# so: sine oculis (J.C. Hall) location: 2-57.1. origin: Spontaneous. discoverer: Milani, 1939. references: 1941, DIS 14: 52. Buzzatti-Traverso, 1946, DIS 20: 63. Milani, 1946, Boll. Soc. Ita. Biol. Sper. 23: 111-13. 1951, DIS 25: 79. 1951, Rend. Ist. Lombardo Sci. Lettere, Ser. 3. Engelmann and Honneger, 1966, Z. Naturforsch. 22B: 1-2. Hofbauer and Campos-Ortega, 1976, Wilhelm Roux's Arch. Dev. Biol. 179: 275-89. Fischbach, 1983, Dev. Biol. 95: 1-18. Fischbach and Lyly-Hunerberg, 1983, Cell Tiss. Res. 231: 551-63. Helfrich and Engelmann, 1983, Physiol. Entomol. 8: 257-72. Fischbach and Technau, 1984, Dev. Biol. 104: 219-39. Helfrich, 1986, J. Neurogenet. 3: 321-43. Dushay, Rosbash, and Hall, 1989, J. Biol. Rhythms 4: 1-27. phenotype: Ocelli always absent; eyes usually reduced to small groups of ommatidia, and occasionally missing; eye field some- times in form of an eye stalk protruding from head with an irregular arrangement of ommatidia; heavy ommatidial disrup- tion with many receptor cells missing. Optic lobes reduced in size, and many flies have no lamina. The reduced volume of adult optic lobes is due to accentuated degeneration of pre- cursor neurons that occurs to a certain degree in normal pupal development (Fischbach, 1983); the increased severity in the mutant includes degeneration of axons in second optic chiasma (Fischbach and Technau, 1984); sol enhances this kind of degeneration, but acts on a separate set of precursors for columnar visual system neurons--as confirmed by anatomical analysis of sol; so double mutant, which ends up with tiny, rudimentary optic lobes (Fischbach and Technau, 1984); sol; so also leads to a central brain that is smaller than normal due to missing afferents from visual system (Fischbach and Tech- nau, 1984); more specifically, there is a reduction in number of axons in anterior optic track in so, and combining so with sol causes a further reduction, but again, these two genes act independently on separate subsets of such axons (Fischbach and Lyly-Hunerberg, 1983). Histological studies reveal that the eye-antenna disc in third-instar larvae appears normal until differentiation begins, at which time cell death is observed (Hofbauer and Campos-Ortega). More extreme at elevated temperatures; lethal at 30; temperature-sensitive period for eye defect in third instar. Survival sensitive to elevated temperature at all developmental stages (Ransom, 1980, DIS 55: 126). Mosaic studies demonstrate that so acts in developing eye tissue and that the resulting reduction in retinal innervation leads to death of cells in the lamina and breakdown of medulla and lobula-complex neuropil (Fischback and Technau). Nonphototactic (Benzer, 1967, Proc. Nat. Acad. Sci. USA 58: 1112-19) and visual orientation almost absent (Bulthoff, 1982, DIS 58: 31). Studies of circadian rhythms in so show eclosion to be normally periodic (Engelmann and Honneger, 1966); adult activity rhythms are robust, in that so, even when thoroughly eyeless, responds to light:dark cues such that it entrains to these conditions (is periodically active vs. inactive, and anticipates the environmental transi- tions) and subsequently free-runs with obvious circadian periodicities in constant darkness (Helfrich and Engelmann, 1983; Dushay, Rosbash, and Hall, 1989); however, these behavioral rhythms are frequently aberrant, e.g., with "split" active components appearing after several days of free-run and with dual periodicities extractable from the locomotor data (Helfrich, 1986); nearly all adults are dual-period when so combined with sol (Helfrich, 1986). allele origin discoverer synonym ref ( comments _________________________________________________________________________ so1 spont. Milani, 2 1939 so+2 spont. Milani, 2 weaker derivative of so1 1939 soD ENU Sakonju, Drl 1 gain-of-function allele| 1982 soDrv1 Ashburner T(2;3)43B1-3;86E14-20 soDrv2 Ashburner T(2;3)43B3-8;91A3-8 ( 1 = Craymer, 1984, DIS 60: 235; 2 = Milani, 1941, DIS 14: 52. | More complete description below. cytology: Placed in 43B1-2 based on the cytology of soD rever- tants (Ashburner). # soD phenotype: Heterozygote has very small glazed eyes; more extreme than Drmio/+;soD/+/+ has a very clear phenotype, but weaker than that of Drmio/+ (i.e., about the size of Gla/+, but not glazed). Heterozygote has excellent viability; homoz- ygous lethal. # Sod: Superoxide dismutase location: 3-32.5 [based on 151 h-gv recombinants (Jelnes, 1971, Hereditas 67: 291-93)]. Mapped to 34.6 by Finnerty using closer markers. synonym: To, Tetrazolium oxidase; cSOD. references: Franklin and Chew, 1971, DIS 47: 38. Lee, Ayala, Misra, 1981, J. Biol. Chem. 256: 8506-09. Lee, Misra, Ayala, 1981, Proc. Nat. Acad. Sci. USA, 78: 7052-55. phenotype: The structural gene for Cu, Zn superoxide dismutase [Superoxide: superoxide oxidoreductase; SOD (EC 1.15.1.1.)], a homodimer of 15,000 subunit molecular weight that contains two Cu++ and two Zn++ per molecule. Enzyme catalyzes the dismuta- tion of the superoxide anion, O2 -, to H2O2, which in turn is converted into H2O by catalase and peroxidases. Enzyme puri- fied by Lee, Ayala, and Misra (J. Biol. Chem. 256: 8506-09); shows homology to homologous mammalian enzymes but does not crossreact with anti-bovine-erythrocyte-SOD antibodies; specific activity 1.5 times that of other species. Amino acid sequence determined by Lee, Friedman, and Ayala (1985, Arch. Biochem. Biophys. 