)2Bd (Belyaeva et al.)] and l(1)2Bc;npr alleles are non-complementing. In the following treatment we retain the subdivisions as defined by Belyaeva et al.; however, as the molecular structure of the complex becomes understood, simpler terminology will be indicated. cytology: Placed in 2B5 based on its deletion by Df(1)S39 = Df(1)1E3-4;2B5 and by the deficiency within Dp(1;Y)Sz280 = Df(1)2B4-5;2B6-7; Df(1)S39/Dp(1;Y)Sz280 males die as puffless third-instar larvae (Belyaeva, Vlassova, Biyasheva, Kakpakov, Richards, and Zhimulev, 1981, Chromosoma 84: 207-19). molecular biology: Region entered by transposon tagging (Chao and Guild, 1986, EMBO J. 5: 143-50) and by microdissection (Galceran, Jimenez, Edstrom, and Izquierdo, 1986. Insect Biochem. 16: 249-54). Chromosomal walk of 230 kb includes polytene bands 2B1-6; coordinate 0 defined as the most distal point of the walk, with positive values extending to the right. Mutational lesions are spread over 50 kb and are con- fined to two disjunct regions, the distal one is between 100 and 115 kb and the proximal is between 150 and 175 kb (Sam- pedro, Galceran, and Izquierdo, 1989, Mol. Cell Biol. 9: 3588-91); both br and l(1)2Bc lesions are found in the proximal group. The region is transcriptionally complex; transcripts from the distal region seem unrelated to BRC func- tion, whereas, the proximal region produces an array of tran- scripts that display alternative initiation and termination sites as well as alternatively spliced exons which show stage specificity, with constitutive and early transcripts originat- ing at coordinate 143 kb and late transcripts at 165 kb (Gal- ceran, Llanos, Sampedro, Pongs, and Izquierdo, 1990, Nucleic Acids Res. 18: 539-45). br: broad Edith M. Wallace, unpublished. # br: broad references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 145, 220 (fig.). phenotype: The br complementation group contains both amorphic and hypomorphic mutant alleles; amorphic alleles cause early prepupal developmental arrest; hypomorphic alleles cause late pupal or pharate adult developmental arrest or are viable. Null alleles display normal larval development but prevent elongation and eversion of discs giving rise to appendages in the pupal stage. Wings of the viable allele, br1, somewhat broader than normal; about 80% of normal length, with round full tip; crossveins closer together. Shape difference visi- ble in middle prepupal stage immediately after eversion [Wad- dington, 1939, Proc. Nat. Acad. Sci. USA 25: 299-307; 1940, J. Genet. 41: 75-139 (fig.)]. A haplo-insufficient locus in that heterozygosity for a deficiency including the br locus leads to a slight br phenotype (Craymer and Roy, 1980, DIS 55: 200-04); furthermore, the deficiency in combination with br1 or br3 leads to drastic reduction in viability, especially at 18, and an extreme phenotype among survivors, including reduced palpi characteristic of rbp alleles, short rounded wings with interrupted veins, and malformed third legs, i.e., shortened and thickened femora and tibiae as well as misshapen basitarsi. The malformed-leg syndrome is enhanced by hetero- zygosity for Sb or sbd alleles (Beaton, Kiss, Fristrom, and Fristrom, 1988, Genetics 120: 453-64). br16/+ and Df(1)S39/+ display slight dominance of br effects in the presence of RpII215Ubl (Mortin and Lefevre, 1981, Chromosoma 82: 237-47). alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________________________________ br1 spont Bridges,15i26 4, 5, 7, 13 viable; 412 insert at 164.4 kb br3 spont Bridges,31e1 4, 5, 13 viable; 412 insert at 164.4 kb + B104 insert at 159.4 kb br4 DNA Fahmy br59j 4, 5 viable; inserts at 109 and 115 kb + small deletion between 102 and 104 kb br5 EMS l(1)t35 1, 2, 7, 8 amorph, prepupal lethal br6 EMS l(1)t103 1, 2 In(1)2B3-4;3C1, hypomorph, pupal lethal; breakpoint at 146 to 151 kb br7 EMS l(1)t336 1, 2, 7 br8 EMS l(1)t366 1, 2, 8 amorph, prepupal lethal br9 / ray Pak l(1)t476 1, 2 viable br10 X ray Lefevre l(1)A18 9 T(1;2)2A4;60E8-9 br11 X ray Lefevre l(1)A64 9 T(1;2)2B7;42 br12 X ray Lefevre l(1)C123 9 T(11;2)2B6;54A br13 X ray Lefevre l(1)GA106 9 In(1)2B6;20F br14 X ray Lefevre l(1)GE222 9 T(1;3)2B6;83E br15 X ray Lefevre l(1)GE246 9 In(1)2B6;3D5-6 (complex) br16 X ray Lefevre l(1)GF325 4, 11 Tp(1;2)2B7;7D;36C br17 X ray Lefevre l(1)N34 In(1)2B6;4D6 br18 EMS Lefevre l(1)VE662 10 br20 EMS Lefevre l(1)VE736 10 br21 EMS Lefevre l(1)VE891 10 In(1)2B6-7;20A br22 EMS Lefevre l(1)VE901 10 T(1;2)2B;25E-F br23 spont Schalet l(1)14-153 br24 spont Schalet l(1)20-68 *br24h spont L.V. Morgan 4 viable br25 X ray 7 Df(1)1E1-2;2B4-5 = Df(1)pn7b breakpoint at 144.5 to 147 kb br26 DEB brJTD1 7 Df(1)1D-E;2B5; hypomorph br27 DEB brJTD2 7 viable, hypomorph br28 HD br32/10B 13 0.2 kb deletion at 102 to 104 kb br29 X ray brX195 13 1.5 kb insert at 174 kb *br33a spont L.V. Morgan 4 viable *br37l spont Bridges 4 viable brD spont Muller, 19h 12 D = Dominant *br1-a spont Muller, 19h 12 *br1-b spont Muller, 19h 12 *brsh spont Bridges, 14g20 3 viable; sh = short *bruq spont Fahmy, 1955 6 viable; uq = unequal wings *brw spont Duncan 4 viable; w = wide ( 1 = Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbetova, Kra- mers, and Zhimulev, 1982, DIS 58: 184-90; 2 = Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelova, and Zhimulev, 1980, Chromosoma 81: 281-306; 3 = Bridges, 1916, Genetics 1: 151; 4 = CP552; 5 = CP627; 6 = Fahmy, 1958, DIS 32: 77; 7 = Kiss, Beaton, Tardiff, Fristrom, and Fristrom, 1988, Genetics 118: 247-59; 8 = Kiss, Szabad, Belyaeva, Zhimulev, and Major, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.) Plenum Press, New York and London, pp. 163-81; 9 = Lefevre, 1981, Genetics 99: 460-80; 10 = Lefevre; 11 = Morton and Lefevre, 1981, Chromosoma 82: 237-47; 12 = Muller and Altenburg, 1921, Anat. Rec. 20: 213. 