# b: black (M. Ashburner) location: 2-48.5. phenotype: Black pigment on body and tarsi and along wing veins. Reflectance of cuticle 40% that of wild type (Peder- sen, 1982, Carlsberg Res. Comm. 47: 391-400). Heterozygote somewhat darker than wild type, especially on trident, but never confused with homozygote. Body color darker at low tem- perature (Sherald, 1981, Mol. Gen. Genet. 183: 102-06). Puparium lighter than wild type. Not easily classified in newly emerged flies (Waddington, 1941, Proc. Zool. Soc. London Ser. A. 111: 173-80). Tyrosinase formed in adult flies (Horowitz). Fails to synthesize beta-alanine (Hodgetts, 1972, J. Insect Physiol. 18: 937-47), and feeding or injection of beta-alanine to b produces normal phenotype [Jacobs, 1974, J. Insect Physiol. 20: 859-66; Hodgetts, Hodgetts and Choi, 1974, Nature (London) 252: 710-11]. Also corrected by feeding 6-azauracil (Pedersen, 1982, Hereditas 97: 329); feeding 6- azathymine produces weak b phenocopy which is suppressed by Su(b) (Pedersen). ERG normal [Hotta and Benzer, 1969, Nature (London) 22: 354-56]. Puparial case structurally abnormal with wide, diffuse, exocuticular lamellae and indistinct endo- cuticular fibrils (Jacobs, 1978, Insect Biochem. 8: 37-41). Pupae UV sensitive (Jacobs 1978). Suppressed by su(b) (Sherald, 1981, Mol. Genet. 181: 102-106) and Su(b) (Peder- sen); enhanced by sp2 (Gubb) and su(r) (Pedersen). su(r) su(b) b is enhanced black; su(r) b not enhanced by feeding 6- azauracil (Pedersen). Possibly structural gene for beta- ureidopropionase (EC 3.5.1.6; Sherald). RK1 in aged flies. alleles: allele origin discoverer ref ( cytology ________________________________________________________________________ b1 spont Morgan, 1910 4, 5, 7, 8 *b14b28 spont Bridges 7 *b18c27 spont Wallace 7 *b23b2 spont L.V. Morgan 7 *b24b15 spont L.V. Morgan 7 *b29 spont Promptov 7 *b34g spont Gottschewski 7 b36f Nichols-Skoog, 11 36f1 b39 spont Glass, 39f22 7, 9 *b39j spont Bryson 7 b40c spont Buzzati- 6, 7 Traverso, 40c15 b50d | UV Meyer, 50d 8, 12 b51f | UV Meyer, 51f 8, 12 b661 / ray Alexandrov 1 b66h b71k1 / ray Alexandrov 1 Tp(2;2)34D2-4; 34D8-E1; 43C2-4; lethal b71k2 / ray Alexandrov 1 b74b2 caffeine + / ray Alexandrov 1 b74b4 caffeine + / ray Alexandrov 1 b74b5 caffeine + / ray Alexandrov 1 b74c2 caffeine + / ray Alexandrov 1 b74c4 caffeine + / ray Alexandrov 1 b74c5 caffeine + / ray Alexandrov 1 b74d2 caffeine + / ray Alexandrov 1 b74d4 caffeine + / ray Alexandrov 1 b74d6 caffeine + / ray Alexandrov 1 b75a / ray Alexandrov 1 b75f EMS 2 b76b1 caffeine + / ray Alexandrov 1 b76b2 caffeine + / ray Alexandrov 1 b76e1 / ray Alexandrov 1 b76e2 / ray Alexandrov 1 b76f3 | / ray Alexandrov 1 b76j1 actin.-D + / ray Alexandrov 1 b76j2 actin.-D + / ray Alexandrov 1 b76j3 actin.-D + / ray Alexandrov 1 b76k1 actin.-D + / ray Alexandrov 1 b76k2 actin.-D + / ray Alexandrov 1 b77a1 actin.-D + / ray Alexandrov 1 b77a2 actin.-D + / ray Alexandrov 1 b77a3 actin.-D + / ray Alexandrov 1 b77a4 actin.-D + / ray Alexandrov 1 b77a5 actin.-D + / ray Alexandrov 1 b77j / ray Alexandrov 1 b77.1X X ray 3 In(2L)CyLtR, Roi b77.2X X ray 3 In(2L)CyLtR, Roi b77.3e EMS 2 b77.4e EMS 2 b77.5X X ray b78.1 DEO / Detwiler 3 b78a / ray Alexandrov 1 b78f1 NaF + / ray Alexandrov 1 b78f2 NaF + / ray Alexandrov 1 b78g NaF + / ray Alexandrov 1 b78k1 NaF + / ray Alexandrov 1 b78k2 NaF + / ray Alexandrov 1 b78k3 NaF + / ray Alexandrov 1 b78k4 NaF + / ray Alexandrov 1 b78k5 NaF + / ray Alexandrov 1 b79a1 0.85 MeV n Alexandrov 1 b79a2 0.85 MeV n Alexandrov 1 b79b1 / ray Alexandrov 1 b79b7 0.85 MeV n Alexandrov 1 b79d2 / ray Alexandrov 1 b79d4 0.85 MeV n Alexandrov 1 b79d5 0.85 MeV n Alexandrov 1 In(2L34D4; 35B10; lethal b79d6 0.85 MeV n + / ray Alexandrov 1 T(2;3)34A2-3; 34D8-E1;79B; 80C; lethal b79d8 | 0.85 MeV n + / ray Alexandrov 1 b79dt0 0.85 MeV n + / ray Alexandrov 1 b79dt1 0.35 MeV n Alexandrov 1 b79dt3 / ray Alexandrov 1 b79df2 / ray Alexandrov 1 b79g2 / ray Alexandrov 1 b79h1 / ray Alexandrov 1 Tp(2;2)34D2-4; 34D8-E1; 41; lethal b79h2 / ray Alexandrov 1 b79h3 / ray Alexandrov 1 b80c1 / ray Harrington b80c2 / ray Angel 3 In(2L)b80c2 b80i2 / ray Harrington b80i3 / ray Harrington b80j1 / ray Harrington T(1;3)CA17 b80j2 / ray Harrington b80k1 / ray Harrington b80k2 / ray Harrington b80l1 / ray Angel Tp(2;2)Sco b80l2 / ray Angel Tp(2;2)Sco b81a / ray Alexandrov 1 Tp(2;2)34D2-4; 34D8-E1; 41D-E1; lethal b81a2 / ray Alexandrov 1 b81c 0.7 MeV n Alexandrov 1 b81c2 / ray Alexandrov 1 b81c17 / ray Alexandrov 1 b81dt b81f1 ` / ray Gubb CyO + Dp(2;2)34D3; 35B2 b81f2 / ray Gubb CyO b81f3 | 0.1 MeV n Alexandrov 1 In(2L)34D2-4; 35B10 b81h2 / ray Gubb CyO b81k | / ray Alexandrov 1 b81l2 / ray Durrant In(2L)Gla b81l17 / ray Alexandrov 1 In(2L)34D2-4; 40F; lethal b81l40 / ray Alexandrov 1 b81l42 / ray Alexandrov 1 lethal bb82a1 / ray Harrington bb82c1 spont Harrington In(2LR)Gla b82c3 252Cf fission n Alexandrov 1 b82c7 252Cf fission n Alexandrov 1 b82c16 252Cf fission n Alexandrov 1 b82c44 252Cf fission n Alexandrov 1 In(2L)34D4; 40F; homozygous sterile b82c54 252Cf fission n Alexandrov 1 homozygous sterile b83b1 / ray Alexandrov 1 homozygous sterile b83b2 / ray Alexandrov 1 In(2L)34D4; 35B10; lethal b83b40 / ray Alexandrov 1 b83c20 / ray Alexandrov 1 b83c25 / ray Alexandrov 1 b83c26 / ray Alexandrov 1 b83c35a / ray Alexandrov 1 homozygous sterile b83c35b / ray Alexandrov 1 b83c36 / ray Alexandrov 1 b83c47 / ray Alexandrov 1 homozygous sterile b83d29b 252Cf fission n Alexandrov 1 b83d35 252Cf fission n Alexandrov 1 b83d36 252Cf fission n Alexandrov 1 b83f17 / ray Alexandrov 1 b83f18 / ray Alexandrov 1 b83f51 / ray Alexandrov 1 b83f52 / ray Alexandrov 1 b83fXD X ray Alexandrov 1 b83l 0.7 MeV n Alexandrov 1 b84b1 / ray Harrington b84g X ray Alexandrov 1 b84h34 X ray Alexandrov 1 b84h40 X ray Alexandrov 1 b84h70 / ray Alexandrov 1 b85b3 / ray Alexandrov 1 b85b4 / ray Alexandrov 1 b85c2 0.85 MeV n Alexandrov 1 T(2;3)34C7-D1; 34E1-2; 95C4-D1; homozygous sterile b85c3 0.85 MeV n Alexandrov 1 bA51 EMS Sherald bA53 EMS Sherald bA54 EMS Sherald bA55 EMS Sherald bD - spont Goldschmidt, 10 1945 ( 1 = Alexandrov and Alexandrova, 1986, DIS 63: 159-61; 2 = Ashburner, Faithfull, Littlewood, Richards, Smith, Vel- issariou, and Woodruff, 1980, DIS 55: 193-95; 3 = Ash- burner, Angel, Detwiler, Faithfull, Gubb, Harrington, Lit- tlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91; 4 = Ashburner, Aaron, and Tsubota, 1982, Genet- ics 102: 421-35; 5 = Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 144 (fig.); 6 = Buzzati- Traverso, 1940, DIS 13: 49; 7 = CP552; 8 = CP627; 9 = Glass, 1939, DIS 12: 47; 10 = Goldschmidt, 1945, Univ. Calif. Berkeley Publ. Zool. 49: 504-20; 11 = Nichols-Skoog, 1937, DIS 7: 60; 12 = Meyer and Edmonson, 1951, DIS 25: 71. | Lighter than b1. / Diepoxyoctane. ` Induced simultaneously with rk81f2. - Synonym = bB; homozygous lethal, said to be associated with Df(2L)35C;35D, but this was almost certainly a misinterpre- tation of ectopic pairing (Ashburner). cytology: Placed in region 34D4-6 (Ashburner). # |: see Tyr2 # B: Bar location: 1-57.0. origin: Spontaneous in a female. discoverer: Tice, 13b. references: 1914, Biol. Bull. 26: 221-30 (fig.). Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 66 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 29-33. phenotype: Eye restricted to narrow vertical bar of about 90 facets in the male and 70 facets in the female, as contrasted with normal numbers of about 740 for males and 780 for females [Sturtevant, 1925, Genetics 10: 117-47 (fig.)]. Homozygous female fully viable. B/+ female has about 360 facets and shows indentation terminating in horizontal fissure on ante- rior margin of eye, producing a kidney-shaped eye. B/B and B/+ completely separable from wild type; in some genetic back- grounds, B/B overlaps B/+ slightly. Classifiable in single dose in triploids by slight anterior nick in eye (Schultz, 1934, DIS 1: 55); is useful in the recognition of triploids. Variegated position effect derivatives of BS(BSVY) exhibit nonmutant phenotypes in XY males but narrow eyes in XYY males; other enhancers of variegation, M(2)S10 and E(var)7, also shift phenotype toward normal (Brosseau, 1960, Genetics 45: 979). Eyes of female heterozygous for a deficiency for B and a normal X are normal (Sutton, 1943, Genetics 28: 97- 107). Log of facet number inversely proportional to tempera- ture of development (Hersh, 1930, J. Exp. Zool. 57: 283-306). Nonautonomous over short distances (Sturtevant, 1932, Proc. Intern. Congr. Genet., 6th, Vol. 1: 304-7). Facet develop- ment enhanced in organ culture by addition of wild type cephalic complexes [Kuroda and Yamaguchi, 1956, Jpn. J. Genet. 31: 97-102 (fig.)]. Disc size reduced; morphogenetic furrow absent; deep cleft at anterior margin of preommatidial cell clusters. Only four to five rows of clusters. Those at cleft edge look mature (Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29). Cell death observed in anterior presumptive ommatidium-forming region of eye disc [D. Fristrom, 1969, Mol. Gen. Genet. 103: 363-79; 1972, Mol. Gen. Genet. 115: 10-18; Michinomae and Kaji, 1973, Jpn. J. Genet. 49: 353-71 (fig.); Michinomae, 1974, Jpn. J. Genet. 49: 353-71; 1976, Jpn. J. Genet. 51: 315-26 (fig.)]; high acid phosphatase levels characteristic of liposomal activity seen at same time (Michi- nomae, 1974, 1976). Reduction in facet number, increase in acid phosphatase activity, and cell death inhibited in larvae grown on medium supplemented with acetamide or lactamide (Kaji, 1954, Annot. Zool. Jpn. 27: 194-200; Fristrom, 1972; Michinomae and Kaji, 1973; Michinomae, 1974, 1976). Double amides more effective than single (DeMarinis and Sheibley, 1968, DIS 43: 138). Facet development responds strongly to environmental factors around 60 hr after oviposition (Luce, Quastler, and Chase, 1951, Genetics 36: 488-99). Pigmented but nonfaceted part of eye shows retinulae and dioptic apparatus lacking, but rudimentary ommatidia present, consist- ing of hypertrophied accessory cells (Wolsky and Huxley, 1936, Proc. Zool. Soc. London 485-89). Introduction of B into a strain of flies characterized by jumping in response to a sud- den decrease in light intensity nearly eliminates response; response rescued by increasing facet number _____________________________________________________________________________________________________________________________________ allele origin ref ( phenotype cytology ` ____________________________________ ___________________________________ | chromosome treatment | | | eye | viability / | | _____________________________________________________________________________________________________________________________________ B3 B spont 6, 7 B + *B36j + spont 6, 7 B + T(1;3)16A;88F B68f + X ray 3 B *Brev-1 B X ray 6, 7 + + no change *Brev-2 B X ray 6 + + In(1)3F8-4A1;16A2-4 *Brev-3 B X ray 6 + + In(1)16A6-A1;20A4-5 BS B X ray 6, 7 >B + T(1;4)16A7-A1;102F BS3i B X ray 7 >B + Tp(1;3)16A7-B1;19-20;66B13-C1 BSR T(1;4)BS spont 5,9 + + no change BSV BSY X ray 1 B = more extreme than B/+, etc. / Viability of males hemizygous and, where testable, of females homozygous for the allele. Where tested the lethal alleles are cell lethal in cuticular spots. ` + = loss of tandem duplication or triplication to produce normal sequence. through lactamide feeding during larval development (Nakashima-Tanaka and Matsubara, 1980, Jpn. J. Genet. 55: 275-82). RK1A. alleles: Derivatives of B with altered phenotypes, including reversions to normal phenotype have been given allelic desig- nations. These derivatives are summarized in the accompanying table. Unless otherwise indicated, fuller descriptions are found in CP627. See table for allele information. cytology: Located in 16A1-2. Associated with Dp(1;1)B = Dp(1;1)15F9-16A1;16A7-B1. molecular biology: Region cloned by transposon tagging from hybrid-dysgenesis-induced B reversion (Tsubota, Rosenberg, Szostak, Rubin, and Schedl, 1989, Genetics 122: 881-90). Analysis of genomic DNA reveals presence of roo element at the junction between 16A7 and 16A1, indicating that original duplication may have arisen by unequal recombination between roo elements inserted at 16A1 and 16A7. Three hybrid- dysgenesis-induced partial revertants have P-element inserts close to the junction as does B3. Breakpoints of B, BM1, BM2, and Bbd span a region of approximately 37 kb. other information: Since B is a tandem duplication, B homozy- gotes may give rise to a nonduplicated chromosome (reversal to normal phenotype) and a triplicated chromosome (i.e., double Bar = BB) as reciprocal products of unequal crossing over (Sturtevant and Morgan, 1923, Science 57: 746-47; Gabay and Laughnan, 1973, Genetics 75: 485-95). From successive unequal crossovers in attached X's, Rapoport (1940, Zh. Obshch. Biol. 1: 235-70; 1941, DIS 15: 36-37) was able to accumulate as many as 7 or 9 Bar regions in a single chromo- some. Bar is the first recorded instance of position effect. Presumably results from the new band association 16A7-16A1 and can be reversed by rearrangements that separate these bands. Also the first case of cis-trans position effect, two 16A7- 16A1 associations in the same chromosome producing greater facet reduction than one association in each of two homologous chromosomes. B: Bar Left: heterozygous female. Right: hemizygous male. From Stur- tevant and Beadle, 1939. An Introduction to Genetics, Saunders, p. 24. # BZ: see BR # b-l33g18: see tri # B2t: see TubB85D # ba: balloon location: 2-107.4. origin: Spontaneous. discoverer: Morgan, 10k. references: Marshall and Muller, 1917, J. Exp. Zool. 22: 457- 70 (fig.). Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 148 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 212 (fig.), 218. Bridges, 1937, Cytologia (Tokyo), Fujii Jub., Vol. 2: 745-55. ba: balloon From Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 148. phenotype: Wings at first inflated with hemolymph to produce blisters and vesicles; venation weak, plexus like; wings smaller, warped, discolored, and divergent. Effect caused by inadequate contraction of epithelium after inflated state of pupal wing [Waddington, 1940, J. Genet. 41: 75-139 (fig.)]