241: 577-89); 151 amino acid residues with molecular weight 15,750. Enzyme levels show little variation during development; slight rise in activity during adulthood (Graf and Ayala, 1986, Biochem. Genet. 24: 153-68). alleles: Two electrophoretic variants, SodF and SodS, whose relative frequencies vary greatly among natural populations. SodS alleles differ from SodF alleles in having a lysine in place of asparagine at residue 96 (Lee and Ayala, 1985, FEBS Lett. 179: 115-19); fast alleles from California and Tunisia differ at two additional residues, tentatively California alleles have a serine and a glutamine or glutamic acid where Tunisian alleles have a histidine and a proline. Slow forms of SOD have specific activity 2-3 times that of fast forms and they are more thermolabile (Lee, Misra, and Ayala, 1981). A low activity allele, SodCA1 isolated from a natural population in California exhibits 3.5% of normal CRM level; low level maps to Sod (Graf and Ayala). In addition to these naturally occurring alleles there is a single ethyl methanesulfonate- induced null allele, Sodn1 (isolated as l-108; Campbell, Hil- liker, and Phillips, 1986, Genetics 112: 205-15). cytology: Placed in 68A8-9 by in situ hybridization (Kirkland and Phillips, 1987, Gene 61: 415-19). molecular biology: Gene cloned and sequenced; cDNA clones have 458 base pairs of open reading frame, encoding 153 amino acids; N-terminal methionine and C-terminal valine do not appear in the mature polypeptide (Seto, Hayashi, and Tener, 1987, Nucleic Acids Res. 15: 5483). Genomic sequence con- tains a 725 base-pair intron between codons 21 and 22, which corresponds to the position of the first intron in the human SOD gene (Seto, Hayashi, and Tener, 1987, Nucleic Acids Res. 15: 10601). # Sodn1 origin: Ethyl methanesulfonate-induced derivative of SodF. references: Phillips, Campbell, Michaud, Charbonneau, and Hil- liker, 1989, Proc. Nat. Acad. Sci. USA 86: 2761-65. phenotype: Originally recovered as a lethal mutation; homozy- gotes die in the process of eclosion; rare eclosing adults are completely sterile, are devoid of SOD activity and die within 2-3 days; however, some derived sublines show higher adult survival. Surviving homozygous males are sterile and homozy- gous females produce few if any offspring. Reduced life span and fertility attributed to reduced capacity of embryos, lar- vae, and pupae to protect developing preimaginal cells from O2 --initiated cytotoxic damage. Homozygotes hypersensitive to the O2 --radical-generating compound, paraquat (1,1'-dimethyl- 4,4'-bipyridinium dichloride) and copper ions. # soft brown: see sb # sog: short gastrulation location: 1-53. references: Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. Zusman, Sweeton, and Wieschaus, 1988, Dev. Biol. 129: 417-27 (fig.). phenotype: Embryonic lethal with weak ventralized phenotype. Invagination and subsequent closing of the posterior midgut and anterior midgut delayed; germ-band extension incomplete; dorsal-most cells fail to assume normal amnioserosal fate; they are abnormally thick and fall into deep dorsal folds at the time of germ-band extension. Mosaic studies indicate that sog expression required only ventrally for normal development. No discernable maternal effect. alleles: Six ethyl methanesulfonate-induced alleles, one of which is temperature sensitive, recorded by Wieschaus et al.; one isolated as sog-92.31 designated sog1 by Zusman et al. Allele sogM4 here designated sog2; XM designated sog3. The remaining alleles designated sog4 through sog6; identity of t.s. allele unknown. sog7 ethyl methanesulfonate induced by Eberl and Hilliker (1988, Genetics 118: 109-20) as EH628. cytology: Placed in 13D1-E7 based on its location between the breakpoints of T(1;Y)B28 = T(1:Y)13D;YS and T(1;Y)W23 = T(1;Y)13E1-7;YL. # sol: small optic lobes (J.C. Hall) location: 1- {65} (Fischbach and Heisenberg, 1981, and Hel- frich, 1986, quote more distal and more proximal meiotic map positions, respectively); Fischbach and Lyly-Hunerberg mapped sol proximal to car. origin: Induced by ethyl methanesulfonate. synonym: PC79; w5000. references: Markow and Merriam, 1977, Behav. Genet. 7: 447-55. Fischbach and Heisenberg, 1981, PNAS 78: 1105-09. Bulthoff, 1982a, DIS 57: 31. Bulthoff, 1982b, Biol. Cybernet. 45: 63-70. Fischbach and Lyly-Hunerberg, 1983, Cell Tissue Res. 231: 551-63. Helfrich and Engelmann, 1983, Physiol. Entomol. 8: 257-72. Fischbach and Technau, 1984, Dev. Biol. 104: 219-39. Helfrich, 1986, J. Neurogenet. 3: 321-43. Coombe, 1986, J. Comp. Physiol. 159: 655-65. Miklos, Kelly, Coombe, Leeds, and Lefevre, 1987, J. Neuro- genet. 4: 1-19. phenotype: Medulla, lobula, and lobula-plate optic ganglia reduced in volume and cell number (anatomical criteria on which several of the mutations, including the most studied allele sol1, were isolated by Heisenberg and Bohl, 1979, Z. Naturforsch. 