# sh: short winged location: 3-56. origin: Spontaneous. discoverer: Bridges, 23d3. synonym: short wing. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 235. 1935, DIS 3: 16. phenotype: Wings small; similar to dy. Appears to be epistatic to vg in that vg sh flies have sh phenotype; by same argument px epistatic to sh (Rudy and Duffy, 1972, J. Hered. 62: 387- 88). RK2. #*sh-5: short-5 location: 3-93.2 (Koliantz, 1969, DIS 44: 52). origin: Spontaneous. discoverer: Spencer, 26j. references: 1934, DIS 1: 35. 1935, Am. Naturalist 69: 223-38. phenotype: Wing veins L5 and L3 short and do not reach wing margin. Expression variable; overlaps wild type. RK3. # Sh: Shaker (M. Tanouye) location: 1-57.6. origin: X ray induced. discoverer: Catsch, 1944. references: Catsch, 1944, Z. Indukt. Abstamm. Vererbungsl. 82: 64-66. Trout and Kaplan, 1973, J. Neurobiol. 4: 495-512. Jan, Jan, and Dennis, 1977, Proc. R. Soc. London Ser. B 198: 87-108. Tanouye, Ferrus, and Fujita, 1981, Proc. Nat. Acad. Sci. USA 78: 6548-52. Salkoff and Wyman, 1981, Nature (London) 293: 228-30. Tanouye, Kamb, Iverson, and Salkoff, 1986, Ann. Rev. Neurosci. 9: 255-76. phenotype: Under moderate ether anesthesia, legs shake abnor- mally, antennae twitch, abdomen pulsates; wings scissor in some alleles; very little effect in deeply etherized flies; unetherized mutants twitch and shudder occasionally; severed legs shake (Kaplan and Trout, 1969, Genetics 61: 399-409; Trout and Kaplan, 1973; Tanouye, Ferrus, and Fujita, 1981; Ganetzky and Wu, 1982a, Genetics 100: 597-614; Tanouye and Ferrus, 1985, J. Neurogenet. 2: 253-71). Structural gene for several types of potassium channel (Iverson, Tanouye, Lester, Davidson, and Rudy, 1988, Proc. Nat. Acad. Sci. USA 85: 5723-27; Timpe, Schwarz, Tempel, Papazian, Jan, and Jan, 1988, Nature 331: 143-45). Abnormal action potential repo- larization of adult giant fiber; repetitive firing of action potentials in larval nerves; prolonged transmitter release at larval neuromuscular junction (Jan, Jan, and Dennis, 1977; Tanouye, Ferrus, and Fujita, 1981; Ganetzky and Wu, 1982b, J. Neurophysiol. 47: 501-14; Tanouye and Ferrus, 1985). Abnor- mal in one class of potassium channel (A channel) present in embryonic myocytes, larval and pupal muscle (Salkoff and Wyman, 1981; Salkoff, 1983, Cold Spring Harbor Symp. Quant. Biol. 48: 221-31; Wu and Haugland, 1985, J. Neurosci. 5: 2626-40; Timpe and Jan, 1987, J. Neurosci. 7: 1307-17; Haugland and Wu, 1990, J. Neurosci.). Sh mutations do not affect four other distinct potassium-channel types (KD, K1, A2, Calcium-gated) (Salkoff and Wyman, 1981; Salkoff, 1983, Nature 302: 249-51; Wu, Ganetzky, Haugland, and Liu, 1983, Science 220: 1076-78; Solc, Zagotta, and Aldrich, 1987, Sci- ence 236: 1094-98; Solc and Aldrich, 1988, J. Neurosci. 8: 2556-70). Males carrying hemizygous deletions of Sh are viable (Tanouye, Ferrus, and Fujita, 1981). Abnormal associa- tive learning in some paradigms (Tully); activity patterns high, but show normal circadian rhythmicity (Konopka). RK1. alleles: allele origin discoverer synonym ref ( comments | ________________________________________________________________________ *Sh1 X ray Catsch 1 1 *Sh2 X ray Novitski 2 1 *Sh3 X ray Novitski 2 1 *Sh4 CB3025 Fahmy 2 Sh5 EMS Kaplan 6, 7, 9, 4 12, 14 Sh6 EMS Homyk Sh101 4 1 Sh7 EMS Homyk Sh102 4, 12, 4 13, 14 Sh8 X ray Merriam ShB55 10, 12 3; T(1;Y)B55 