13 = Sampedro, Galceran, and Izquierdo, 1989, Mol. Cell Biol. 9: 3588-91. other information: Some br and br/rbp genotypes display reduced palpi, leading Kiss et al. to place br and rbp in the same complementation group. # l(1)2Bab phenotype: So named because of its failure to complement lethality of br and rbp mutations. Homozygotes and hemizy- gotes die in pupal stage; puparium formation delayed three [l(1)2Bab3] to six [l(1)2Bab1] hr. l(1)2Bab1 pupae have nor- mal imaginal organs, and escapers have faded wings and reduced bristles on palpi. Prepupal lethal in combination with npr11 or Df(1)S39. other information: Surviving l(1)2ab1/rbp1 and l(1)2ab1/l(1)2Bc1 exhibit malformed-leg syndrome. alleles: allele origin synonym ref ( _______________________________________________ l(1)2Bab1 EMS l(1)t4 1, 2, 3, 4 l(1)2Bab2 EMS l(1)t126 1, 2, 3 l(1)2Bab3 EMS l(1)t143 1, 2, 3, 4 l(1)2Bab4 l(1)d.norm.24 3, 5 ( 1 = Aizenzon and Belyaeva, 1982, DIS 58: 3-7; 2 = Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbetova, Kramers, and Zhimu- lev, 1982, DIS 58: 184-90; 3 = Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelova, and Zhimulev, 1980, Chromosoma 81: 281-306; 4 = Kiss, Beaton, Tardiff, Fristrom and Fristrom; 5 = Kiss, Bencze, Fekete, Fodor, Gausz, Maroy, Szabad, and Szidonya, 1976, Theoret. Appl. Genet. 48: 217-26. # l(1)2Bc phenotype: Die in prepupal or early pupal stage after formation of a gas bubble. Imaginal discs fail to fuse, especially dor- sally, to produce a continuous integument. Puparium formation variably delayed: 6 hr in l(1)2Bc1, 12 hr in l(1)2Bc2, and 9 hr in l(1)2Bc3 and l(1)2Bc4. Many late ecdysone puffs both in larvae and prepupae either absent or underdeveloped [l(1)2Bc1] [Zhimulev, Belyaeva, and Aizenzon, 1980, Genetika (Moscow) 16: 1613-31]. l(1)2Bc1 an amorphic allele fully complements the amorphic br5 (Kiss et al.). alleles: allele origin synonym ref ( comments _______________________________________________________________________ l(1)2Bc1 EMS l(1)t10 1, 2, 3, 4, 5 amorph l(1)2Bc2 EMS l(1)t76 1, 2, 3, 4 amorph l(1)2Bc3 EMS l(1)t149 1, 2, 3 l(1)2Bc4 EMS l(1)t197 1, 2, 3 l(1)2Bc5 HD l(1)2Bclp14 6 defective P at 172 kb l(1)2Bc6 HD l(1)2Bclp69 6 defective P at 172 kb ( 1 = Aizenzon and Belyaeva, 1982, DIS 58: 3-7; 2 = Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbetova, Kramers, and Zhimu- lev, 1982, DIS 58: 184-90; 3 = Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelova, and Zhimulev, 1980, Chromosoma 81: 281-306; 4 = Kiss, Beaton, Tardiff, Fristrom and Fristrom; 5 = Kiss, Szabad, Belyaeva, Zhimulev, and Major, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall and Hall, eds.) Plenum Press, New York and London, pp. 163-81. 6 = Sampedro, Galceran, and Izquierdo, 1989, Mol. Cell Biol. 9: 3588-91. # l(1)2Bd phenotype: Males and homozygous females display normal pheno- type and viability; however, in heterozygous combination with deficiencies or npr mutations, l(1)2Bd acts as a temperature- sensitive lethal; completely lethal at 29; at 25 or 18 most individuals die in late pupal stage, and survivors have faded wings, swollen abdomen, and reduced bristle number on palpi. alleles: allele origin synonym ref ( comments _____________________________________________________ l(1)2Bd1 EMS l(1)t252 1, 2, 3, 4 hypomorph ( 1 = Aizenzon and Belyaeva, 1982, DIS 58: 3-7; 2 = Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbetova, Kramers, and Zhimu- lev, 1982, DIS 58: 184-90; 3 = Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelova, and Zhimulev, 1980, Chromosoma 81: 281-306; 4 = Kiss, Beaton, Tardiff, Fristrom and Fristrom. # npr1: nonpupariating phenotype: Hemizygous male larvae fail to pupariate, although they survive 10-15 days after their normal sibs have pupari- ated. Four-day-old larvae appear normal as do their imaginal discs; normal ecdysteroid levels achieved. Discs become abnormal beginning on the sixth day; peripodial membrane becomes enormously distended and highly distorted; partially evaginated structure becomes visible in the disc lumen; do not undergo detailed morphological changes characteristic or metamorphosis, either in situ or in transplants into normal larvae [Fristrom, Fekete, and Fristrom, Wilhelm Roux's Arch. Dev. Biol. 190: 11-21 (fig.)]. Both salivary glands and fat bodies fail to undergo histolysis in situ or in vitro. Mutant flies able to produce ecdysone, but tissues unable to respond normally. In gynandromorphs, the female tissue forms a puparium, whereas npr1 male tissue remains larval; no adults survive (Kiss, Szabad, and Major, 1978, Mol. Gen. Genet. 