34: 143-147); lamina seems unaffected; degree of reduction in the three more proximal visual-system ganglia is allele dependent; after isogenization the severity ranking of nine alleles was as follows: sol2 = sol3 (ca. 50% normal volume)>sol6 = sol9 = sol16 >sol1 = sol4 = sol5 = sol8 (ca. 30% normal volume). Three sol mutants isolated on basis of fast phototaxis; Markow and Merriam (1977) showed that one such allele, sol4, causes flies to be anomalously photo posi- tive and highly geonegative in maze tests. Anatomically, sol mutations cause specific cell types in medulla to be missing (Fischbach and Heisenberg, 1981); stratifications in outer medulla are missing; in general, however, mutant optic lobes are grossly well structured, and there are no disorders in the optic chiasma; special classes of transmedullary columnar neu- rons as well as intramedullary cells are absent; numbers of columns in the visual ganglia are normal, but numbers of neu- rons per column are reduced; certain neurons called T1 cells are present in each column in sol1, as usual; these reductions in cell numbers are caused by cell-type-specific degeneration of presumptive optic lobe neurons during pupation, with no degeneration apparent in neuropiles of these ganglia (Fisch- bach and Technau, 1984); the number of axons severely reduced in anterior optic track, and the combining of so with sol1 showed that these two mutations act independently on nearly exclusive subsets of these axons (Fischbach and Lyly- Hunerberg, 1983). Mosaic study showed that aberrant morphol- ogy of visual ganglia is autonomous in these optic lobes (Fischbach and Technau, 1984); adult eye and lamina optic lobe appear normal. In combination with rol and mnb mutations, sol causes diminished amplitudes of light-on and light-off tran- sient spikes in electroretinogram (Coombe, 1986); visual fixa- tion behavior notably defective (Fischbach and Heisenberg, 1981) [e.g., in the walking mode, fixation behavior is actu- ally reversed in all sol alleles (Fischbach)] as, to a lesser degree, are landing responses and "figure/ground" discrimina- tion; on the other hand, optomotor yaw response is nearly nor- mal (Fischbach and Heisenberg, 1981); orientation to spots in multiple Y-maze quite subnormal (Bulthoff, 1982a,b). Shock- avoidance learning of sol1 (Heisenberg, Borst, Wagner, and Byers, 1985, J. Neurogenet. 2: 1-30) and color discrimination in sol1, sol2, and sol3 (Fischbach) are normal; there are, however, deficits in visual plasticity (Gotz, 1983, Dtsch. Zool. Ges. Gustav Fischer Verlag, Stuttgart, pp. 83-99) and in the flexibility that wild types can exhibit in optomotor flight control tests (Gotz, 1985, Biol. Chem. Hoppe Seyler 366: 116-17). Circadian rhythms of adult locomotor activity basically normal (Helfrich and Engelmann, 1983; Helfrich, 1986), but when sol1 combined with so, all flies tested showed complex periodicities, with a given behavioral record having one component at approximately 21 and another at approximately 26 h (Helfrich, 1986). alleles: allele origin discoverer synonym ref ( comments | ___________________________________________________________ sol1 EMS KS58 4 histology sol2 EMS KS84 4 histology sol3 EMS KS160 4 histology sol4 EMS EE111 1 phototaxis sol5 EMS KS91 1 phototaxis sol6 EMS PC79 1 phototaxis sol7 EMS 542 3 histology sol8 EMS 648 3 histology sol9 EMS 2303 3 histology sol10 EMS 3056 3 histology sol11 EMS 3447 3 histology sol12 EMS 3575 3 histology sol13 EMS 3596 3 histology sol14 EMS 3819 3 histology sol15 EMS w5000 3 histology sol16 EMS Bulthoff nofEB12 2 behavior sol17 Heisenberg 1048 ( 1 = Benzer and Merriam; 2 = Bulthoff, 1982, DIS 58: 31; 3 = Fischbach and Heisenberg, 1981, Proc. Nat. Acad. Sci. USA 78: 1105-09; 4 = Heisenberg and Bohl, 1979, Z. Natur- forsch. 34: 143-47. | Criterion used in selection of mutant. cytology: Tentatively placed in 19F4, along with slgA, these two genetically separable mutations being flanked by l(1)19Fe and l(1)19Ff; this determination (Miklos et al., 1987) was based the behavioral defects and anatomical abnormalities of sol in heterozygous combination with Df(1)GA104, but not by Df(1)16-129, located distally or Df(1)JA117, located proxi- mally; none of the three has cytologically determined break- points. molecular biology: Maps within the distal 15 kb of a 40 kb interval defined by the proximal breakpoint of Df(1)16-129 and the distal breakpoint of Df(1)JA117. This region is further subdivided by a breakpoint of a deficiency, Df(1)2/19B, which separates sol and slgA. Only one transcription unit has been detected within this 15 kb segment by Northern blotting (should contain both l(1)19Fe and sol); a 5.3 kb cDNA comple- mentary to the one transcript has been isolated and sequenced (Delaney, Hayward, Fischbach, and Miklos, unpublished). The conceptual translation product is ca. 35% identical to human or chicken calcium-activated neutral protease (calpain); sequence data also reveal an opa repeat and cysteine repeats of the zinc-finger type. Spatial expression studies so far reveal sol transcript to be expressed in a few cells (probably glia) within the embryonic CNS (F. Barleben and K. F. Fisch- bach, unpublished), although there are no apparent anatomical defects in mutant embryos or larvae. other information: In behavioral tests, sol1 was complemented by alleles of l(1)19Ff and also by mutations at the nearby slgA, uncl, and stn loci (Miklos et al., 1987). #*som: sombre location: 1-40.8. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1953. references: 1958, DIS 32: 75. phenotype: Pigmentation of body and eyes dark and dull. Wings occasionally divergent or blistered. Good viability and fer- tility. RK2. other information: One allele induced by CB. 1414. # sonless: see snl # sp: speck location: 2-107.0. references: Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 128 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 211 (fig.), 236. phenotype: Axils of wings have black specks. Body color dark. In pupa, region of anal papilla is dark (Waddington). Displays a marked decrease in the amount of the A2 component of phenoloxidase; levels restored to normal in presence of su(s)2 (Warner, Grell, and Jacobsen, 1975, Biochem. Genet. 