Sh9 EMS Ferrus/Ganetzky ShE62 3, 5, 4 12, 13 Sh10 P Kreber/Ganetzky ShHD1 8 1 Sh11 / ray Kreber ShK82a 3, 8, 13 2 Sh12 / ray Kreber ShK82b 8, 13 2 Sh13 P Kreber ShK83f 8, 13 2 Sh14 EMS Searcy ShKS133 6, 10, 12 4 Sh15 EMS Crosby ShLC 12, 13 3; T(1;3)16F1-2;80 Sh16 spont. Ganetzky ShM 11, 14 4 Sh17 / ray Paulus ShP 8, 13 2 Sh18 / ray Paulus ShRP1 8 1 Sh19 / ray Paulus ShRP2 8 1 Sh20 / ray Paulus ShRP2 8 1 Sh21 EMS O'Hara ShrKO120 3, 6, 9, 4 12, 14 Sh22 spont. Barbel ShSB2 5, 13 4 Sh23 P Barbel ShSB3 5, 13 4 Sh24 spont. Barbel ShSB13 5, 13 4 Sh25 X ray Merriam ShW32 10, 12 3; T(1;Y)16F3-6 Sh26 spont. Kreber ShX 8 1 ( 1 = Catsch, 1944, Z. Indukt. Abstamm. Vererbungsl. 82: 64- 66; 2 = CP627; 3 = Haugland and Wu, 1990, J. Neurosci.; 4 = Homyk, 1977, Genetics 87: 105-28; 5 = Jan, Barbel, Timpe, Laffer, Salkoff, O'Farrell, and Jan, 1983, Cold Spring Harbor Symp. Quant. Biol. 48: 233-45; 6 = Jan, Jan, and Dennis, 1977, Proc. R. Soc. London Ser. B 198: 87-108; 7 = Kaplan and Trout, 1969, Genetics 61: 399-409; Trout and Kaplan, 1973, J. Neurobiol. 4: 495-512; 8 = Kreber and Ganetzky; 9 = Salkoff and Wyman, 1981, Nature (London) 293: 228-30; 10 = Salkoff, 1983, Cold Spring Harbor Symp. Quant. Biol. 48: 221-31; 11 = Tanouye and Ferrus, 1985, J. Neurogenet. 2: 253-71; 12 = Tanouye, Ferrus, and Fujita, 1981, Proc. Nat. Acad. Sci. USA 78: 6548-52; 13 = Timpe and Jan, 1987, J. Neurosci. 7: 1307-17; 14 = Wu and Haugland, 1985, J. Neurosci. 5: 2626-40. | Sh phenotype has been assessed in four ways: (a) abnormal leg shaking under ether anesthesia; (b) abnormal A-type potassium currents in larval muscle and/or pupal flight mus- cle; (c) abnormal action potentials in the adult cervical giant fiber; and (d) abnormal synaptic transmission at the larval neuromuscular junction and multiple firing of larval motoneurons. Numbers above indicate the tests that have been performed on each allele: 1 = a; 2 = a + b; 3 = a + b + c; and 4 = a + b + c + d. All tests performed produced mutant results. cytology: Located in 16F1-8 (Tanouye, Ferrus, and Fujita, 1981). Associated with T(1;Y)B55 = T(1;Y)16F1-4, with T(1;3)Sh15 = T(1;3)16F1-2;80, and with T(1;Y)W32 = T(1;Y)16F3-6; covered by Dp(1;3)16E2-4;17A-B;99D. molecular biology: Structural gene for a potassium channel cloned by chromosomal walking; large transcription unit spans >110 kb of chromosomal DNA with multiple transcripts generated by differential splicing; at least twelve different tran- scripts formed from at least 25 different exons; all tran- scripts contain a conserved central portion (863 bp) built from six common exons; the transcripts contain variable 5' and 3' domains; Northern blots show a heterogeneous pattern of transcripts with a broad band of 5.5-6.5 kb and major bands at 7.8, 8.5, and 9.5 kb (Kamb, Iverson, and Tanouye, 1987, Cell 50: 405-13; Baumann, Krah-Jentgens, Mueller, Mueller- Holtkamp, Seidel, Kecskemethy, Casal, Ferrus, and Pongs, 1987, EMBO J. 6: 3419-29; Papazian, Schwarz, Tempel, Jan, and Jan, 1987, Science 237: 749-53; Tempel, Papazian, Schwarz, Jan, and Jan, 1987, Science 237: 770-75; Kamb, Tseng-Crank, and Tanouye, 1988, Neuron 1: 421-30; Pongs, Kecskemethy, Muller, Krah-Jentgens, Baumann, Kiltz, Canal, Llamazares, and Ferrus, 1988, EMBO J. 7: 1087-97; Schwarz, Tempel, Papazian, Jan, and Jan, 1988, Nature (London) 331: 137-42). Two forms of gene product are deduced: a small-protein