. Sensitive to temperature. RK3 above 25; RK2 at 19 or below. alleles: *ba2 (CP627). cytology: Located in 60C5-D2 based on inclusion within Df(2R)Px = Df(2R)60B8-10;60D1-2 and within Df(2R)Px2 = Df(2R)60C5- 6;60D9-10 (Bridges, 1937). other information: May be part of a pseudoallelic complex with bs and Px. # ba2: see blo # ba33f26: see blo # Ba: Brista location: 2-107.8 (0.8 unit to right of sp). synonym: Dll: Distal-less. references: Sato, 1984, DIS 60: 180-82 (fig.) Sunkel and Whittle, 1987, Wilhelm Roux's Arch. Dev. Biol. 196: 124-32. Cohen and Jurgens, 1989, EMBO J. 8: 2045-55. phenotype: Null alleles are recessive embryonic lethals, with dominant developmental defects of distal appendages. Lethal embryos lack certain sensilla, including Keilin's organs, and antennal, maxillary, labial, and labral sense organs, all of which are thought to correspond to vestiges of the distal sen- silla of rudimentary larval appendages. No other embryonic sensilla are affected, nor are the neurons innervating the rudementary apppendages detectably abnormal. In homozygous- viable or pharate-adult-lethal hypomorphic alleles defects are found in all appendages represented by the above larval struc- tures. Heterozygotes for lethal alleles are characterized by transformations of distal antennal segments (i.e., AII, AIII, and arista) to mesothoracic leg and by variable loss of distal leg segments, depending on severity of allele. Transformation in the case of Ba1 sensitive to low-temperature pulses throughout larval development, whereas the TSP for leg trunca- tion is at end of the third larval instar. Clones of homozy- gous Ba- cells incapable of contributing to any but the coxal segment of the legs, and for the most part, the first antennal segment; in the relatively infrequent cases, in which Ba- clones involve distal antennal segments, Ba- portions, which always include at least the arista, are absent, and Ba+ por- tions develop normally indicating cellular autonomy. alleles: allele origin discoverer synonym ref ( comments | ______________________________________________________________________________ Ba1 / ray Whittle 2, 3, 6 cold sensitive allele *Ba2 EMS Sunkel 6 Ba3 EMS Sunkel 6 recessive pharate-adult lethal Ba5 EMS Tiong, 1983 3, 6 Ba6 2 Ba7 2 Ba8 2 Ba9 spont Sato BaM 2, 5, 6 recessive; homozygous viable Ba10 HD Adler E(Arp) 1, 2, 3 8-kb insert in 13-kb intron at ~ 120 + P insert distal to transcription unit at 30 kb; recovered as enhancer of Arp Ba11 X ray Botas Art3, BaB 2, 3, 6 In(2LR)48E-F;60E5-6; break at ~ 115 kb / Ba12 EMS Kennison BaE1 4 Ba13 Gelbart BaG 2, 3 Tp(2;3)52E;60E;81; break at ~ 100 to 110 kb Ba14 spont Bussey anto, BaIB 2 Ba15 / ray Jurgens BaJ 2, 3, 6 T(2;3)60E5-6;64B12-C12; break at ~ 105 kb; 3 to putative coding region ` Ba16 HD Posakony BaP 2 insert of ? at ~ 125 kb Ba17 BaSA1 2, 3 ~ 6 kb deletion around ~ 120 kb; removes middle exon Ba18 spont Williams Art1, BaW 2, 3, 6 T(1;2)3C3-7;60E5-6; break at ~ 120 kb ( 1 = Brunk and Adler, 1990, Genetics 124: 145-56; 2 = Cohen, Bronner, Kuttner, Jurgens, and Jackle, 1989, Nature 338: 432-34; 3 = Cohen and Jurgens, 1989, EMBO J. 8: 2045-55; 4 = Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40; 5 = Sato, 1984, DIS 60: 180-82; 6 = Sunkel and Whittle, 1987, Wilhelm Roux's Arch. Dev. Biol. 196: 124-32. | Coordinates estimated from figure of Cohen et al.; origin undefined; positive values extend to left. / Differs from other tested alleles in showing some dominance in combination with two + alleles. ` Differs from other tested alleles in being embryonic rather than pupal lethal in combination with Ba3 and Ba9. cytology: Placed in 60E5-6 based on its inclusion in Df(2R)Ba = Df(2R)60E3;60E6 and on common breakpoints of Ba rearrange- ments. molecular biology: Region isolated in a chromosome walk of 180 kb (Cohen, Jurgens, and Jackle, 1989, Nature 338: 432-34). Ba lesions extend over a region of 38 kb. A single transcrip- tion unit detected that is homologous to transcripts of ~2.5 and ~3.4 kb which hybridize to restriction fragments extending over 25 kb of genomic sequence; three exons identified; sequence of genomic fragments hybridizing transcript indicate the presence of a putative homeodomain that is interrupted by an intron between residues 44 and 45 as is the homeodomain of lab. # Ba1 phenotype: Homozygous lethal; dies in first instar and has nor- mal morphology. Heterozygote shows antenna-to-leg transformation; entire arista and part of third antennal seg- ment transformed to distal metathoracic leg structures. Expression temperature sensitive; transformation complete at 19; phenotype normal at 29. Ba/Df(2R)Ba4 shows abnormal seg- mentation both dorsally and ventrally and loss of head struc- tures; antennal, maxillary, and labial segments affected. "H" piece malformed or absent as are Keilin's organs in all three thoracic segments. Recessive to two doses of 60D-F. # Ba3 phenotype: Ba3/+ wild type; Ba3/Ba1 fail to eclose; pharate adults lack third antennal segment; second segment transformed to leg; distal arista normal. Legs lack all structures distal to tibiae; tibiae enlarge and bear ectopic bristles; no remaining leg bristles are bracted. # Ba5 phenotype: Ba5/+ like Ba1/+. Ba5/Ba5 and Ba5/Ba1 are late embryonic lethals; show loss of antennae, maxillary, and labial sense organs, as well as the "H" piece and Keilin's organs from all three thoracic segments. Occasional abnormal- ities in setal bands of segments posterior to prothorax; setal bands or spinules may be deleted or adjacent bands fused. Posterior end of larva normal. # Ba9 phenotype: Recessive allele. Homozygotes show partial transformation of antennae to legs as well as deletions of some leg structures. Tarsal tissue, sometimes including claws, develops in place of arista and part of third antennal segment. Third segment usually contains patchwork of incom- pletely differentiated leg tissue; first and second segments normal. Leg effects distal to mid tibia; legs proximal to mid tibia normal. In extreme cases number of tarsal segments reduced to two or three; basitarsus and distal tibia may be missing; in most extreme cases claws may also be missing. In the case of mild expression abnormal bristle patterns, includ- ing polarity reversal, occur around basitarsus-tibia joint, where there may also develop cuticular hyperplasia. Penetrance greater in females than males, in antennae than legs, and in metathoracic than other legs. Ba1/BaM die as pharate adults with extreme malformations of antennae and legs. # Ba12 phenotype: Ba12/+ wild type; recessive lethal. Heterozygote exhibits nearly complete suppression of extra-sex-combs pheno- type of Pc4/+. # bab: see ybab # Bag: see Bg # bag of marbles: see bam # Baksa: see Fs(3)Sz3 #*bal: bandy legged location: 2- (not located). origin: Spontaneous. discoverer: Stroher, 1958. references: Mainx, 1958, DIS 32: 82. phenotype: Legs extremely shortened and crippled. All parts of legs from femur to tarsi shortened, broadened, and irregularly curved. Deformities most extreme in metathoracic legs. Move- ment unsteady and tottering. Manifestation increased by selection. Viability poor, especially in males; fertility good. RK2. # bald: see ra2 # balding: see bd # bald: see bld # baldhead: see bh # ballet: see blt # balloon: see ba # Balloon: see Bb # balloon wing: see bs3 # bam: bag of marbles location: 3-{85}. origin: Hybrid dysgenesis. references: Gonzalez, Molina, Casal, and Ripoll, 1989, Genetics 123: 371-77. genetics: Homozygous males and females sterile. cytology: Placed in 96A-E based on its inclusion in Df(3R)L16 = Df(3R)96A1;96E. # band: see bn # bandy legged: see bal # bang senseless: see bss # bang sensitive: see bas # Bar: see B # Bar + Bar: see BB # Bar double: see BB # bar eye: see at # bar-3: see hh # Bar-infra double: see BiBi # Barlike eye: see Ble # baroid: see Bbd # barrel: see hbrr # Barsa: see Fs(2)Sz1 # bas: bang sensitive (J.C. Hall) location: 1-50.7 (based on 31 m - f recombinants). origin: Induced by ethyl methanesulfonate. references: Grigliatti, L. Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-14. Ganetzky and Wu, 1982, Genetics 100: 597-614. synonym: bas-A. phenotype: Striking culture vial sharply on hard surface immo- bilizes bas flies for 30-40 seconds. Rapid recovery followed by refractory period of an hour. Suppressed by napts at per- missive temperatures; at temperatures above 37.5 bas flies quickly paralyzed; no detectable physiological abnormalities at neuromuscular junction in bas larvae (Ganetsky and Wu). In experiments on photoreceptor function, recovery of prolonged depolarization afterpotentials (induced by strong blue light) abnormally slow following exposure to orange light (Homyk and Pye, 1989, J. Neurogenet. 5: 37-48). cytology: Included in neither Dp(1;4)r+ = Dp(1;4)13F;16A1-2 nor Df(1)sd72b = Df(1)13F1-14B1; therefore bas to the left of 13F1. Placed in 12F by Homyk. other information: Jan and Jan (1978, Proc. Nat. Acad. Sci. USA 75: 515-19) erroneously termed what is now bss1 a bas allele. # bas-B: see bss # Bashed: see Mhc-m5 # basket: see bsk # bat: bat location: 2-71.0. discoverer: Bridges, 22j26. synonym: ext-b: extended-b. phenotype: Wings extended and bent backward. RK2. #*baton: baton location: 2-52. phenotype: Abdomen elongated with defective plates; eye resem- bles L4. Extremely inviable; most homozygotes die in larval and pupal stages, appearing as elongated corpses. Heterozy- gote shows some eye effect. RK3. # baz: bazooka location: 1-56.7. origin: Induced by ethyl methanesulfonate. references: Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. Wieschaus and Noell, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 63-73. phenotype: Homozygous lethal, large dorsal and ventral hole in embryo. Homozygous baz germ-line clones undergo oogenesis, but the heterozygous progeny produced display major reductions in viability (Wieschaus and Noell). alleles: Three alleles, baz1 = D9, baz2 = K7, and baz3 = i1. cytology: Placed in 14A1-B1, or 14E1-F6, or 15A6-16A2 based on its being covered by Dp(1;4)exd+82b = Dp(1;4)14A1-2;14B5-18 + 14E1-4;16A1-2 but not included in Df(1)r-D17 = Df(1)14F6;15A6. an extreme bobbed Edith M. Wallace, unpublished. # bb: bobbed (K.D. Tartof and R.S. Hawley) location: 1-66.0 (Bridges) and on YS (Stern, 1927; Cooper, 1959, Chromosoma 10: 535-88). Proximal to ks-1 and ks-2 (Kennison, 1981, Genetics 98: 529-48). origin: Many alleles. In laboratory stocks, bb mutants may arise spontaneously or inadvertently while selecting for mutagen-induced mutations at other loci. bb mutations may be induced at high frequency by carcinogenic hydrocarbons such as 7,12-dimethyl benz[(]anthracine (DMBA) (Fahmy and Fahmy, 1969, Nature 224: 1328-29; 1970, Mutat. Res. 9: 239-43) or multi- functional alkylating agents such as triethylenemelamine (Tar- tof). Mutations of the X chromosome bb locus may be specifi- cally induced genetically in four different ways. First, alterations of the X chromosome bb locus may occur bb in males or females carrying the aberrant chromosome Ybb-. These are high frequency (10-2-10-1) events and may be observed as either stable reversions from bb to bb+ (magnification: Ritossa, 1968, Proc. Nat. Acad. Sci. USA 60: 509-16; Komma and Endow, 1986, Genetics 114: 859-74) or as mutations (10-3-10-2) from bb+ to bb or from bb to bbl (reduction: Tartof, 1973, Cold Spring Harbor Symp. Quant. Biol. 38: 491-500; Tartof, 1974, Proc. Nat. Acad. Sci. USA 71: 1272-76; Locker and Prud'homme, 1973, Mol. Gen. Genet. 124: 11-19). It has been suggested that both magnification and reduction may be the result of unequal sister-chromatid exchanges occurring at the X chromosome bb locus in the germ line of X/Ybb- males (Tartof, 1974); evidence for this is from studies of ring-X bb chromosomes (Endow, Komma, and Atwood, 1984, Genetics 108: 969-83); alternatively, a model of exci- sion and reintegration of circular molecules rDNA has been proposed by Ritossa [1972, Nature (London), New Biol. 240: 109-11]. C(1)RM stocks carrying Ybb- accumulate modif- iers that suppress the bb phenotype (Marcus, Zitron, Wright, and Hawley, 1986, Genetics 113: 305-19). Second, in males carrying mei-41, bb+ mutates to bb at a frequency of 10-3-10-2 (Hawley and Tartof, 1983, Genetics, 104: 63-80). mei-41 does not induce reversions of bb to bb+ as does Ybb- nor does it induce bb mutations on the Y. Third, when males carrying cer- tain XY chromosomes are mated to females heterozygous for Rex, free Y chromosomes carrying bb mutants are generated at high frequency (10-2; Robbins, 1981, Genetics 99: 443-59). Fourth, hybrid dysgenic crosses may also generate bb (Thompson and Woodruff, 1980, Proc. Nat. Acad. Sci. USA 77: 1059-62). Despite such high frequency genetic mutations, homozygous stocks of bb2, bb4, bb6, and bb8 have been maintained for 10 years with no evidence of reversions (Tartof). Unless oth- erwise stated, the origin of most bb mutations is unclear. discoverer: Sturtevant, 20b. references: Stern, 1927, Z. Indukt. Abstamm. Vererbungsl. 44: 187-231. Ritossa, Atwood, and Spiegelman, 1966, Genetics 54: 819-34. Ritossa, 1976, Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 801-47. phenotype: Three phenotypes are associated with bobbed mutants: thinning and shortening of bristles, etching of the abdomen, and, in extreme cases, lethality. Of these pheno- types, bristle size and lethality are the most reliable. These phenotypes are somewhat variable from fly to fly and the bristle abnormality may be obscured by such mutations as f, sn, and ty to name a few. bb/0 males, and bb/In(1)sc4Lsc8R females have phenotypes similar to, but more extreme than, that of homozygous females. bb/Y males are wild type, owing to presence of a normal allele of bb in YS; bb/bb/Y females are similarly normal in phenotype. Viability is variable. Ritossa, Atwood, and Spiegelman (1966) showed that bb contains about half as many ribosomal RNA genes (rDNA) as bb+. They conclude that the bb locus is the site of ribosomal RNA syn- thesis and interpreted bb mutations as partial deletions of the locus. They postulated that in bb flies the rate of pro- tein synthesis is limited by the amount of ribosomal RNA, and the bb phenotype results in part because normal bristle pro- duction requires maximum