164: 77-83; Kiss, Bencze, Fodor, Szabad, and Fristrom, 1975, Nature 262: 136-38). Implantation of wild-type ring glands into npr1 larvae does not rescue pupariation; however implanted wild-type or npr1 ring glands are able to rescue npr3 larvae [Kiss, Szabad, Belyaeva, Zhimulev, and Major, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.) Plenum Press, New York and London, pp. 163-81]. No maternal effect of either npr13 or npr14 (Perrimon, Engstrom, and Mahowald, 1984, Dev. Biol. 105: 404-14). npr16 homozygous and hemizygous larvae die without exhibiting any sign of ecdysone-inducible puff forma- tion; culture of slivary glands in 20-OH ecdysone produces partial development of some early, but none of late ecdysone- inducible puffs, and extraneous puff appears at 75CD (Belyaeva, Vlassova, Biyasheva, Kakpakov, Richards, and Zhimu- lev, 1981, Chromosoma 84: 207-19). npr1+ gene product also required for regression of the intermolt 68C glue puff [Belyaeva, et al. (npr6); Crowley, Mathers and Meyerowitz, 1984, Cell 39: 149-56 (npr3)] and for the transcription of the three 68C glue protein genes (Crowley et al). alleles: allele origin discoverer synonym ref ( comments ______________________________________________________________________________ npr1 EMS Stewart l(1)d.norm.-1a 2, 4, 6, 7, 8, 9, 12 npr2 EMS Stewart l(1)d.norm.-1b 8, 10, 12 npr3 EMS Kiss l(1)npr-1 2, 4, 6, 7, 9 l(1)d.norm.-12 5 npr4 EMS Kiss l(1)npr-2 2, 6, 9 npr5 EMS l(1)t324 1, 2, 5 npr6 EMS l(1)t435 1, 2, 3 npr7 DEB nprJTD3 6 T(1;3)2B5;61F3-4 nprfs P fs(1)de12 11 ( 1 = Aizenzon and Belyaeva, 1982, DIS 58: 3-7; 2 = Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelova, and Zhimulev, 1980, Chromosoma 81: 281-306; 3 = Belyaeva, Vlas- sova, Biyasheva, Kakpakov, Richards, and Zhimulev, 1981, Chromosoma 84: 207-19; 4 = Fristrom, Fekete, and Fristrom, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 11-21; 5 = Kiss, Bencze, Fekete, Fodor, Gausz, Maroy, Szabad, and Szidonya, 1976, Theoret. Appl. Genet. 48: 217-26; 6 = Kiss, Beaton, Tardiff, Fristrom, and Fristrom; 7 = Kiss, Bencze, Fodor, Szabad, and Fristrom, 1976, Nature 262: 136-38; 8 = Kiss, Szabad, Belyaeva, Zhimulev, and Major, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.) Plenum Press, New York and London, pp. 163-81; 9 = Kiss, Szabad and Major, 1978, Mol. Gen. Genet. 164: 77-83; 10 = Murphy, 1974, Dev. Biol. 39: 23-36; 11 = Orr, Galanopoulos, Romano, and Kafatos, 1989, Genetics 122: 847-58 (fig.). 12 = Stewart, Murphy, and Fristrom, 1972, Dev. Biol. 27: 71-83. # rbp: reduced bristles on palpus phenotype: Late pupal lethal; most animals reach the pharate adult stage. rbp2 homozygotes and males survive with fewer than normal bristles on the palpus; when raised at 29, females exhibit faded wings and swollen abdomens; when raised at 18 males have faded wings. rbp2/Df(1)RA19 females virtually lethal; females carrying rbp2 and any of the other rbp alleles are completely viable when reared at 18, but at higher tem- peratures most die and escapers have reduced bristles on the palpus, shortened bristles on the scutellum, shrivelled or swollen abdomen shrivelled wings and eyes with crumpled sur- face. alleles: allele origin synonym ref ( comments __________________________________________________ rbp1 EMS rbpt99 1, 2, 3, 4 rbp2 EMS rbpt132 1, 2 hypomorph rbp3 EMS rbpt144 1, 2 rbp4 EMS rbpt358 1, 2 rbp5 EMS rbpt376 1, 2 ( 1 = Aizenzon and Belyaeva, 1982, DIS 58: 3-7; 2 = Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelova, and Zhimulev, 1980, Chromosoma 81: 281-306; 3 = Kiss, Beaton, Tardiff, Fristrom, and Fristrom; 4 = Kiss, Szabad, Belyaeva, Zhimulev, and Major, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.) Plenum Press, New York and London, pp. 163-81; #*brd: broadened location: 1-33. origin: X ray induced. discoverer: Muller, 26l27. references: 1935, DIS 3: 29. phenotype: Wings expanded. Viability 20% wild type. RK3. # Brd: Bearded (M. Leviten) location: 3-42 (between Gl and th). phenotype: Causes production of supernumerary chaetae and sen- silla at or near normal positions. Brd1 homozygotes survive and exhibit more severe phenotypes than heterozygotes. Brd1/+ = Brd1/Df(3L)Brd. Brd alleles affect all classes of adult sensory organs. Brd1 strongly affects macrochaetae and other imaginal-disc sensilla (i.e., trichoid, campaniform, basi- conic), but only mildly increases microchaete density. Brd3 and other alleles produce more severe microchaete phenotypes, in both disc and histoblast derived tissues, as well as exhi- biting the Brd1 phenotypes. In addition to sensillum multi- plication, Brd1 homozygotes also exhibit bristle loss, with anterior orbitals absent (>90%) and a less frequent loss of ocellar macrochaetae (<5%). This bristle loss occurs in other Brd genotypes and is most severe for Brd3 homozygotes. The combination of sensilla multiplication and loss phenotypes is made more severe by loss-of-function mutations at Notch and neuralized, and are decreased in the presence of three wild- type copies of these genes. The ethyl-methanesulfonate- induced point revertants of Brd1 tested (Brdrv1-4) are homozy- gous viable, viable in trans to Brd deficiencies, and display no mutant phenotypes in either situation. alleles: Alleles other than Brd1 are primary or secondary