form with three hydrophobic segments has unknown function; a larger form with six potential membrane-spanning segments has potas- sium channel function as demonstrated electrophysiologically by expression in Xenopus oocytes, mammalian cell lines, and insect cell lines; at least six different transcript variants express potassium channels with different physiological pro- perties; the channel may be a tetramer formed from four Sh subunits; a heteromultimer may be indicated from results on heterozygous combinations and co-injections into Xenopus oocytes; conserved region may be responsible for voltage dependence of activation, voltage dependence of inactivation, potassium selectivity, and toxin sensitivity which are similar among all products; variable amino termini are responsible for different potassium channel inactivation rates; variable car- boxyl termini are responsible for differences in inactivation recovery rates; a current loss in myotubes may be rescued by germline transformation (Iverson, Tanouye, Lester, Davidson, and Rudy, 1988; Timpe, Schwarz, Tempel, Papazian, Jan, and Jan, 1988; Timpe, Jan, and Jan, 1988, Neuron 1: 659-67; Leo- nard, Karschin, Jayashree-Aiyar, Davidson, Tanouye, Thomas, Thomas, and Lester, 1989, Proc. Nat. Acad. Sci. USA 86: 7629-33; Zagotta, Germeraad, Garber, and Aldrich, 1989, Soc. Neurosci. Abstracts 15: 338; Iverson and Rudy, 1990, J. Neurosci.; Wu and Haugland, 1990; Iverson and Rudy; Stuhmer; Isakoff; Miller). An S4 motif, consisting of 7 repeats of the triplet, R-X-X, where R is sometimes replaced by K, and X is a hydrophobic residue, is present in all Sh channels and is highly conserved in virtually all other known voltage-gated ion channels; mutagenesis of S4 results in alterations of voltage sensi- tivity; the motif is thought to be a voltage-sensor (Tempel, Papazian, Schwarz, Jan, and Jan, 1987; Kamb, Tseng-Crank, and Tanouye, 1988; Pongs, Kecskemethy, Muller, Krah-Jentgens, Bau- mann, Kiltz, Canal, Llamazares, and Ferrus, 1988; Papazian, Timpe, Jan, and Jan, 1989, Soc. Neurosci. Abstracts 15: 337). A leucine-heptad repeat located adjacent to the S4 motif may participate in the channel gate; mutagenesis causes altera- tions in voltage sensitivity and subunit interactions (McCor- mack, Campanelli, Ramaswami, Mathew, Tanouye, Iverson, and Rudy, 1989, Nature 340: 103; McCormack, Ramaswami, Mathew, Tanouye, Iverson, McCormack, Rudy, 1989, Soc. Neurosci. Abstracts 15: 337). A truncated product that acts as an antimorph is associated with Sh7; an amino acid substitution is associated with the Sh14 product, which acts as an antimorph; an amino acid sub- stitution in the leucine-heptad repeat motif is associated with the Sh5 product; an alteration of a splice site is asso- ciated with the Sh9 mutation; Sh16 contains an insertion into coding sequence (Kamb, Iverson, Tanouye, 1983; Gisselmann, Sewing, Madsen, Mallart, Angaut-Petit, Mueller-Holtkamp, Ferrus, and Pongs, 1989, EMBO J. 8: 2359-64; Pongs; Gautam and Tanouye). The Sh product is highly homologous to three other potassium channel genes: Shab, Shal, and Shaw, isolated by DNA crosshybridization using Sh probes (Butler, Wei, Baker, and Salkoff, 1989, Science 243: 943-47). Tissue in situ hybridization shows Sh transcript in the cell bodies of retina, optic lobe, central brain, thoracic gan- glion, and muscle; antibody studies show a major polypeptide