13: 353-56). RK1. alleles: allele origin discoverer synonym ref ( comments _____________________________________________________________________________ sp1 spont Morgan, 10c ol-2: olive-2 1, 2, 5 412 and roo inserted in region sp2 Bridges, 25f stronger than sp1 *spS61 spont Shuman, 61c 4 like sp1 *spu UV Meyer, 52d 3 weaker than sp1 ( 1 = Morgan and Bridges, 1919, Carnegie Inst. Wash. Publ. No. 278: 128 (fig.); 2 = Morgan, Bridges, and Sturtevant, 1925, Bibliogr. Genet. 2: 211 (fig.), 236; 3 = Meyer, 1955, DIS 29: 74; 4 = Meyer, 1963, DIS 37: 51; 5 = Searles and Voelker, 1985, Proc. Nat. Acad. Sci. USA 83: 404-08. cytology: Placed in 60B13-60C5 on the basis of its inclusion in the 2RPXD element of T(1;2)Bld = T(1;2)1C3-4;60B12-13 and Df(2R)Px = Df(2R)60B8-10;69D1-2 but not in Df(2R)Px2 = Df(2R)60C5-6;60D9-10 [Bridges, 1937, Cyto- logia (Tokyo), Fujii Jub., Vol. 2: 745-55]. sp: speck From Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 129. # sp: see sdsp # Sp: Sternopleural location: 2-22.0. origin: Spontaneous. discoverer: M. (Mann) Lesley. synonym: Br: Bristled. references: 1923, Genetics 8: 27-36. phenotype: Sternopleural bristles increased in number. At 19, wild type; at 25, overlaps wild type; at 28-30, no overlap. Apparently does not affect sternopleural bristles on metathoracic segment converted by bx to a mesothoracic segment (Waddington, 1939, Growth Suppl. 1, pp. 37-44). Homozygous lethal. RK2. cytology: Placed in salivary chromosome region 27C1 to 28C1 (E. H. Grell). Salivary chromosomes apparently normal (Mor- gan, Bridges, and Schultz, 1937, Year Book - Carnegie Inst. Washington 36: 301). Sp: Sternopleural Edith M. Wallace, unpublished. # sp-w: see wsp # spa: sparkling location: 4- [probably most distal visible locus on chromosome 4 (Abrahamson, Herskowitz, and Muller, 1956, Genetics 41: 410-19)]. origin: Spontaneous. discoverer: L. V. Morgan, 34k6. references: 1941, DIS 14: 52. 1947, Genetics 32: 200-19. Hochman, 1971, Genetics 67: 235-52. Hochman, 1974, Cold Spring Harbor Symp. Quant. Biol. 38: 581-89. phenotype: Eyes rough in varying degrees and somewhat bulging. Affected by genetic modifiers. More extreme at 17-19 than at 22-25. Heterochromatin and sex affect expression so that X/0 > X/X > X/Y > X/X/Y; also enhanced by Df(2R)M41A10; spa haplo-4s have an exaggerated phenotype. RK2. cytology: Placed in 102D-F on the basis of the absence of spa+ from the 4P2LD element of T(2;4)b = T(2;4)25E;102C15-D1 (E. B. Lewis). Observations on its further location conflict. Fahmy restricts its location to 102D on the basis of its inclusion in Df(4)M62e = Df(4)101E;102D13-E1, whereas Hochman places it between 102E2 and 102F10 on the basis of its inclu- sion in Df(4)11 = Df(4)102E2-10;102F2-10. # spaA references: Craymer, 1980, DIS 55: 197-200. phenotype: Dominant rough-eye allele; more extreme than spaCat. spaA/spapol shows extreme poliert phenotype; spaA/spaCat lethal. RK1A. cytology: Associated with T(3;4)UbxA, an extremely complex rearrangement with one breakpoint in 102E-F. # spaCat: sparkling-Cataract origin: X ray induced. discoverer: Belgovsky, 1936. synonym: Cat. references: 1937, DIS 8: 7. Morgan, 1941, DIS 14: 52. phenotype: Posterior third or half of eye of heterozygote rough; facets irregular and fused. Homozygous lethal. Stocks vary in expression, presumably because of genetic modifiers. X/X and X/0 flies that are spaCat/spa show the bulging eyes and roughening of spa and the posterior fused facets of spaCat; X/X/Y and X/Y flies have only the spaCat phenotype. spaCat/spapol has fusion of facets over entire surface of eye and roughness in posterior region of eye. spaCat/4-sim is wild type. spaCat/+ more extreme than spaCat/+/+ (Davis, 1969, Genetics 61: 577-94). RK2. other information: spaCat behaves as a deficiency in that it fails to complement l(4)102EFa, l(4)102EFb, l(4)102EFc, and l(4)102EFd; complements sv and l(4)102EFe. # spae(lz): sparkling-enhancer of lozenge origin: Spontaneous. discoverer: H. A. Bender, 65b23. phenotype: Homozygote wild type in absence of lz; eyes strongly roughened in presence of heterozygous lz3, lz34, lz36, or lzD. Slight eye roughening when both spae(lz) and a lz allele are heterozygous. spae(lz)/spapol and spae(lz)/spap65 have very rough eyes but normal tarsal claws and spermathecae. RK3. # spap61: sparkling-poliert type origin: Spontaneous. discoverer: Sturtevant, 1961. phenotype: Eyes small, rough, and glazed. More extreme than spapol or spap65. Nonpigmented tarsal claws. RK1. # spap65 origin: Spontaneous. discoverer: H. A. Bender, 65j11. phenotype: Eyes somewhat reduced in size, rough and partially glazed. More extreme than spapol but less so than spap61. Tarsal claws unpigmented and possibly reduced; reminiscent of certain lozenge mutants. Pulvilli and accessory female repro- ductive structures appear normal. Heterozygote with spapol and spap61 has affected tarsal claws as well as rough eyes. Heterozygote with spa has slightly roughened eyes at 25 but markedly roughened eyes at 18; female somewhat more extreme than male. Viability and fertility good. RK1. # spapol: sparkling-poliert origin: Spontaneous. discoverer: Hadorn, 51a. synonym: pol. references: Rickenbacher, 1953, DIS 27: 59. 1954, Z. Indukt. Abstamm. Vererbungsl. 86: 62-68 (fig.). phenotype: Eyes rather small; surface smooth and glassy. Dur- ing second day of pupal life, retinula cells withdraw from other cells of eye disk. SEM studies show irregular disposi- tion and morphology of ommatidial hairs as well as numerous necrotic pits over surface of eye [Oster and Crang, 1972, Trans. Am. Microsc. Soc. 91: 600-02 (fig.); Strum-Tegethoff and Dicke, 1974, Theor. Appl. Genet. 