derivatives of Brd1. Brdrv5 and Brdrv6 are revertants of Brd3, and the BrdPrv alleles are revertants of BrdP1. allele origin discoverer phenotype ( comments _________________________________________________________________________ Brd1 spont Groger Brd2 / ray Posakony > Brd1; severe eye In(3L)71A;71F defects; homozygous early pupal lethal Brd3 P Leviten homozygotes -> fz-like In(3L)70D-E;71A rough-eye and bristle polarity defects Brd4 / ray Posakony < Brd1; homozygous viable In(3)71A1-2;80-81 Brd5 / ray Posakony << Brd1; homozygous viable In(3)71A1-2;80-81 Brd6 / ray Posakony < Brd1; homozygous lethal In(3)71A1-2;80-81 Brdrv1 EMS Shim wild type; homozygous viable Brdrv2 EMS Shim wild type; homozygous viable Brdrv3 EMS Leviten wild type; homozygous viable Brdrv4 EMS Leviten wild type; homozygous viable Brdrv5 EMS Leviten wild type; homozygous lethal Brdrv6 EMS Leviten wild type; homozygous lethal BrdP1 P Leviten < Brd1; homozygous viable BrdPI1 __2-3 Leviten > Brd1; homozygous lethal BrdPI2 __2-3 Leviten > Brd1; homozygous viable BrdPI3 __2-3 Leviten > Brd1; homozygous viable BrdPrv1 __2-3 ( Leviten wild type; homozygous viable BrdPrv2 __2-3 Leviten wild type; homozygous viable BrdPrv3 __2-3 Leviten wild type; homozygous viable ( P-element excisions from BrdP1 induced by __2-3. other information: Possibly Hi was a Brd allele. #*bre: bright eye location: 1-24.6. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 68. phenotype: Eye color brighter red. Wings shorter, often crum- pled or waved. Abdomen disproportionately large. Male via- bility and fertility good; females have reduced fertility. Not easily classified. RK3. alleles: One allele induced by methyl methanesulfonate. # brevis: see bv # brh: brown head location: 2-61. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.). Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Embryonic lethal. Defect in head involution; denti- cle bands abnormal. alleles: Two retained, brh1 and brh2 isolated as IB and IID; plus six discarded alleles. # bri: bright location: 2-54.3. origin: Spontaneous. discoverer: Nichols-Skoog, 34b23. references: Beadle and Ephrussi, 1937, Am. Naturalist 71: 91- 95. phenotype: Eye color bright red, like cn2 or v2; difficult to separate from wild type. Malpighian tubules pale yellow (Bea- dle, 1937, Genetics 22: 587-611). RK3. # bride of sevenless: see boss # Bridged: see Br # brief: see bf # bright: see bri # bright eye: see bre # Brista: see Ba # Bristle: see Bl # Bristled: see Sp # brl: braille (M.P. Scott) origin: Enhancer trap P-element mutagenesis. discoverer: L.E. Rost and M.P. Scott, 1989. phenotype: Recessive mutation with complete penetrance and variable expressivity. Strongest phenotypes include partial to full transformation of one or both eyes into antennae. Less severe adult phenotypes include excess bristles under the eyes, duplication of the more anterior set of scutellar bris- tles (macrochaetae), and a spoon-like curvature of the wings. Homozygotes are viable and fertile. cytology: P-element insertion in 60B-C; mobilization of the P- element restored wild-type morphology. molecular biology: Gene cloned by plasmid rescue from bacterial sequences in the P-element. other information: Presumed additional alleles obtained by mobilization of P-element. All are recessive lethals that die during early larval stages. # brm: brahma (J.A. Kennison) location: 3-43.0. origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1983. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Dominant suppressor of Pc and Pcl alleles. Reces- sive embryonic lethal with strong maternal contribution. Maternal effect lethality is non-rescuable even by two wild- type zygotic alleles. There is a single 5.5 kb mRNA present throughout development with the greatest amounts in the unfer- tilized egg and early embryo. brm1 isolated as a dominant suppressor of the antennal to leg transformation associated with a Pc2 AntpNs double heterozygote. alleles: Fifteen alleles induced by ethyl methanesulfonate, three alleles induced by gamma irradiation, and four alleles induced by hybrid dysgenesis. cytology: Placed in 72A3-5 based on in situ hybridization to salivary gland chromosomes. # brn: see caG # broad: see br in BRC # broad abdomen: see brb # broad head: see bhe # broad head: see l(2)gl # broadened: see brd # broader wing: see brw # bronze: see sf2 # bronzy: see malbz # brown: see bw # brown head: see brh # brown-like: see red # brown spots: see bsp # brr: see hbrr # brunette: see Hnr2 #*brw: broader wing location: 1-39.8. origin: X ray induced. discoverer: Fahmy, 1956. references: 1959, DIS 33: 83. phenotype: Wings broad and rounded at the tips. Males show reduced viability and are sterile. RK3. # bs: blistered location: 2-107.3. origin: Spontaneous. discoverer: Bridges, 11k16. references: Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 155 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 219 (fig.). phenotype: Wings blistered, small, pointed; venation thick and plexus-like with branches from and parallel to L5 beyond second crossvein, where there is a semidominant free vein effect. Temperature sensitive. RK2 at 19; RK3 at 25. alleles: bs2, bs3, *bs4, bs8, *bs52d, *bs54j, *bsbl, *bs38i, bscy, *bsP, and