of about 70-80 kd; differential temporal and spatial expres- sion may be indicated (Pongs, Kecskemethy, Muller, Krah- Jentgens, Baumann, Kiltz, Canal, Llamazares, and Ferrus, 1988; Tseng-Crank and Tanouye; Schwarz, Papazian, Carretto, Jan, and Jan, 1988, Soc. Neurosci. Abstracts 14: 454). allele molecular biology ( ref | _______________________________________________________ Sh5 phe371 to ile 1, 2 Sh7 trp404 to stop 1, 3 Sh8 break at 33.4 to 34.9 4, 5, 6 Sh9 splicing defect at gly480 2 Sh11 break at 61 4 Sh13 insertion at 44 4 Sh14 val413 to asp 2 Sh15 break at 54.1 to 59.1 4, 5, 6 Sh16 insertion at 45.5 to 46.1 5 Sh25 break at 95.2 to 98.7 4, 5, 6 T(1;Y)B27 break at -22 to -21 6 ( Locations are relative to the Sh chromosomal walk in kb (Kamb, Iverson, and Tanouye, 1987). Amino acid changes are relative to the deduced H37 protein (Kamb, Tseng-Crank, and Tanouye, 1988). | 1 = Gautam and Tanouye; 2 = Pongs; 3 = Gisselmann, Sewing, Madsen, Mallart, Angaut-Petit, Muller-Holtkamp, Ferrus, and Pongs, 1989, EMBO J. 8: 2359-64; 4 = Papazian, Schwarz, Tempel, Jan, and Jan, 1987, Science 237: 749-53; 5 = Kamb, Iverson, and Tanouye, 1987, Cell 50: 405-13; 6 = Baumann, Krah-Jentgens, Mueller, Mueller-Holtkamp, Seidel, Kecskemethy, Casal, Ferrus, and Pongs, 1987, EMBO J. 6: 3419-29. other information: Some Sh phenotypes are suppressed by nap and para alleles; i.e., in double mutant combinations, abnormal leg-shaking, repetitive firing of larval action potentials, and transmitter release at larval neuromuscular junction are nearly normal; the interactions are not allele-specific (Ganetzky and Wu, 1982a,b). Some Sh phenotypes are enhanced by eag; i.e., in double mutant combinations, abnormal leg- shaking, repetitive firing of larval action potentials, and transmitter release are more extreme; also, adults have down- turned wings, and dented-in thoraces at the sites of the dor- sal longitudinal muscle insertions; the interactions are not allele-specific (Ganetzky and Wu, 1983, J. Neurogenet. 1: 17-28). Some Sh phenotypes are enhanced by dnc; i.e., in double mutant combinations, abnormal leg-shaking is more extreme; abnormal spontaneous activity is seen in the giant fiber (Ferrus and Tanouye). The breakpoint of T(1;3)B27 = T(1;3)16E3-5;36D-F, induced in a Sh14 background, causes an alteration in the pattern of leg-shaking (Tanouye and Ferrus). # sha: shavenoid location: 2-62. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Trichomes missing or very short. Flies cannot fly or walk on glass. In larvae, the number of denticles is reduced with remaining denticles thin and bent. Hairs are largely absent, but sensory hairs not affected. Autonomous in nuclear transplants. Causes disoriented and abbreviated hairs on larval cuticle; useful as a larval-cuticle marker (Struhl and Lawrence, 1982, Cell 31: 285-92). alleles: sha1 and sha2 (originally designated IN and IIP) plus two discarded alleles. cytology: Placed in 47E3-48A6 based on its location in the area of overlap between Df(2R)en-A = Df(2R)47D3; 48A5-6 and Df(2R)en-B = Df(2R)47E3;48B2. # Shab: Shaker cognate b (J.C. Hall) location: 3- {15}. origin: Isolated by screening a cDNA library with a Sh cDNA probe. references: Butler, Wei, Baker, and Salkoff, 1989, Science 243: 943-47. cytology: Mapped to 63A by in situ hybridization. phenotype: Expression in Xenopus oocytes reveals a delayed- rectifier type