44: 762-65]. ERG absent [Grossfield, Handbook of Genetics (King, ed.). Plenum, New York, pp. 679-702]. spapol/spaCat has extreme phenotype; spapol/spa slightly more extreme than spa (Sturtevant, 1961, DIS 35: 47). Homozygote has excellent viability and fertil- ity. RK1. # spade: see spd # spaghetti squash: see sqh # spalt: see sal # sparkling: see spa # sparse arista: see crmsa # sparge hairs: see sph # spastic: see sps # spaztle: see spz # spc: see gra # spd: spade location: 2-21.9 [to the left of Sp (E. H. Grell)]. origin: Spontaneous. discoverer: Bridges, 30d15. phenotype: Wings short and broad, pointed at tip, and warped at base. Effect on wing shape arises from excessive contraction of epithelium from inflated stage onward (Waddington, 1940, J. Genet. 41: 75-139). Overlaps wild type in existing stock. RK3. cytology: Placed in 27D based on its inclusion in Df(2L)spd = Df(2L)27D-E;28C (E. H. Grell) and location distal to T(Y;2)A171 = T(Y;2)h3;27D breakpoint (Kotarski, Pickert, and MacIntyre, 1983, Genetics 105: 371-86). # spdfg: spade-flag origin: Spontaneous. discoverer: Doane, 60f14. synonym: fg. references: 1960, DIS 34: 49. 1961, DIS 35: 45-46. phenotype: Wings about two-thirds the length and three-fourths the width of wild type, held tentlike over abdomen. Alulae absent or vestigial; proximal posterior wing margins often irregular with tendency to fold under about vein L4. Venation usually normal with occasional blistering. spdfg/spd has phenotype varying from slight shortening of wings to a shape midway between the two homozygotes. Excellent viability and fertility. RK1. # spe: see lzs # (Spec: alpha Spectrin location: 3- {1.5}. references: Dubreuil, Byers, Branton, Goldstein, and Kiehart, 1987, J. Cell Biol. 105: 2095-2102. Byers, Dubreuil, Branton, Kiehart, and Goldstein, 1987, J. Cell Biol. 105: 2103-10. phenotype: Structural gene for alpha spectrin, a 234 kd polypeptide that forms an elongated heterodimer with beta spectrin to form an important cytoskeletal component. Product crossreacts with antibodies against mammalian spectrins; can be shown to bind to beta spectrin subunits. cytology: Placed in 62B1-7 by in situ hybridization to a single polytene site. molecular biology: cDNA sequences isolated by antibody screen- ing of an expression library prepared from Drosophila adult head polyadenylated RNA. Northern blots reveal a single homo- logous 8 kb messenger RNA. Derived probes bind to a single polytene region, suggesting the presence of a single Droso- phila alpha spectrin gene. cDNA clones indicate (Spec con- tains a single open reading frame that encodes a polypeptide 2,415 residues long of molecular weight 278,364 daltons. Con- ceptual sequence indicates two stretches of nine 106-residue repeats separated by a short non-repetitive segment; the repeats are defined by a consensus sequence of 54 residues, 50 of which are shared by chicken ( spectrin. Drosophila ( spectrin is 63% identical with chicken brain ( spectrin (Dubreuil, Byers, Sillman, Bar-Zvi, Goldstein, and Branton, 1989, J. Cell Biol. 109: 2197-2205). # |Spec: beta Spectrin location: 1-{57}. references: Byers, Hussain-Chishti, Dubreuil, Branton, and Goldstein, 1989, J. Cell Biol. 109: 1633-41. phenotype: Structural gene for beta spectrin; The subunit of beta spectrin associates with the subunit of alpha spectrin, forming heterodimers which associate to form tetramers, presumably the most important functional state for spectrin. cytology: Located in 16C1-4 by in situ hybridization to the salivaries (Byers et al., 1989). A single polytene site was detected. molecular biology: Drosophila |Spec cDNA clones were isolated from cDNA expression library using chicken alpha spectrin as a probe. These cDNAs express polypeptides that bind to alpha spectrin. Antibodies from fusion proteins expressed by these sequences react with Drosophila spectrin. Nucleotide and predicted amino acid sequences for the 5' end of spectrin determined; the amino acid sequence predicted for this region shows 62% identity to the deduced sequence for the erthyrocyte beta spectrin in man. A single mRNA of about 8.0 kb was detected on Northern blots of poly A+ RNA from Drosophila heads (Byers et al., 1989). # speck: see sp # spectacled: see lzs # Spectrin: see (Spec and |Spec # sperm amotile: see sam # spermatheca: see spt # spg: sponge location: 3-95. discoverer: Rice. synonym: early-D; mat3(6). references: Rice and Garen, 1975, Dev. Biol. 43: 277-86 (fig.). Rickoll and Counce, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 245-51 (fig.). phenotype: Maternal-effect lethal; embryos produced by homozy- gous females produce pole cells, but syncytial blastoderm fails to cellularize completely; cells form at the anterior and posterior ends of the embryo but are separated by a non- cellular region comprising 70% of the embryo surface. Abortive gastrulation signified by formation of posterior midgut rudi- ment. alleles: Five ethyl methanesulfonate-induced alleles; spg1 through spg5, isolated as 145, 242, 805, 842, and rm6, respec- tively. # sph: sparse hairs location: 1- {65}. references: Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 16, pp. 847- 902. Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31. phenotype: Thoracic hairs sparse, eye roughening variable, wings extended and margins incised. This phenotype observed in flies heterozygous for Df(1)17-87, Df(1)22, and sph1, sph3, or sph4 (Schalet and Lefevre). No effect on central or peri- pheral nervous system in sph5 or sph6; both alleles cell lethal in female germline clones (Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52). alleles: allele origin discoverer synonym ref ( comments _____________________________________________________________ sph1 X ray l(1)4P1 5, 7, 8, 9 sph2 EMS Lifschytz l(1)M147 4 on y_Ymal_ sph3 EMS Lifschytz l(1)R-9-5 3, 7, 8 sph4 X ray Lifschytz l(1)X4 2, 3, 7, 8 sph5 EMS Lefevre l(1)VE829 1, 5 L/P sph6 spont Schalet sphS1 5, 6 L l(1)7-96 ( 1 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 2 = Lifschytz and Falk, 1968, Mut. Res. 6: 235-44; 3 = Lifschytz and Falk, 1969, Mut. Res. 8: 147-55; 4 = Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84; 5 = Perrimon, Smouse, and Miklos, 1989, Genet- ics 121: 313-31; 6 = Schalet, 1986, Mutat. Res. 163: 115- 44; 7 = Schalet and Lefevre, 1973, Chromosoma 44: 183-202; 8 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902; 9 = Schalet and Singer, 1971, DIS 46: 131-32. cytology: Placed in 20E by Lefevre (1981, Genetics 99: 461- 80). # spi: spitz location: 2-54. 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. Mayer and Nusslein-Volhard, 1988, Genes Dev. 2: 1496-1511 (fig.). phenotype: Embryonic lethal. Normal allele required for normal development of blastoderm cells just lateral to the ventral mesodermal precursors. Denticle bands narrower than normal; first row often missing; reversal of polarity between anterior and posterior rows not seen; irregular fusion in midline of adjacent dentical bands. Keilin's organs missing or strongly reduced. Labrum, antennal-maxillary complex and labial sense organ reduced in size; right and left halves of head skeleton fused to produce pointed appearance. Tail region normal. Right and left halves of ventral ganglia of the central ner- vous system closer together than normal resulting in shorter commissures. The cells in the CNS that stain with anti-eve+ antibodies are closer together in spi than in wild type. spi+ required in the female germ line; spi pole cells transplanted into normal embryos produce no progeny. alleles: Three ethyl methanesulfonate-induced alleles, spi1, spi2, and spi3, isolated as IIA, IIT, and *IIIA. cytology: Placed in 37E2-38A1; in the region common to Df(2L)E55 = Df(2L)37D2-E1;37F5-38A1 and Df(2L)TW9 = Df(2L)37E2-F4;38A6-C1. molecular biology: spitz region cloned from 37F [Rutledge, Zhang, Perrimon, Bier, and Y. Jan, 1990 (Asilomar)]. # spindle: see spn # spineless: see ss # spiny legs: see sple # spir: spire (T. Schupbach) location: 2- {54.5}. origin: Induced by ethyl methanesulfonate. references: Manseau and Schupbach, 1989, Genes Dev. 3: 1437- 52. phenotype: Maternal-effect lethal; homozygous females lay eggs which sometimes (5-10%) have a "peak" (spire) of dorsal appendage material sitting over the anterior end of the egg, instead of two distinct dorsal appendages. Such eggs are similar to eggs formed by the female-sterile mutation fs(1)K10, but the extent of dorsal appendage material on spir eggs is much more variable than that of fs(1)K10 eggs. Mutant females produce embryos lacking polar granules, pole cells, and normal abdominal segmentation. In combination with Bic-D, however, abdominal segmentation does develop in the anterior half of the embryo; improper localization of abdominal deter- minants also indicated by the lack of posterior localization of vasa protein. Cellularization of the blastoderm irregu- larly defective with nuclei of different sizes and densities. Resemble embryos formed by other grandchildless-knirps-like mutations, such as vasa or tudor, but in addition, some of the embryos from spire females appear also to be dorsalized. alleles: Twelve alleles, presumably induced by ethyl methanesulfonate; spir1 to spir6 isolated as RP, HP, HJ, QF, O3, and 41, respectively. cytology: Placed in 38A6-C10, based on its inclusion in Df(2L)pr21 = Df(2L)37E3-F1;38C6-10 but not Df(2L)TW50 = Df(2L)36E4-F1;38A6-7. # spiracles: see gra # spire: see spi # spl: see under N # Spl: Splayed location: 3-51.6. references: Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero, 1972, Genetics 71: 157-84. Tasaka and Suzuki, 1973, Genetics 74: 509-20. Suzuki, Kaufman, and Falk, 1976, Genetics and Biology of Dro- sophila (Ashburner and Novitski, eds.). Academic Press, Lon- don, New York, San Francisco, Vol. 1a, pp. 208-51. phenotype: Legs extended; movements awkward; some melanization of leg joints. Originally described as the phenotype of a heterozygous deficiency for region 81F-82A by Lindsley et al.; subsequently a temperature-sensitive lethal isolated by Tasaka and Suzuki that mapped to the region and which produced the same phenotype, presumably in homozygotes reared at permissive temperatures. alleles: Only one mutant allele, Splts. cytology: Placed in 81F-82A based on the phenotype of heterozy- gotes for the segmental deficiency produced from T(Y;3)J139 = T(Y;3)80-81 and T(Y;3)J17 = T(Y;3)82A. # splay wing: see splw # splc: see tor11D # sple: spiny legs location: 2-55.3 [between pk and pwn (Grau and Simpson, 1987, Dev. Biol. 122: 186-200)]. origin: Spontaneous. references: Goldschmidt, 1945, Univ. Calif. (Berkeley) Publ. Zool. 49: 503-4, 521. Gubb and Garcia-Bellido, 1982, J. Embryol. Exp. Morph. 