bsPP (CP627). cytology: Located between 60C5 and 60D2, based on its inclusion within Df(2R)Px = Df(2R)60B8-10;60D1-2 and within Df(2R)Px2 = Df(2R)60C5-6;60D9-10 (Bridges, 1937, Cytologia (Tokyo), Fujii Jub., Vol. 2: 745-55). other information: May be part of a pseudoallelic complex with ba and Px. bs2: blistered-2 Edith M. Wallace, unpublished. # Bsb: Blunt short bristle location: 3-100.6 (based on distribution of Bsb among 387 crossovers between ro and ca from Bsb/ca ro females). origin: Induced by ethyl methanesulfonate. references: B.S. Baker, 1980, DIS 55: 197. phenotype: Bristles markedly shortened; sharply tapered at tip resembling sharpened pencil under compound microscope. Excel- lent cell marker. Bristles reduced to very short stubs in Pr Bsb heterozygotes. Homozygous lethal; viability and fertility of heterozygote excellent. cytology: Salivary-gland chromosomes normal. #*bsc: bent scutellars location: 1-1.1. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 68. phenotype: One or more scutellars bent on themselves in form of inverted V. Other bristles irregularly bent. Eyes slightly smaller. Wings slightly abnormal in shape. Male viability about 50% wild type; fertility much reduced. RK3. alleles: One allele each induced by L-p-N,N-di-(2- chloroethyl)amino-phenylalanine and D-p-N,N-di-(2- chloroethyl)amino-phenylalanine. # Bsg: Blastoderm-specific gene Three loci identified in a differential screen of a genomic library with labeled blastoderm cDNA plus competing amounts of unlabeled preblastoderm cDNA; localized by in situ hybridiza- tion to polytene chromosomes. genetic cytological locus location location synonym ref ( _________________________________________________ Bsg25D 2-{16} 25D3 2, 3 Bsg75C 3-{45} 75C1-2 term 1, 3 Bsg99D 3-{101} 99D4-8 3 ( 1 = Balderelli, Mahoney, Salas, Gustavson, Boyer, Chang, Roark, and Lengyel, 1988, Dev. Biol. 125: 85-95; 2 = Boyer, Mahoney, and Lengyel, 1987, Nucleic Acids Res. 15: 2309-25; 3 = Roark, Mahoney, Grahm, and Lengyel, 1985, Dev. Biol. 109: 476-88. # Bsg25D molecular biology: Genomic subclone hybridizes to overlapping 2.7-, 3.0-, and 4.5-kb mRNA's on Northern blots. The two larger transcripts present in 0-8 hr embryos; whereas the 2.7-kb transcript is found only in the blastoderm stage. The 2.7- and 4.5-kb messages encode the same polypeptide; they come from a transcript with three exons, the first two of which are shared, and the third of which differs between the two in the length of its 3 untranslated region. The concep- tual amino-acid sequence contains 741 amino acids and contains a 96-amino-acid domain with 22% identity to c-fos and a 21- amino-acid domain that resembles repeated actin-binding seg- ments of tropomyosin. # Bsh: see Mhc-m5 # bsk: basket location: 2-33. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.). Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Homozygous lethal; embryos have large dorsal ante- rior hole. alleles: Three, bsk1, bsk2, and bsk3, isolated as IIJ, IIP, and *IL. cytology: Placed in 31B-32A based on its inclusion in Df(2L)J27 = Df(2L)31B-E;32A. # bsp: brown spots location: 2-40.6. origin: Spontaneous. references: Di Pasquale, 1959, DIS 33: 128. Di Pasquale and Zambruni, 1963, DIS 37: 73 (fig.). 1965, DIS 40: 80. 1966, DIS 41: 119. 1967, DIS 42: 74. phenotype: Spots of brown pigment appear in integument of bsp/bsp females only after they have mated. Di Pasquali and Zambruni (1963) showed that copulation with any male, sterile or fertile, triggers formation of brown spots in cuticle and brown masses in tissues. Courtship without copulation inef- fective; virgin females never show brown spots. Simulated copulation with a glass needle, with or without accessory- gland fluid, leads to phenotype. Mating of etherized females less effective in inducing brown spot formation. No phenotype in males. Penetrance of 60-80%; viability excellent. RK3. # bss: bang senseless (J.C. Hall) location: 1-54.6. origin: Induced by ethyl methanesulfonate. synonym: basMW1: bang sensitive. references: Jan and Jan, 1978, Proc. Nat. Acad. Sci. USA 75: 515-19. Ganetzky and Wu, 1982, Genetics 100: 597-614. phenotype: Mechanical shock or vortexing induces paralysis lasting for 2-3 minutes; heterozygous female are paralized for 40-50 seconds. Homozygotes and hemizygotes have abnormally prolonged release of neurotransmitter at larval neuromuscular junctions, which is associated with multiple firing of action potentials in the nerves; behavioral and electrophysiological phenotypes suppressed by napts at its permissive (low) tem- perature. alleles: bss1 (formerly basMW1) and bss2 phenotypically alike. cytology: Placed between 14B5 and 14B13 based on its being deleted by Df(1)81l12h = Df(1)14B5-18;15A6-11 (Steller) but not carried by Dp(1;2)r+75c = Dp(1;3)14B13;15A9;35D-E (Ganet- sky and Wu). other information: Separable by recombination from eas, which causes a similar phenotype and to which bss is closely linked. # bt: bent location: 4-1.4 [mapped in diplo-4 triploids by Sturtevant (1951, Proc. Nat. Acad. Sci. USA 37: 405-7)]. origin: Spontaneous. references: Muller, 1914, J. Exp. Zool. 17: 325-36. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 216 (fig.), 219. Bridges, 1935, Biol. Zh. 4: 401-20. phenotype: Wings held out at base and bent sharply backward. Rear legs often lumpy at first tarsal joint. May have one to four "preleg" or "first ventral" bristles on ventral surface of thorax anterior to first pair of legs, in space otherwise devoid of bristles or hairs. Overlaps wild type at 25, very much at 19, and little if any at 29 (Metz, 1923, Proc. Soc. Exp. Biol. Med. 20: 305-10). RK2 at 28. cytology: Tentatively placed in 102B10-E9 between Df(4)M4 = Df(4)101E-F;102B9-10 and Df(4)G = Df(4)102E2-10;tip (Hochman, 1971, Genetics 67: 235-52). other information: First mutant found on chromosome 4. bt: bent From Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 216. # btD: bent-Dominant origin: X ray induced. discoverer: Schultz, 33a11. references: Bridges, 1935, Biol. Zh. 4: 401-20. phenotype: When found, btD/+ showed regularly divergent wings with some angular bend near base. Legs lumpy at low tempera- ture. Preleg bristles present as in bt. Homozygous lethal. Fails to complement l(4)2 and l(4)23 [Hochman, 1976, The Genetics and Biology of Drosophila (Ashburner and Novistki, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 903-28]. RK3 as lethal. other information: Balanced stocks in existence today show only preleg bristle character and recessive lethality (Lewis). #*Bt: Branchlet location: 1- (rearrangement). origin: Induced by 32P. discoverer: Bateman, 1950. references: 1950, DIS 24: 54. 1951, DIS 25: 77. phenotype: Heterozygous female has posteriorly directed bran- chlet on posterior crossvein as well as other extra venation. Abdominal segments often poorly chitinized. Male lethal. RK3A. cytology: Associated with Dp(1;1)Bt = Dp(1;1)3B2-C1;6F6-7. other information: Phenotype may be Co effect in 3C7 or more likely dx in region 6. # btd: buttonhead location: 1-31. origin: Induced by ethyl methanesulfonate. references: Wieschaus, Nusslein-Volhard and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307 (fig.) phenotype: Homozygous lethal; head involution incomplete. cytology: Localized to 8A5-9A1 by segmental aneuploidy. # btdl: buttonheadlike location: 1-65. origin: Induced by ethyl methanesulfonate. references: Eberl and Hilliker, 1988, Genetics 118: 109-20. phenotype: Mouthparts sclerotized but not completely internal- ized; the head is often open. A fraction of btdl1/+ females have bristled growths on the head; those in eye region resem- ble eye-to-antenna transformations. alleles: btdl1 and btdl2 isolated as l(1)EH564 and l(1)EH793. cytology: Placed in 18B4-19A1 based on its being covered by XPYDB50 from T(1;Y)18B4-11;YL but not by Ymal+, which carries 18F3-19A1 to 20F from the X. #*bu: bulging location: 1-58. origin: X ray induced. discoverer: Muller, 26l8. references: 1935, DIS 3: 29. phenotype: Eyes rough and bulging. Semilethal. RK3. # bu: see Hnr2 # bu-w61j: see vs61j # Bubble: see Bb # bubble wing: see vs61j # buckled: see bk # buckledlike: see bkl # bul: bulge location: 3-43.6. origin: Spontaneous. discoverer: Spencer, 36d28. references: 1937, DIS 7: 6. Curry, 1939, DIS 12: 45. phenotype: Eyes very large and bulging; facets rounded, in irregular rows, and some quite large. Wing margin heavy; end of wing somewhat squared off to L3. RK3. cytology: In 72E4-5 (Velissariou and Ashburner, 1981, Chromo- soma 84: 173-85). # bulbp: bulge-bumpy origin: Spontaneous. synonym: bp. references: E. H. Grell, 1955, DIS 29: 72. phenotype: About one-half the eye surface erupted into irregu- lar yellowish blisters. Facets larger than normal in non- blistered areas. Homozygotes occur with 1% of expected fre- quency. Surviving homozygotes vigorous and male fertility high; females lay eggs abundantly, but only rarely does an egg hatch. RK3. # bulD: bulge-Dominant (E.H. Grell) origin: Induced by ethyl methanesulfonate. phenotype: Eyes rough with large facets in both heterozygote and homozygote. Good viability. # bulging: see bu #*buo: burnt orange location: 2-57.1. origin: Spontaneous. discoverer: T. Hinton and Kleiner, 1941. references: Hinton, 1942, DIS 16: 48. phenotype: Eye color bright orange-brown. Malpighian tubules colorless in larva (Brehme and Demerec, 1942, Growth 6: 351- 56). RK2. other information: Not an allele of cn. Allelism with ltd (2- 56) apparently never tested. # bur: burgundy location: 2-55.7. origin: Ultraviolet induced. references: Meyer and Edmondson, 1949, DIS 23: 60. phenotype: Eye color dull, darkish brown (like pr), brilliant orange in combination with cn. burgua supplementable by guanosine but not other ribonucleosides or nucleic acid bases; inosine-5 -monophosphate dehydrogenase activity reduced com- pared to normal (Johnston, Nash, and Naguib, 1985, Biochem. Genet. 23: 539-55). Classification and viability excellent. Fertility of females good; of males, variable. RK1. alleles: bur2 (CP627) and burgua. cytology: In 42B1-3 (Johnstone). other information: bur not allelic to lt, ltd, or pr. Allelism of burgua inferred from map position of 2-54 and phenotype. # burgua origin: Induced by ethyl methanesulfonate. synonym: gua2-1. phenotype: Recessive auxotroph for guanosine; supplementable by 3.2 mM of guanosine but not by other ribonucleosides or nucleic acid bases. Homozygotes have dark red eyes; this character segregates with the nutritional requirement. Ino- sine dehydrogenase activity of burgua larval extracts an order of magnitude lower than that of wild type (Johnston, Nash, and Naguib, 1985, Biochem. Genet. 