of potassium current expressed by Shab; the rate of current activation in Shab is somewhat faster than in Shaw. molecular biology: Isolated by screening a cDNA library with a Sh cDNA probe containing all of the presumptive membrane- spanning domains, which form the core of the potassium channel proteins encoded by Sh, and which thus very likely character- ize the Shab gene product as well. Sequencing of six Shab cDNAs identifies alternatively spliced mRNAs from this locus; this involves, at least in part, the coding portion of the gene (e.g., one cDNA contains an additional exon not found in two others). Sequencing data reveal, in addition to homolo- gies to Sh, as expected, homologies to two other Sh-type genes, Shaw and Shal. Similarities among products of these four genes are greater than those between D. melanogaster's Sh gene family and sodium or calcium channel proteins. Shab shares opa (poly-Gln) repeats with some of the alternatively spliced Sh products (relatively near N- and C-termini of the respective proteins), and there are possible cAMP-dependent phosphorylation sites in one of the corresponding regions of the two gene products (C-terminal to the intramembrane por- tions of the proteins); in Shab, but not Shaw conceptual pro- tein, there is a large sequence N-terminal to the first membrane-spanning region, which includes Ser-Gly and Thr-Gly repeats (possible sites of O-linked glycosylation); the "S4" region of Shab, which is the presumed voltage sensor of the channel, contains a string of five positive charges (vs. seven and four in Sh and Shaw proteins, respectively). Shab cDNA probes found to detect two late embryonic transcripts, 4.3 and 6.8 kb, the latter being more abundant; in pupae, relative abundances of these two switch; these RNA species not detected in adults. other information: A rat potassium channel gene (drk1), iso- lated by expression cloning in a frog oocyte system, has greater sequence similarity to Shab than to Sh (Frech, Van- Dongen, Schuster, Brown, and Joho, 1989, Nature (London) 340: 642-645); drk1 is not the same as two other mammalian K+ channel genes, cloned by homology to Sh. # shade: see shd # shadow: see sad # shaggy: see sgg # shakA: shaking A (J.C. Hall) location: 1-38.2 (Homyk). origin: Induced by ethyl methanesulfonate. discoverer: Homyk. references: Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. phenotype: Vigorous shaking of legs when flies under ether; both mutant alleles cause temperature-sensitive phenotypes: shakA1 exhibits generally hyperactive behavior (irrespective of anesthetic) when raised at 22; after rearing at 29, flying and jumping abilities severely subnormal, and males show abnormal wing usage in courtship; shakA2 causes lethality when raised at 29; after rearing at 22, adults are hypoactive and uncoordinated. alleles: Two alleles, shakA1 and shakA2. # shakB: shaking B (J.C. Hall) location: 1-64. synonym: nj-156: non-jumper; pas: passover. references: Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. Thomas, 1980, Neurosci. Abstr. 6: 742. Wyman and Thomas, 1983, Cold Spring Harbor Symp. Quant. Biol. 48: 641-52. Thomas and Wyman, 1984, J. Neurosci. 4: 530-38. Baird and Hillis, 1985, Neurosci. Abstr. 11: 627. Baird, 1986, Neurosci. Abstr. 12: 1164. Miklos, Kelly, Leeds, and Lefevre, 1987, J. Neurogenet. 4: 1-19. Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 313-31. Baird, Schalet, and Wyman, 1990, Genetics 126: 1045-59. phenotype: Some of the shakB mutants are viable but defective in their neural phenotypes as homo-, hemi-, or heterozygotes, but other mutants are homozygous lethals that may or may not complement the viable shakB alleles. The viable mutants have difficulty in controlling leg movements and show leg tremors under ether anesthesia (Homyk et al., 1980). They show no escape response; the flies are unable to jump into the air and fly away at a light off stimulus (Thomas, 1980; Thomas and Wyman, 1984). Unlike the mutant Sh, the leg tremors of shakB are weak and end when the legs are severed from the body (indicating a central nervous system defect). In wild-type flies, the thoracic muscles involved in the escape response are driven by the giant fiber (GF) neuron pathway connecting the brain and thoracic ganglia. In the mutant shakB, the synapse between the GF axon and the post- synaptic interneuron (PSI) or between the PSI and the dorsal longitudinal muscle (DLM) seems to be defective; thus the DLM does not respond to visual stimulation by depressing the wings in flight. The synapse between the GF axon and the motor neu- ron of the tergotrochanter muscle (TTM) also seems to be defective, resulting in a weak response or no response from the TTM, the muscle that extends the leg in jumping. The motor neurons "pass over" the midline of the thoracic central nervous system and send aberrant branches into each contrala- teral mesothoracic ganglion. The abnormal neural phenotype is more pronounced if shakB is uncovered by a deficiency (Wyman and Thomas, 1983; Baird and Hillis, 1985; Baird et al., 1990). The muscles themselves and their neuro-muscular junctions are not abnormal (Thomas and Wyman, 1984). Viable shakB mutants are also characterized by electrore- tinogram (ERG) abnormalities; the corneal negative component is reduced and the on- and off- transients are reduced or absent. Neurons in the brain are affected, as indicated by failure of one of the superoesophageal brain commissures to fill with cobalt when the antennal nerve is backfilled (Aceves-Pina). shakB3 (= Pas) is partially dominant to wild type in regard to the mutant's elimination of the jump response, but the other viable alleles are recessive. +/Df(1)16-3-35 and +/Df(1)A118 are behaviorally normal, but Df(1)16-3- 35/Df(1)A118 females are shakB in phenotype. alleles: A number of homozygous lethal alleles have been located in the shakB region. Six of them do not complement the shakB neural phenotype; two of the remainder have been tested and found to complement this neural phenotype, but do not complement the lethality of the other lethal alleles. The six noncomplementing lethals also fail to complement Df(1)16- 3-35 (distal deficiency) and Df(1)A118 (proximal deficiency), while the two complementing lethals complement Df(1)A118 but not Df(1)16-3-35. 