68: 37-57. Held, Duarte, and Devakhshanian, 1986, Roux's Arch. Dev. Biol. 195: 145-57 (fig.). phenotype: Polarity of chaetae and trichomes on legs irregular; relations between bracts and bristles disrupted. High incidence of ectopic tarsal joints with inverted polarity, especially in tarsae 3 and 4; incomplete intersegmental mem- branes between tarsal segments, especially between segments 3 and 4; no extra sensilla companiformia despite extra joints. Chaetae on abdominal tergites turned toward midline instead of pointing posteriorly as in wild type; polarity of bristles on sternites disrupted as well. alleles: allele origin discoverer synonym ref( comments _________________________________________________________________ sple1 spont Goldschmidt 1, 2 sple2 X ray Garcia-Bellido sple78a 1 also mutant for pk sple3 EMS splebor 3 described below ( 1 = Gubb and Garcia-Bellido, 1982, J. Embryol. Exp. Morph. 68: 37-57; 2 = Held, Duarte, and Derakhshanian, 1986, Roux's Arch. Dev. Biol. 195: 145-57; 3 = Sharma, Chitnis, and Shyngle, 1985, DIS 61: 216 (fig.). cytology: Placed in 42C1-43C7 based on its inclusion in the region common to Df(2R)pk78r = Df(2R)43A1;43C7 and Df(2R)pk78s = Df(2R)42C1-7;43F5-8 (Ashburner, Angel, Detweiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91). # sple3 synonym: Bristle orientation reversed. phenotype: A low-temperature-sensitive allele. Legs of flies raised at 19 highly condensed with incomplete joints, hapha- zard bristle pattern, occasional increase in number of bristle rows, and absence of some prominent markers. Flies unable to walk and soon get stuck in food. In sple3 flies raised at 28 53% of legs, though apparently normal, display abnormalities such as swollen second, third, and fourth tarsal segments, abnormal tarsal joints and reversals in bristle orientation in the middle of every segment; such flies able to walk and breed. About 30% of legs show phenotype intermediate between the two phenotypes described above. Mutant phenotype expressed in the homeotic legs of Antp and ssa; also expressed in mitotic clones. # spliced: see tor11D # split: see spl under N # split thorax: see spx # Splotched: see Sl # splw: splay wing location: 1-58.6. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 75. phenotype: Wings shortened and usually slightly divergent. Eyes small and occasionally rough and deformed. Body size reduced slightly. Emergence delayed. Male sterile; viability about 10% wild type. RK3. other information: One allele induced by CB. 1246. # spn-A: spindle A location: 3-96. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal-effect lethal. Egg shape affected; in extreme cases dorsal appendages are lacking and eggs have lit- tle or no dorsal-ventral polarity; some eggs have one fused dorsal appendage. Low fecundity; eggs often slightly col- lapsed. alleles: Four alleles designated as spn-A1 through spn-A4 iso- lated as 003, 050, 057, and 215, respectively. # spn-B: spindle B location: 3-52. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal-effect lethal. Similar to spn-A but normal eggs also recovered; eggs always unfertilized and abnormal eggs often long. alleles: Three alleles designated as spn-B1 through spn-B3 iso- lated as 056, 153, and 225, respectively. cytology: Placed in 88A10-C3 based on its inclusion in Df(3R)red-P93 = Df(3R)88A10-B1;88C2-3. However, not in 88B1-4 based on its not being uncovered by Df(3R)red-52P = Df(3R)88A12-B1;88B4-5. # spn-C: spindle C location: 3-17. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal-effect lethal. Similar to spn-A. alleles: Three alleles designated as spn-C1 through spn-C3 iso- lated as 094, 422, and 660, respectively. # spn-D: spindle D location: 3-91. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal-effect lethal. Similar to spn-A; embryos sometimes hatch. alleles: Two alleles, spn-D1, a weak allele isolated as number 150, and a strong allele with isolation number 349. # spn-E: spindle E location: 3-62. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal-effect lethal. Similar to spn-A. alleles: Two alleles, spn-E1 and spn-E2, isolated as 616 and 653. # spn-F: spindle F location: 3-100. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal-effect lethal. Similar to spn-A. alleles: spn-F1, the only allele, isolated as 234. # spo: spook location: 3-19. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. phenotype: Embryonic lethal. No differentiation of cuticle and mouthparts. alleles: spo1 and spo2 isolated as 4G9 and 7J. #*spot: spot location: 3- (not located). discoverer: Hersh, 34h15. references: 1935, DIS 4: 14. phenotype: Dark spot appears below eye on posterior margin of head. Expression variable. RK3. # spotted white: see wsp # spotty: see stt # spotty-tergum: see stt2 # spr: spread wings location: 3- [right arm associated with In(3R)P]. origin: Spontaneous. discoverer: Bridges, 36c16. phenotype: Wings held out at wide angle. Both sexes sterile. RK3A. #*Spr: Spread location: 3- (rearrangement). origin: X ray induced. discoverer: Oliver, 32k21. references: 1935, DIS 4: 15. phenotype: Wings held outstretched perpendicular to body axis, droop in older fly. Homozygous lethal. Heterozygote viabil- ity somewhat low. Female fertile; male quite infertile. RK2A. cytology: Associated with In(3L)Spr; breakpoints unknown. #*sprd: spread location: 3-65. origin: Spontaneous in In(3R)C. discoverer: Dexter, 13k. synonym: sd (preoccupied). references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 105. phenotype: Wings spread at right angles to body. RK2A. other information: Probably separable from In(3R)C = In(3R)92D1-E1;100F2-3. # Spread: see Spr # spread wings: see spr # spreadex: see sdx # spready: see egspy # sps: spastic location: 2-63.6. origin: Ultraviolet induced. discoverer: Edmondson and Meyer, 49d. references: 1951, DIS 25: 73. phenotype: Pupal and postpupal lethal. Fly that emerges from pupal case unable to walk or fly. Spastic contraction and jerking of leg and wing muscles. Fly becomes overturned and stuck; survives less than 24 hr; sterile. Muscles so relaxed in etherized fly that mutant indistinguishable from normal fly. RK3. # spt: spermatheca location: 2-63.3. origin: Spontaneous. discoverer: Hadorn, 43e. references: Hadorn and Graber, 1944, Rev. Suisse Zool. 51: 418-23. Graber, 1949, Z. Indukt. Abstamm. Vererbungsl. 