23: 539-55). # burnt orange: see buo # buttonhead: see btd # buttonheadlike: see btdl # bv: brevis location: 3-102.7 (recalculated from Sturtevant, 1956, Genetics 41: 118-23). discoverer: Bridges, 33e25. phenotype: Bristles uniformly short and stubby. Body chunky. Hatches late but viability excellent. RK1. cytology: Tentatively placed in distal to 100B7-8 by Frisardi and MacIntyre (1984, Mol. Gen. Genet. 197: 403-13) based on the retention of bv+ by Df(3R)ca48 = Df(3R)98F14;100B7-8. # bw: brown location: 2-104.5. discoverer: Waaler, 19j15. references: 1921, Hereditas 2: 391-94. Dreesen, Johnson, and Henikoff, 1988, Mol. Cell Biol. 8: 5206-15. Sullivan and Sullivan, 1975, Biochem. Genet. 13: 603-13. Mount, 1987, Nature (London) 325: 487. phenotype: Eye color light brownish wine on emergence, darken- ing to garnet. Red pigments lacking. Xanthommatin mostly replaced by dihydroxanthommatin (Phillips, Forrest, and Kul- karni, 1973, Genetics 73: 45-56). Pigment granules present but somewhat smaller than in wild type. Adult testes and vasa colorless. Larval Malpighian tubules pale yellow (Beadle, 1937, Genetics 22: 587-611). Produces white eyes in combina- tion with v, cn, or st. Eye color autonomous when transplanted into wild-type host (Beadle and Ephrussi, 1936, Genetics 21: 230). RK1. alleles: Mutant alleles of bw are listed in the accompanying table and their phenotypes compared to those of alleles described below. More complete descriptions in CP627 unless otherwise indicated. allele phenotype ( ____________________________ bw1 bw *bw2 bw5 bw2b bw5 *bw2c bw4 bw4 bw4 bw5 bw5 bw6 bw6 *bw+21 bw4 *bw24 bw4 *bw30 bw *bw33f bw *bw33g bw *bw37g bw5 bw38j | bw5 bw45a bw4 *bw47j bw5 bw59 bw4 *bw72 bw bw75 bw5 bw81 bw5 *bw53l bw5 *bw609 bw bw979 / bwa bwa *bwAD bw *bwau bw *bwCB bw *bwle bw *bwM58 bw5 *bwM590 bw *bwptm bwptm bwRa ` bw ( The phenotype column lists the allele described below that the allele listed resembles; bw5 is homozygous lethal, but other bw5-like alleles are not. | Ives, 1968, DIS 43: 64. / Valade del Rio, 1983, Genet. Iberica, 35: 47. ` Trippa, Loverre, and Cichetti, 1980, Genetics 95: 399-412. cytology: Placed betweeen 59E1-2 or the 59E2-3 interband by examination of In(2LR)bw85f4 = In(2LR)30A;59E2-3 (Nash and Tiong) and by in situ hybridization of a brown (Dreesen, et al., 1988). molecular biology: The genomic locus as well as cDNAs have been cloned and sequenced. The genomic region contains six small introns. The bw mutation is an insertion of about 8 kb of unknown origin into the coding portion of the locus. In the heads of newly eclosed wild-type flies there are two major transcripts of 2.8 and 3.0 kb that differ as a consequence of alternative poly(A) addition and encode the same predicted protein of 675 amino acids. The 8 kb bw insertion results in termination of transcription to give two truncated poly(A+) transcripts (Dreesen, et al., 1988). other information: Uptake studies indicate that bw, like w, blocks the transport of guanine and xanthine, likely pteridine precursors (Sullivan and Sullivan, 1975). Sequence comparis- ons between the predicted bw- and w-encoded proteins show that they are similar to one another and to subunits of active transport family members (Mount, 1987; Dreesen, et al., 1988). # bw4 origin: Spontaneous. discoverer: Mohr, 31k28. phenotype: Homozygotes have normal eye color; in heterozygotes with other alleles, red pigment is reduced. bw4/bw5 is pur- pleoidlike. bw4/bw like bw but darker. RK3. # bw5 origin: Spontaneous. discoverer: Mohr, 31k28. phenotype: bw5/bw4 is purpleoidlike (see bw4); bw5/bw is light yellowish brown; bw5/+ is wild type; bw5/bw5 is lethal. RK2A. cytology: Shown to be a deficiency based on failure to hybri- dize in situ with clones derived from this region (Dreesen, Johnson, and Henikoff). # bw6 origin: Spontaneous. discoverer: Farmer, 1974. references: 1977, Heredity 39: 297-303. Farmer and Fairbanks, 1986, DIS 63: 50-51. synonym: Su(wco2)+; Su(wcoJ)+. phenotype: A subliminal recessive allele of bw; homozygotess are wild type in all combinations except in flies that are homozygous or hemizygous for wco2, which are like bw or wco. bw6/bw4 suppresses wco2, but all other heterozygotes between bw6 and bw alleles which were tested did not suppress. RK1 in combination with wco2. # bw61j: see vs61j # bwa: brown-amber origin: Spontaneous. discoverer: R. C. King, 48f15. references: Poulson and King, 1948, DIS 22: 54. phenotype: Eye color light brownish yellow. Adult testes and vasa colorless. Larval Malpighian tubules slightly paler yel- low than wild type. bwa/bw gives eye color slightly lighter than bw. RK1. #*bwA: brown-Auburn origin: X ray induced. discoverer: Dubinin. synonym: A; PmD1. references: Dubinin and Heptner, 1935, J. Genet. 30: 423-46 (fig.). Dubinin, 1936, Biol. Zh. (Moscow) 5: 851-74. phenotype: Nearly uniform brown but with extra Y chromosome shows strong variegation. Homozygote usually lethal. RK1A. cytology: Associated with In(2R)bwA = In(2R)41;59D. # bwD: brown-Dominant origin: Spontaneous. discoverer: T. Hinton, 1940. references: 1940, DIS 13: 49. 