25 alleles, viables and lethals, are listed in the following table. allele origin discoverer synonym ref ( comments ________________________________________________________________________________ *shakB1 EMS Homyk 2 viable; neurological defect shakB2 EMS Homyk 1,2 viable; neurological defect shakB3 EMS Thomas Pas 1,9 viable; neurological defect shakB4 EMS Homyk pasTH73 viable; neurological defect shakB5 X ray Lifschytz l(1)B220 4,6 shakB6 | EMS Lifschytz l(1)E81 1,5,6,8 shakB7 EMS Lifschytz l(1)P81 5,7 shakB8 EMS Lifschytz l(1)P525 5,7 shakB9 EMS Lifschytz l(1)Q212 5,7 shakB10 EMS Lifschytz l(1)R-9-21 5,7 shakB11 | EMS Lifschytz l(1)R-9-29 1,5,7,8 shakB12 EMS Lifschytz l(1)R10-3 5,7 shakB13 EMS Lifschytz l(1)R10-7 5,7 shakB14 EMS Lifschytz l(1)R10-14 5,7 shakB15 EMS Lifschytz l(1)N36 5 shakB16 EMS Lifschytz l(1)YT7 5 shakB17 EMS Lifschytz l(1)YT14 5 shakB18 neutrons Munos l(1)17-96 8 shakB19 | neutrons Munos l(1)17-189 1 shakB20 | neutrons Munos l(1)17-360 1 shakB21 / X ray Lefevre l(1)L41 1,4 shakB22 | EMS Lefevre l(1)EC201 1,5 shakB23 EMS Lefevre l(1)EF481 5 shakB24 / EMS Lefevre l(1)EF535 1,5 shakB25 | HMS Kramers l(1)HM437 1,3 ( 1 = Baird, Schalet, and Wyman, 1990, Genetics 126: 1045-59; 2 = Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet., 177: 533-65; 3 = Kramers, Schalet, Paradi, and Huiser- Hoogteyling, 1983, Mutat. Res. 107: 187-201; 4 = Lefevre, 1981, Genetics 99: 461-80; 5 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 6 = Lifschytz and Falk, 1968, Mutat. Res. 6: 235-44; 7 = Lifschytz and Falk, 1969, Mutat. Res. 8: 147-55; 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 = Thomas, 1980, Neurosci. Abst. 6: 742. | Fails to complement shakB3. / Complements shakB3. cytology: Placed in 19E3-4 based on the mutant neurological phenotype of heterozygotes for Df(1)16-3-35 = Df(1)19D2- 3;19E3-4 and Df(1)A118 = Df(1)19E3-4;19E7-8 (Baird et al.). # Shaker cognate: see Shab, Shal, and Shaw # shaking: see shak # Shal (J.C. Hall) location: 3- {45}. origin: Isolated by screening a cDNA library with a Sh cDNA probe. references: Butler, Wei, Baker, and Salkoff, 1989, Science 243: 943-47. phenotype: Expression of Shal cDNA-derived mRNA in Xenopus oocytes (Wei, Covarrubias, Butler, Baker, Pak, and Salkoff, unpublished) leads to potassium currents intermediate in kinetic properties between those associated with Sh (using the heterologous egg system) and Shaw (same kind of experiment), i.e., between very rapid activation/inactivation (Sh-encoded "A"-type channels) and quite slow kinetics (Shaw-encoded, delayed-rectifier-type channels). cytology: Mapped to 76B by in situ hybridization. molecular biology: Identified, as was Shab, via screening for Sh-like cDNAs; mixed probe of these two types plus a Shaw probe was used to isolate Shal. No structural details of the latter's coding sequence explicitly presented by the authors cited above, yet there are inferences about homology domains among the four known members of Drosophila's Sh family, including Shal, e.g., they are conserved at least insofar as each one's encoding of six similar putative membrane-spanning segments and the putative S4 voltage sensor. Also, whereas Sh, Shab, and Shaw conceptual proteins have strings of seven, five, and four positively charged amino acids in the presumed gating charge region, Shal has five such charges. # shaven: see svb # shaven baby: see svb # shavenoid: see sha # Shaw (J.C. Hall) location: 2- {10}. origin: Isolated by screening a cDNA library with a Shab cDNA probe. references: Butler, Wei, Baker, and Salkoff, 1989, Science 243: 943-47. phenotype: In Xenopus oocyte mRNA injection experiment, protein encoded by Shaw transcripts leads to potassium currents with slow activation and inactivation kinetics (Wei, Covarrubias, Butler, Baker, Pak, and Salkoff, unpublished). cytology: Mapped to 24B-C by in situ hybridization. molecular