protein synthesis on the part of the trichogen cells during a particular interval in development. The rate of rRNA synthesis is reduced in bb (Mohan and Ritossa, 1970, Dev. Biol. 22: 495-512; Mohan, 1975, Genetics 81: 723-38; Shermoen and Kiefer, 1975, Cell 4: 275-80) alleles: Many independent occurrences of bb have been recovered and designated without a superscript; consequently, alleles designated as bb are often unrelated. We redesignate Sturtevant's original bb5 as bb1, but, given the propensity for bb alleles to change spontaneously and the ambiguities of labeling, it is unlikely than any particular bb stock contains the original allele. The same arguments apply to Ybb origi- nally described by Bridges. The accompanying tables summarize the specifically designated bb alleles on both the X and the Y chromosomes. X-linked bb alleles allele origin discoverer ref ( comments __________________________________________________________________________ bb1 Sturtevant 20b 2 bb2 Schultz 13 severe; ~120 genes bb2r reduction Tartof 14 lethal; ~20 genes of bb2 bb2m magnification Tartof 14 normal; ~220 genes of bb2 bb4 Schultz 13 standard bb; ~160 genes bb5 not bb5 of Fahmy and 3 Sturtevant Fahmy bb6 Schultz 13 severe; ~150 genes bb7 Schultz 13 severe; ~140 genes bb8 Schultz 21 severe; ~100 genes bb11 in C(1)RM Gabritschevsky 2 *bb20 spont Bridges 30b24 2 lethal *bb28l spont 2 bb41 mei-41 induced Hawley 6 severe bb68F Lee 7 bb69d 7-bromomethyl Fahmy and 4 12 methyl benz[(] Fahmy anthracine bb83 in Binsc bb84 in Binsc bbamg abnormal male genitalia *bbD X ray Lefevre 48g28 2 dominant allele bbds spont Goldschmidt 9 no longer defi- ciency sensitive; ~100 genes *bbG1 spont Goldschmidt 2 *bbG2 spont Goldschmidt 2 bbG3 spont Goldschmidt 2 *bbG4 spont Goldschmidt 2 *bbG5 spont Goldschmidt 2 *bbK EMS Merrakechi 5 bbl spont Bridges, 1926 2 lethal; ~20 genes *bbl2 spont Stern, 28k 2 bbN 1 bbn5 *bb0f X ray 2 *bbOf-2 X ray 2 bbP2 8 bbP7 8 bbRex Rex | Robbins 11, 12 bbS1 Schultz 13 ~130 genes bbT6 EMS 10 ( 1 = CP552, 2 = CP627; 3 = Fahmy and Fahmy, 1970, DIS 45: 74; 4 = Fahmy and Fahmy, 1971, Mut. Res. 13: 19; 5 = Gans, Audit, and Masson, 1975, Genetics 81: 683-704; 6 = Hawley and Tartof, 1983, Genetics 104: 63-80; 7 = Lee, 1972, DIS 48: 18; 8 = Lenevea and Prud'homme, 1974, Euro- pean Drosophila Conference Abstracts 4; 9 = Lindsley, Eding- ton, and Von Halle, 1960, Genetics 45: 1645-90; 10 = Makai and Marrakechi, 1978, Biol. Cell. 33: 39a; 11 = Robbins, 1981, Genetics 99: 443-59; 12 = Swanson, 1984, Ph.D. dissertation, Michigan State University; 13 = Tartof, 1973, Genetics 73: 57-71; and 14 = Tartof, 1974, Proc. Nat. Acad. Sci. USA 71: 1272-76. | A group of bb alleles regularly produced by Rex-induced mitotic exchange in YSX+YL or in X chromosomes having separated blocks of rDNA (e.g. In(1)wm51bLwm4R; In(1)scS1Lsc4R). Phenotype ranges from bobbed-lethal to wild-type. Y-linked bb alleles allele origin discoverer ref / comments ____________________________________________________________ Ybb spont Bridges 1 designated several unrelated Y-linked bb mutations Ybb- spont Schultz 1, 7 ~40 genes; lacks cr+ Ybb- spont Schultz 2 ~10 genes, mostly with type II inserts, does not participate in nucleolus formation YbbP2 Tartof ~50% normal gene content YbbN2 spont? Ritossa 4 weak; viable over bbl; ~100 genes YbbN3 spont Ritossa 4 weak; viable over bbl; ~100 genes YbbRex Rex ` Robbins 5, 6 YbbsuVar 4 strong; viable over bbl; ~50 genes Ybbts1 EMS Williamson 3 ~117 genes; extreme bb at 18; normal at 29 Ybbts2 EMS Williamson 3 ~127 genes; extreme bb at 18; normal at 29 / 1 = CP627; 2 = Endow, 1982, Genetics 102: 91-99; 3 = Pro- cunier and Williamson, 1974, Dev. Biol. 39: 198-109; 4 = Ritossa, 1968, Proc. Nat. Acad. Sci. USA 59: 1124-31; 5 = Robbins, 1981, Genetics 99: 443-59; 6 = Swanson, 1987, Genetics 115: 271-76; 7 = Tartof, 1973, Genetics 73: 57- 71. ` A regular product of Rex-induced mitotic exchange in progeny of crosses of Rex/+ or Rex/Rex females to YSX+YL/0 males; X/YbbRex males are fertile. cytology: Shown to be to the right of 20E-F by Schalet and Lefevre [1976, Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 848-902)]. The bb locus lies approxi- mately in the center of the proximal heterochromatin and accounts for about one-third of its length, or about 3.2 x 106 bp. The nucleolus organizer, located between heterochromatic regions hB and hC (Cooper, 1959), = h29 of Gatti and Pimpinelli, and the rDNA are probably the same (Ritossa, Atwood, and Spiegelman, 1966). Presence of bb+ on Y chromosome postulated by Burlingame and demonstrated by Stern (1927). This bb+ is located on YS proximal to ks-1 and ks-2 (Kennison, 1981); it is located in the Hoechst-33258 dully fluorescing segment of YS designated h20 by Gatti and Pim- pinelli (1983, Chromosoma 88: 349-73). The rDNAs of the X and Y chromosomes combine to form a single nucleolus in which the rDNA components of each chromosome can be discerned by elec- tron microscopy (Schultz, 1965, Brookhaven Symp. Biol. 18: 116-47). Positions of X-chromosome inversion breakpoints with respect to the rDNA. Thin line represents euchromatin and shaded box represents ribosomal DNA. molecular biology: The X and Y chromosome bb loci each contain approximately 225 rRNA genes organized as a large tandem array of transcription units separated by nontranscribed spacers. (Ritossa et al., 1966, Tartof, 1973, Genetics 73: 57-71). Copy number of Y-linked sequences varies over a six-fold range in Y chromosomes sampled from a natural population (Lyckegaard and Clark, 1989, Proc. Nat. Acad. Sci. USA 86: 1944-48). Sequences of nontranscribed spacers and external transcribed spacers determined (Simeone, deFalco, Macino, and Boncinelli, 1982, Nucleic Acid Res. 10: 63-72; Simeone, LaVolpe, and Bon- cinelli, 1985, Nucleic Acid Res. 13: 1089-1101). There are three kinds of repeating units in the array as defined by digestion with the restriction enzyme, EcoRI. The first class is the functional 11-kb gene containing an external transcribed spacer followed by the sequence encoding 18S rRNA and then an internal transcribed spacer within which is the sequence encoding 5.85 rDNA; this is followed by the sequence encoding 28S rRNA, which is interrupted by a short transcribed spacer and finally there is a long non-transcribed spacer (White and Hogness, 1977, Cell 10: 177-92; Wellauer and David, 1977, Cell 10: 193-212; Pellegrini, Manning, and Davidson, 1977, Cell 10: 213-24). A second class is composed of repeats that contain a 0.5- to 5-kb insert known as Type I (White and Hogness; Wellauer and Dawid). The third class of repeats possesses a different insertion, Type II (Dawid, Wel- lauer, and Long, 1978, J. Mol. Biol. 126: 749-68). Type I and Type II insertions are located at different but nearby sites within the 28S coding region (Rioha, Miller, Woods, and Glover, Nature (London) 1981, 290: 749-53; see also Rae, 1981, Nucleic Acids Res. 9: 4997-5010). Type I and Type II containing genes appear to be transcriptionally inactive under normal conditions (Long and Dawid, 1979, Cell 18: 1185-96; Long, Rebbert, and Dawid, 1980, Cold Spring Harbor Symp. Quant. Biol. 45: 667-72) and are intermingled at random with the noninsert-bearing genes throughout the array (Tartof and Dawid, 1976, Nature 263: 27-36; Hawley and Tartof, 1983, J. Mol. Biol. 163: 499-503). During magnification, however, all types of sequences appear to be transcribed (deCicco and Glover, 1983, Cell 32: 1217-25; Labella, Vicari, Manzi, and Graziani, 1983, Mol. Gen. Genet. 