83: 106-35 (fig.). phenotype: At 28, female has two spermathecae but ducts partly fused; at 25, only one enlarged spermatheca on one duct; at 18, a duct with three branches, each bearing a spermatheca. Temperature-sensitive period in third larval instar. Female fertility not greatly affected. RK3. # spt: see stt2 #*spw: spur wing location: 3- (right arm). origin: Spontaneous. references: Wallbrunn, 1942, DIS 16: 54. phenotype: Wings vary from normal to large fan-shaped struc- tures with extra veins; often a spur-shaped lobe from costal margin. Penetrance better in female and in old cultures. RK3. # spx: split thorax location: 1-22.6. origin: X ray induced. discoverer: Fahmy, 1956. references: 1959, DIS 33: 91-92. phenotype: In extreme manifestation, thorax split into two seg- ments by longitudinal furrow; abdominal tergites also split along mid-dorsal line. Eyes deformed. In least abnormal fly, always a hairless stripe along the dorsal midline of thorax. Wings often slightly divergent. Occasionally, one or both palpi abnormal in position or structure. Viability and fer- tility rather low in male, very low in female. RK3. other information: One allele each induced by CB. 2511 and CB. 3007. Two alleles induced by CB. 1528. # spx: see sdx # spy: see egspy # spz: spaztle location: 3-92. references: Anderson and Nusslein-Volhard , 1984, Nature (Lon- don) 311: 223-27. 1986, Symp. Soc. Dev. Biol. 44: 177-94. Seifert, Muller-Holtkamp, Marcey, and Jackle, 1987, Roux's Arch. Dev. Biol. 196: 78-82 (fig.). Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal-effect lethal. Embryos dorsalized, germ- line dependent. Phenotypic rescue achieved by injection of cytoplasm or poly(A)+RNA from wild-type embryos into young embryos produced by spz females; cytoplasm more effective than RNA (Seifert et al.). Temperature-sensitive period of spz3 extends from oogenesis through fertilization until about the time of pole-cell formation. Strong alleles amorphic by defi- ciency testing. Pole-cell-transplantation studies indicate that spz acts in germ line and not soma of mother (Seifert et al.). alleles: Four ethyl methanesulfonate-induced alleles: spz1 (weak), spz2 (strong), spz3 (temperature sensitive), and spz4 (strong), originally isolated as 145, 197, 670, and rm7, respectively. cytology: Placed in 97D15-E4 based on its inclusion in Df(3R)9Q-RX1 (breakpoints not given) but not Df(3R)ro80b = Df(3R)97D1;97D15 or Df(3R)D605 (breakpoints not given). #*sq: square location: 2-8.4. discoverer: Bridges, 17h17. phenotype: Wings truncated with squarish or oblique tip. Over- laps wild type. Viability erratic. RK3. #*Sq: Squat location: 2-38. origin: Spontaneous. discoverer: Bridges, 15k29. references: Bridges and Morgan, 1929, Carnegie Inst. Washington Publ. No. 278: 283-84 (fig.). phenotype: Wings short, broad, blunt, arched, and less transparent than normal. Thorax and head short and broad. Legs short and weak. Overlaps wild type. Homozygous lethal. RK3. # sqh: spaghetti squash (D. P. Kiehart) location: 1-14. origin: P element insertion. references: Chang, Edwards, and Kiehart, in prep.; Karess, Kulkarni, and Aguilera, unpublished. phenotype: The structural gene for cytoplasmic myosin light chain (Chang et al.) In the homozygous sqh1 mutant, the nor- mally diploid larval tissues (e.g., brain, imaginal disc, and gonad) possess numerous polyploid cells resulting from an intermittent failure of cytokinesis. Repeated rounds of apparently normal mitosis without cytokinesis produce cells containing hundreds of chromosomes. The mutant is a late larval-early pupal lethal with an extended larval period (10- 14 days), during which the brain grows to enormous size. Ima- ginal discs are small and poorly formed (Karess). alleles: sqh1 (isolation number 569) was found among a collec- tion of larval and pupal lethals generated by Dennell and Johnson. Probably a hypomorph. cytology: Located in 5D5-6 by in situ hybridization with cytoplasmic-myosin-regulatory light chain and P element probes. Uncovered by Df(1)5D1,2;5E. molecular biology: The gene was cloned independently by P- element tagging (Karess et al.) and oligonucleotides corresponding to partial peptide sequence of purified cyto- plasmic myosin light chain (Chang et al.). The 2.1 kb tran- scription unit contains two introns, of 1 kb and 73 bp. It expresses transcript(s) of approximately 1.1 kb at all developmental stages. Sequenced cDNAs encode a 174 amino acid protein of 19.9 kd, which is more similar to vertebrate smooth muscle regulatory light chains (80% identity) than to the Dro- sophila muscle homolog Mlc2. sqh1 has an 800 bp internally deleted P element inserted in the 5' untranslated region of the transcription unit, 48 bp from the first codon of the open reading frame.