1942, DIS 16: 48. Slatis, 1955, Genetics 40: 246-51. phenotype: Eye color varies with age from purple to brown. Shows slight variegation in combination with st (Slatis, 1955). Wings pebbled. bwD/+ shows nearly a 100-fold reduc- tion in pteridine levels; no accumulation of bw RNA detect- able. bwD/bwVI > bwD/+ > bwD/bwD in severity of effect (Henikoff, and Dreesen, 1989, Proc. Nat. Acad. Sci. USA 86: 6704-08). Variegation suppressed by extra Y chromosomes (Brosseau, 1959, DIS 33: 123). Homozygote viable and fer- tile. Larval Malpighian tubules bright yellow (Brehme and Demerec, 1942, Growth 6: 351-56). RK1A. alleles: bwD114, X ray induced (Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-285). cytology: Schultz reports an extra band in 59E that tends to pair with a band in the homolog, suggesting a duplication of one band from 59E. Slatis (1955) reports insertion of three or four bands, probably of heterochromatic origin. Reverts to wild type when extra bands separated from bw locus (Hinton and GoodSmith, 1950, J. Exp. Zool. 114: 103-14). Examination of stained metaphase preparations reveals a block of hetero- chromatin in the approximate position of bwD (Dimitri and Pim- pinelli). other information: Since 1950 some and perhaps all lines of bwD have undergone a secondary event that removed a portion of the coding region of the brown gene, generating a null allele (Dreesen and Henikoff). #*bwptm: brown:pteridine modifier origin: Naturally occurring allele. synonym: ptm. references: Clancy, 1967, DIS 42: 57. phenotype: Undetectable in wild-type background. In wsat or wcf flies that are at the same time v, cn, or st, the amount of red eye pigment in +/+ > +/bwptm > bwptm/bwptm. # bwR: brown-Rearranged origin: X-ray-induced derivatives of bw or bw+. discoverer: Slatis, 48k16. references: 1955, Genetics 40: 5-23. phenotype: These rearranged derivatives exhibit variegated phenotype in combination with +. Mostly homozygous lethal; survivors have brown eyes. alleles: These derivatives and those associated rearrangements are listed in the accompanying table. More complete descrip- tions in CP627. cytology: All associated with chromosome rearrangements with one breakpoint in 59DE and one in proximal heterochromatin. allele rearrangement ( ___________________________________________________________ bwA In(2R)41;59D bwD heterochromatic insertion in 59E *bwR3 In(2LR)40F;51F;55E;57E;58D8-9 *bwR4 T(2;3)59E2-3;80-81 *bwR12 T(2;3)59D;80C *bwR14 T(2;3)59E2-3;80 *bwR15 T(2;3)59D;80C *bwR18 In(2)40-41;59E4-F1 *bwR20 In(2LR)40D;59D5-6 *bwR25 T(2;4)59D;101E *bwR27 T(Y;2)59D11-E1 *bwR32 In(2R)41A;59D *bwR33 In(2R)41;59DE *bwR35 In(2)40F-41A;59D11-E1 *bwR40 Df(2R)59C5-6; *bwR45 In(2)40F-41A;59E3-4 *bwR47 In(2)40-41;59D-E1 *bwR50 breakpoint at 59D2-3 *bwR55 In(2LR)24E1-D;42E + In(2R)40F-41A;59D4-5 *bwR56 In(2)40F-41A;59DE *bwR57 T(Y;2)59D5-6 *bwR58 T(2;3;4)59D;65;101C *bwR67 In(2)40F-41A;59E4-F1 *bwR68 breakpoint near 58F *bwR73 In(2)40F-41A;59E4-F1 *bwR79 In(2)40F-41A;59F2-3 bwV1 In(2LR)21C8-D1;60D1-2 + In(2LR)40F;59D4-E1 *bwV2 In(2R) *bwV3 T(2;3) bwV4 T(2;3) bwV5 T(2;3) *bwV6 T(2;3) *bwV7 In(2R) *bwV8 T(2;3) *bwV29l In(2LR) *bwV30a *bwV30k1 In(2LR) *bwV30k10 In(2R) *bwV30k12 T(2;3) *bwV30k13 T(2;3) bwV30k18 T(2;3;4) bwV32g In(2LR)40F;59E bwV34k In(2R)41;59E + In(2R)Cy *bwV40b In(2R)41A-B;59D-E *bwV54a In(2R)41A-B;59D4-9 *bwV54b In(2R)41A;60D9-11 *bwV54c In(2R)41;59E1 bwV57e SM1 derivative bwVA T(2;3) bwVD T(2;3) bwVDe1 In(2R)41B2-C1,59E2-4 bwVDe2 In(2R)41A-B;59D6-E1 bwVDe3 T(2;3)59D;81F bwVDe4 T(2;3)59D2-4;80 *bwVI In(2R)41A;59D ( Polytene analysis unavailable where breakpoints not indi- cated. # bwV1: brown-Variegated origin: X ray induced. discoverer: Muller, 1929. synonym: Pm: Plum. references: 1930, J. Genet. 22: 299-334 (fig.). Glass, 1934, J. Genet. 28: 69-112 (fig.). 1934, Am. Naturalist 68: 107-14. Bridges, 1937, Cytologia (Tokyo), Fujii Jub., Vol. 2: 745-55. phenotype: Eye color like bw or pr, mottled with darker spots that deepen in red color with age. With st or v, has pale orange ground with dark orange spots. bwVI/bw shows sharply reduced levels of transcript from both the bw+ allele in cis with the rearrangement and the bw allele on the homologous second chromosome (Henikoff, and Dreesen, 1989, Proc. Nat. Acad. Sci. USA 86: 6704-08). Extra Y chromosome, as with other variegated browns, suppresses brown color, giving red eye sparsely speckled or splotched with darker spots. Amount of wild-type eye color also responds to fourth-chromosome con- stitution; 4/C(4) > C(4) = 4/4 > 4/0, with the first approach- ing wild type and the latter nearly bw (Lindsley and Rokop). Larval Malpighian tubules normal (Glass, Brehme). Generally lethal homozygous and in combination with other brown- Variegateds. Heterozygotes fully viable and fertile. RK1A. alleles: Other variegated alleles of bw, all of which are asso- ciated with X-ray-induced chromosome aberrations, are listed in the accompanying table. More complete descriptions in CP627. cytology: Associated with In(2LR)bwV1 = In(2LR)21C8-D1;60D1-2 + In(2LR)40F;59D4-E1 (Schultz and Bridges). # bw-b: see ca # bwnG: see caG