190: 487-93). The ribosomal genes of only one homolog are amplified in polytene nuclei of both males and females (Endow, 1980, Cell 22: 149-55). A single rDNA gene is inserted ectopically into euchromatic locations by P-element transformation capable of high-level transcription in polytene chromosomes and micronucleolus for- mation; also able to partially alleviate effects of partial deletions of bb (Karpen, Schaefer, and Laird, 1988, Genes Dev. 2: 1745-63). Map of basic repeating unit of ribosome DNA. Thick segments represent rDNA sequences; segments of intermediate width represent internal (ITS) and external (ETS) transcribed spacer sequences. Thin line represents non-transcribed (NTS) spacer sequences. Inverted triangle denotes positions of type I and type II inserts. X and Y chromosome rDNA differ from each other in three important respects. (1) 65-70% of the X rDNA contains Type I-bearing genes (Wellauer, Dawid, and Tartof, 1978, Cell 14: 269-78). The Y contains type-I repeats detectable by in situ hybridization to metaphase chromosomes (Hatsumi and Endow, 1990); however, the major type-I class is greatly reduced in amount in Y chromosomes (Tartof and Dawid, 1979, Nature 263: 27-30; Komma, Glass and Endow, 1990). (2) Yagura, Yagura, and Muramatsu (1979, J. Mol. Biol. 133: 533-47) showed that the 18S RNA transcribed from X rDNA differs from that of the Y by at least one base substitution. (3) Coen, Thoday, and Dover (1982, Nature 295: 564-68) found that the 5' end of the nontranscribed spacer is different in X and Y rDNA. These data indicate that there is little, if any, interchange of rDNA between X and Y chromosomes. However, rDNA is apparently responsible for regular pairing and segre- gation of X and Y chromosomes in males (McKee and Karpen, 1990, Cell 61: 61-72). other information: Exchange between Xh and the Y chromosome at the bobbed locus results in YSXh. and X.YL products that arise at a frequency of about 2 x 10-4 (for review, see Lindsley, 1955, Genetics 40: 24-44; Hawley and Tartof, 1983, Genetics 104: 63-80). Orientation of the X rDNA cluster has no effect on the frequency of exchange (Maddern, 1981, Genet. Res. 38: 1-7). Similar events occur in females [Williamson and Parker, 1976, Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Vol. 1b, pp. 701-20]. Recombination events involving rDNA sequences of X chromosomes and X and Y chromosomes investigated using restriction-fragment-length polymorphisms (Williams, Kennison, Robbins, and Strobeck, 1989, Genetics 122: 617-24). # bba px sp: see bbG1 # bba px sp hi: see bbG2 # bbpoi: see bbG3 # bbpoi47: see bbG4 # bpoi hi: see bbG5 # bbx: see bb28l # Bb: Bubble location: 1- (not located) or 3-48. origin: X ray induced. discoverer: R. L. King, 32d. synonym: Balloon. phenotype: Wings of heterozygous female smaller, trimmed, and inflated. Bubble in first posterior cell. In extreme cases and usually in males, the wing is a small inflated sac. Sex- ual difference in expression may indicate that Bb is on the X. Female fertile; male entirely sterile; therefore, homozygous females not obtainable. RK3A. cytology: Associated with T(1;3)Bb = T(1;3)13E;84F (Morgan, Bridges, and Schultz, 1937, Year Book - Carnegie Inst. Wash- ington 36: 301). Bb: Bubble From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 23. # BB: Bar + Bar origin: Spontaneous through unequal crossing over in B/B (see description of B). discoverer: Zeleny. synonym: Bar double; Ultra-bar; double Bar. references: 1920, J. Exp. Zool. 30: 292-324 (fig.). Sturtevant, 1925, Genetics 10: 117-47 (fig.). phenotype: Eye more reduced than in B. Facet numbers are 25, 29, and 45 in BB/BB female, BB male, and BB/+ female, respec- tively. Median ocellus lacking or strongly reduced (Lefevre, 1941, DIS 14: 40). Optic disc reduced (Power, 1942, Genetics 27: 161); deep cleft anteriorly; cell clusters at cleft look mature (Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29). RK1A. alleles: Different alleles of B that are not involved in gross chromosome aberrations can be combined in all pair-wise combi- nations by means of unequal crossing over in heterozygous females. Described combinations are *BBi, *BiB, and BiBi (Sturtevant, 1925, Genetics 19: 117-47); *Bi40bBi40b (Stein- berg, 1942, DIS 16: 53); *BB3, BB36b, and BBL (Muller). cytology: Associated with a tandem triplication of the region duplicated in Dp(1;1)B = Dp(1;1)15F9-16A1;16A7-B1 [Bridges, 1936, Science 83: 210-11 (fig.)]. # Bc: Black cells location: 2-80.6. origin: Induced by ethyl methanesulfonate. references: Grell, 1969, DIS 44: 46. Rizki, Rizki, and Grell, 1980, Wilhelm Roux's Arch. Dev. Biol. 188: 91-99 (fig.). phenotype: Quadrate crystalline bodies in crystal cells of hemolymph replaced by amorphous melanotic mass. Black cells appear in 11-hour embryos in Bc/Bc and in late first-instar larvae in Bc/+. Crystal cells replaced by black cells during first instar in Bc/+. Numerous black cells visible through the integument of larvae, pupae, and of head, thorax, and abdomen in adults. Bc/Bc larvae have no phenol oxidase activity and larval hemolymph fails to darken upon exposure to air; Bc/+ intermediate between +/+ and Bc/Bc in these respects. Bc/Bc adults viable and fertile when separated from a closely linked simultaneously recovered lethal. RK1 in lar- vae; RK2 in pupae and adults. cytology: Placed in 55A based on its inclusion in Df(2R)PC4 = Df(2R)55A;55F but not Df(2R)Pd-w5 = Df(2R)55A-B;55C (Deng and Rizki, 1988, Genome 30, Suppl. 1: 192). other information: Suppressed by some lz alleles (Rizki and Rizki, 1981, Genetics 97: s90). Dox-A1 and Phox reside in the same cytological interval. # bch: branch location: 3-46 (approximately). origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. phenotype: Homozygous lethal; incomplete fusion of denticle bands. # bd: see ra2 #*bd: balding location: 2-56.1 (between Bl and L). origin: Spontaneous. discoverer: Ives, 71j25. synonym: bald (preoccupied). references: 1972, DIS 49: 38. phenotype: Semicircular, medial bald spot on thorax, about one-third width of thorax. Very little variation at 25. RK1. Bd: Beaded From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 152. # Bd: Beaded location: 3-91.9 [based on 102 ro-ca and 182 Pr-ca recombinants in crosses involving BdS (Curry, 1939, DIS 12: 46)]. references: Dexter, 1914, Am. Nat. 48: 712-58. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 37, 152 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 45. Fleming, Scottgale, Diederich, Artavanis-Tsakonas, 1990, (manuscript). phenotype: Originally recovered alleles were recessive lethal with a dominant incised-wing phenotype; Bd1 was very weak and highly variable when first recovered, but gained expressivity with selection; subsequently isolated alleles were stronger. Wings reduced by marginal excision both anteriorly and poste- riorly. Phenotype of Bd1/Bd1/+ extreme (Peter Lewis). Expression and interaction studied by Goldschmidt and Gardner [1942, Univ. Calif. (Berkeley) Publ. Zool. 49: 103-24]. Expression of Bd1, Bd3, and BdS suppressed by H (DIS 9) and Ax alleles (Bang). In combination with several different Minutes, causes incomplete development of anal and genital imaginal discs in males and less frequently in females (Goldschmidt, 1948, Proc. Nat. Acad. Sci. USA 34: 245-52; Sturtevant, 1949, Proc. Nat. Acad. Sci. USA 35: 311-13). BdS (originally designated Ser: Serrate) homozygous viable; ini- tially thought to be homozygous lethal, but lethality remov- able by recombination (Belt, 1971, DIS 46: 116). The closely linked recessive lethal persists in many BdS-bearing chromo- somes. Recessive lethal alleles, which lack the dominant wing phenotype, recovered as revertants of BdS (symbolized BdSrv) or selected on the basis of their failure to complement the lethality of Bd3 (symbolized Bdr). Allelism of Bdr1 (origi- nally designated std: serratoid) inferred from enhanced wing incising in heterozygotes with BdS and genetic map position similar to that of BdS; homozygous viability unknown. Cuticle preparations of embryos homozygous for BdS revertants reveal lack of germband retraction, improper deposition of cuticle, lack of head and thoracic structures, lack of Filzkorper, and in severe cases, only a remaining patch of cuticle (either ventral or dorsal). Central-nervous-system defects revealed by anti-horseradish peroxidase preparations include breaks in the longitudinal and/or commissure nerve tracts, twisted or unretracted nerve tracts, only a single nerve tract, and occa- sionally only the presence of groups of staining cells scat- tered throughout the embryo (Fleming, et al.). Each BdSrv allele displays the whole range of embryonic phenotypes but the proportions of individuals with a particular phenotype varies between alleles. alleles: allele origin discoverer synonym ref ( comments ___________________________________________________________________________________ Bd1 spont Morgan, 10e 1, 2 10 dominant wing phenotype; homozygous lethal; fails to complement Bd3 *Bd2 spont Wallace, 15i10 BdW 2 more extreme; ends of L3 and L4 split or disturbed Bd3 heat Goldschmidt, 1934 BdG 2, 3, 4 dominant wing phenotype; homozygous lethal; molecular polymorphisms at 0 to 1.0 and 14 to 17 kb *Bd4 spont Goldschmidt BdG45 2, 6 more extreme scalloping effect *Bd5 X ray Piternick, 1949 BdP 2, 5 more highly penetrant; 100% when heterozygotes *Bd6 X ray Ohnishi, 49l16 Bd49 2, 11 like extreme Bd; variable; overlaps wild type Bdr1 spont Lee std 7, 8 Bdr2 EMS Hecht Bd43.5 3 homozygous lethal; no dominant phenotype Bdr3 EMS Hecht Bd862.5 3 homozygous lethal; fails to complement Bd3; no dominant phenotype Bdr4 EMS Hecht homozygous lethal; fails to complement Bd3 associated with pll11; possible small inversion in 97F region; molecular lesion at 17 to 19 kb Bdr5 X ray 3, 9 fails to complement Bd3; no dominant phenotype; T(Y;3)R128 = T(Y;3)YS;97F; breakpoint at 25 to 28 kb BdS spont Spencer, 35l7 Ser 2, 3 dominant wing phenotype; homozygous viable; 5.5-kb insert at 0 to 3.0 kb | BdSrv1 X ray Fleming Serrev2-3 3 homozygous lethal; complements Bd3 BdSrv2 X ray Fleming Serrev2-11 3 homozygous lethal; fails to complement Bd3; In(3R)97F;98C BdSrv3 X ray Fleming Serrev3 3 homozygous lethal; fails to complement Bd3 T(2;3)56E;97F BdSrv4 X ray Fleming Serrev5-5 3 homozygous lethal; fails to complement Bd3 BdSrv5 X ray Fleming Serrev6-1 3 homozygous lethal; fails to complement Bd3 ( 1 = Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 37, 152 (fig.). 2 = CP627; 3 = Fleming, Scottgale, Diederich, Artavanis-Tsakonas, 1990, (manuscript); 4 = Gottschewski, 1935, DIS 4: 14, 16; 5 = Goldschmidt, 1953, J. Exp. Zool. 123: 79-114; 6 = Goldsch- midt, 1942, Univ. Calif. (Berkeley) Publ. Zool. 49: 520; 7 = Lee, 1972, DIS 48: 18-19; 8 = Lee, 1973, Aust. J. Biol. Sci. 26: 189-99; 9 = Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, and Gould-Somero, 1972, Genetics 71: 157-84; 10 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 45; 11 = Ohnishi, 1950, DIS 24: 61. | More detailed description follows. cytology: Placed in 97F by T(2;3)BdSrv3 = T(2;3)56E;97F, In(3R)BdSrv2 = In(3R)97F;98C, Df(3R)Ser = Df(3R)97D;97F-98A1, and T(Y;3)128 = T(Y;3)97F;YS. Also in situ chromosomal studies displayed hybridization at 97F. molecular biology: An 85 kb walk and Southern analysis showed that BdG and BdS contain molecular lesions in the 97F region (BdS contains a 5.5 kb repeated DNA sequence, and BdG has a complex rearrangement). Two major transcripts of 5.5 and 5.6 kb appear to differ at their 5 ends. Sequencing of two over- lapping cDNAs produced a sequence of 5561 base pairs that con- tained a large open reading frame of 4329 nucleotides. Con- ceptual translation indicates a protein of 1404 amino acids that contains a signal peptide, a region of sequence homology to the neurogenic locus Delta, a partial EGF-like repeat, 14 EGF-like repeats with interruptions in the 4th, 6th, and 10th repeats, a transmembrane domain, and an intracellular domain of ~160 amino acids. Analyzing whole mount in situs using probes that recognize both transcripts, revealed a complex and dynamic pattern of embryonic mRNA expression in the head seg- ments; the dorsal, ventral, and lateral epidermis in the thorax and abdomen; the proventriculus, and hindgut; the tra- chea; and a reiterated array of cells in the CNS. Expression appears to be limited to tissues of ectodermal origin (Fleming et al., 1990). other information: Bd/In(3R)C, l(3)a was the first described case of a balanced lethal [Muller, 1918, Genetics 3: 422-99 (fig.)]. BdS: Beaded-Serrate Edith M. Wallace, unpublished. # BdS: Beaded-Serrate phenotype: Wings of BdS/+ and BdS/Df(3R)Ser notched at tip; deepest notch at second posterior cell. In triploids, one dose of BdS overlaps wild type. BdS is homozygous viable; initially thought to be homozygous lethal, but lethality removable by recombination (Belt, 1971, DIS 46: 116); the closely linked recessive lethal persists in many BdS-bearing chromosomes. Homozygous BdS produces extreme incision of wing margins especially in second posterior cell (Belt, 1971). As with other Bd alleles expression suppressed by H and Ax (Bang). # bdw: see osbdw #*be-3: benign tumor in chromosome 3 location: 3-25. origin: Spontaneous. discoverer: Stark, 16k. references: 1919, Proc. Nat. Acad. Sci. USA, 5: 573-80 (fig.). Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 179 (fig.). Stark and Bridges, 1926, Genetics 11: 249-66. Stark, 1935, DIS 4: 62. phenotype: Melanotic tumors appear in larvae and persist in adults. Subject to modification by genetic factors. Nonlethal. RK3. # Beaded: see Bd # Beadex: see Bx # Beadexoid: see Bxd # Bearded: see Brd # bef: beta lobes fused location: 1- (not located). origin: Induced by ethyl methanesulfonate. synonym: befBG17b. references: Heisenberg, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). pp. 373- 90. phenotype: Beta lobes of mushroom bodies (in anterior supraeso- phageal ganglion) are fused across midline. Mutant isolated on basis of this morphological defect in strain with aberrant visual responses and optic lobes, but genetic etiology of aberrant mushroom bodies is apparently separable from X- chromosome factor(s) causing the visual defects. # bel: belle (M.T. Fuller) location: Just proximal to p. synonym: l(3)L3; ms(3)neo30. references: Bender, Turner, and Kaufman, 1987, Dev. Biol. 119: 418-32. Jones and Rawls, 1988, Genetics 120: 733-42. Deuring, Wolf, Schuske, Cooley, Spradling, and Fuller, (unpub- lished). phenotype: Recessive larval lethal. Homozygous null individu- als hatch, but remain as first instar larvae until their death several days later. allele synonym origin ref ( phenotype ______________________________________________________ bel1 EMS belleb3 1 larval lethal bel2 EMS belleb10 1 larval lethal bel3 EMS belleb58 1 larval lethal bel4 EMS belleb68 1 larval lethal bel5 EMS belleeke24 1 larval lethal bel6 EMS belleprl34 1 larval lethal bel7 P ms(3)neo30 2 male sterile | ( 1 = Bender, Turner, and Kaufman, 1987, Dev. Biol. 119: 418-32; 2 = Deuring, Wolf, Schuske, Cooley, Spradling, and Fuller, (unpublished). | Male sterile with defects in meiosis and spermatid differen- tiation. Hemizygotes are more extreme than homozygotes, and poorly viable if raised at 18. Female fertile, but hemizy- gous females sterile and produce eggs with weak chorion. cytology: Placed in region 85A4-6 on the basis of the position of the P-element insert in bel7, and on the basis of being uncovered by Df(3R)p7 but not Df(3R)p5. molecular biology: The 4 kb bel transcript is present in unfer- tilized eggs, embryos, larvae, pupae, and adult males and females; it encodes a protein of 781 amino acids with a cen- tral core region of 414 residues that is highly homologous to vasa (Deuring et al., unpublished). Based on this core homol- ogy, the bel gene product is a member of the DEAD box family and is likely to be a nucleic-acid-dependent ATPase. # bellyache: see bly # ben: bendless (J. Hall; R. Wyman) location: 1-45.0 (1.2 cM to the left of na). origin: Induced by ethyl methanesulfonate. synonym: nj-262: nonjumper-262. references: Thomas, 1980, Neurosci. Abstr. 6: 742. Thomas and Wyman, 1982, Nature (London) 298: 650-51. Thomas and Wyman, 1983, Cold Spring Harbor Symp. Quant. Biol. 48: 641-53. 1984, J. Neurosci. 4: 530-38. phenotype: Adults have an aberrant startle response; they do not jump when presented with a lights-off stimulus. The cerv- ical giant fiber, a brain neuron, has abnormal morphology. The normal giant fiber terminates in the thorax at a synapse onto the motoneuron innervating the tergo-trochanteral (TT) muscle (= jump muscle). In ben, this synapse is abnormal or absent. The normal lateral bend of the giant fiber toward the TT motoneuron in the mesothoracic neuromere is absent; the axon usually terminates at the midline with fine branches extending from its tip. Latency of response of the TT muscle to stimulation of the giant fiber is abnormally long, and mus- cles cannot follow stimulation at rates above 5 Hz. Rhab- domeres of the photoreceptor cells in the ommatidia heart shaped in cross section with indentation centrally oriented rather than round as is normal. Furthermore, the axons from photoreceptor cells R7 and R8 fail to make the right-angle turn into the optic medulla after traversing the lamina (Benzer). ben flies choose visible over ultraviolet wave lengths whereas wild-type flies make the opposite choice (Benzer). alleles: Six ethyl-methanesulfonate-induced alleles; all are jumpless; all but ben1 have normal giant-fiber physiology (Tanouye). allele discoverer synonym _____________________________ ben1 Wyman, and Thomas ben2 Tanouye ben1372 ben3 Tanouye ben1394 ben4 Tanouye ben1499 ben5 Tanouye ben1561 ben6 Tanouye ben1682 other information: ben/Df(1)HA92 said to be indistinguishable from ben/ben, indicating that the mutation is amorphic (Thomas and Wyman, 1983). cytology: Located within salivary gland chromosome region 12A6-B based on its inclusion in Df(1)HA92 = Df(1)12A6-7;12D3 (Thomas and Wyman, 1984), but not the segmental deficiency YPXDB166/XPYDB89 = Df(1)12A-B;12B9-C1 (Tanouye). # ben(2)gcn: see bgcn # bending wings: see osbdw # bendless: see ben # benign gonial cell neoplasm: see bgcn # benign tumor in chromosome 3: see be-3 # bent: see bt # bent scutellars: see bsc #*ber: berrytail location: 1-52.4. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1953. references: 1958, DIS 32: 67. phenotype: Abdomen narrow, ending in a berry-like protrusion carrying defective genitalia. Wings opaque, with areas of deranged hairs (some with cut inner margins and interrupted or abnormally positioned longitudinal veins). Anterior scutel- lars often acutely bent; eyes occasionally misshapen. Males sterile and viability about 40% wild type. RK3. # Bercel: see Fs(3)Sz4 # beta: see Tyr2 # beta lobes fused: see bef # bf: brief location: 3-95. origin: Spontaneous. discoverer: Curry, 38i3. references: 1939, DIS 12: 45. phenotype: Fly small; bristles Minute like. Classification perfect; viability fair. Male completely sterile; female with low fertility. RK3. # Bg: Bag location: 1-51.6 (to the right of sd). origin: Spontaneous. discoverer: Bridges, 33d22. phenotype: Heterozygous female with wings shorter and blunter, shortened L5, extra veins or gaps near anterior crossvein, and inflated bag centering in first basal cell. Frequently over- laps wild type. Lethal in male. RK2 as a lethal; RK3 as a dominant. alleles: Lost alleles described in CP627: *Bg1, *Bg2, *Bg49h, and *Bg52c. cytology: Probably in 13C, based on Bg-like variegation of Tp(1;3)rasv = Tp(1;3)9E;13C;81F. other information: Possibly an allele of Bb, although published information suggests that sd lies between Bb and Bg. # bgcn: benign gonial cell neoplasm location: 2- (between dp and b). origin: Induced by ethyl methanesulfonate. synonym: ben(2)gcn. references: Gateff, 1981, DIS 56: 191. phenotype: Gametocyte differentiation defective; gonial proli- feration unchecked; gonads of both males and females become engorged with gonial cells. Ovarioles appear sausage like; testes smaller than normal. Autonomous in transplants of young adult ovaries and testes into body cavity of wild-type females. # bh: baldhead location: 3-81. origin: Spontaneous. references: Robertson, 1973, DIS 50: 24 (fig.). phenotype: Ocelli and associated bristles absent; wings shor- tened. Both sexes sterile. # bhe: broad head (C. Nusslein-Volhard) location: 2-0. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. phenotype: Embryonic lethal; embryos have incompletely invo- luted heads. In double mutants with Pc-like mutants, abdomi- nal transformations occur. At least one bhe allele fails to complement l(2)gl, which is a larval lethal (Kennison). alleles: bhe1 (formerly bheIJ) and bhe2 (formerly bheIM). cytology: Placed in 21A on basis of being covered by terminal 2L duplications that cover l(1)gl.