biology: Identified by screening a cDNA library for Sh-like cDNAs, using a Shab cDNA probe. Sequencing the Shaw cDNA resulted in conceptual protein of approximately 500 amino acids (some 400 residues smaller than that deduced from Shab's longest correctly spliced cDNA); hence Shaw polypeptide more similar in size to that of Sh than other putative potassium channel proteins; differs in length of charged amino acid string, in voltage-sensor region, from other members of the Sh family; for example, the position corresponding to the first (positive) gating charge in Sh occupied by negatively charged Asp in Shaw and Shab; Shaw also has a negative residue (Glu) at second position (defined by a positive amino acid in Sh). Northern blotting experiment using a Shaw cDNA probe showed one 4.9 kb transcript, which was similar in abundance in late embryos, pupae, and adults. #*shb: shortened bristles location: 1-39.0. origin: Induced by S-2-chloroethylcysteine (CB. 1592). discoverer: Fahmy, 1957. references: 1959, DIS 33: 90. phenotype: Bristles slightly short and thin. Wings broad, often convex or concave. Fly somewhat large. Male fertile; viability about 50% wild type. Female sterile. RK3. # shd: shade location: 3-41. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. Roark, Mahoney, Graham, and Lengyel, 1985, Dev. Biol. 109: 476-88. Tearle and Nusslein-Volhard, 1987, Dis 66: 209-26. phenotype: Embryonic lethal. No differentiation of cuticle or head skeleton. alleles: shd1, shd2, and shd3 (originally designated 6J, 7C, and I9K) plus two discarded alleles; all induced by ethyl methanesulfonate. cytology: Placed in 70D-71C; covered by Dp(3;Y)B162 = Dp(3;Y)65E;71A-C but not by Dp(3;Y)G145 = Dp(3;Y)68D;70D. # shd: see spl #*she: sherry location: 3-0. origin: Kaliss, 36a13. references: 1937, DIS 8: 9. phenotype: Eye color sherry. Sterile inter se but both sexes crossfertile. RK3. # Shell: see Cpl5 #*shf: shifted location: 1-17.9. discoverer: Bridges, 13a. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 63. phenotype: Vein L3 fails to reach wing margin and is shifted toward L4. Anterior crossvein usually lacking. Wings diver- gent. Postscutellar bristles small and erect. Body small. Viability 60% wild type. Female often sterile. RK2. cytology: Placed between 6A3 and 6F11 based on deficiency analysis using shf2 (Demerec, Kaufmann, Fano, Sutton, and San- some, 1942, Year Book - Carnegie Inst. Washington 41: 191). # shf2 origin: X ray induced. discoverer: Oliver, 29j29. references: 1935, DIS 3: 28. 1935, DIS 4: 10. phenotype: Veins closer together than in wild type. L3 and L4 tend to fuse near anterior crossvein; anterior crossvein shor- tened, knotted, or absent. Phenotypic effect visible in prepupal wing bud, the two longitudinal veins diverging at a smaller-than-normal angle [Waddington, 1940, J. Genet. 41: 75-139 (fig.)]. Eyes sometimes slightly rough. Scutel- lar bristles often absent. Scutellum short. Wings narrow and often warped downward. Fertility and viability good. RK2. #*shf3 origin: Spontaneous. discoverer: Curry, 37d26. phenotype: Like shf2 but more extreme. Viability about 70% wild type. Frequently infertile. RK2. shf3: shifted-3 From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 173. # shfov: shifted-oval origin: Induced by P32. discoverer: Bateman, 1950. references: 1950, DIS 24: 55. phenotype: Eyes rough and narrow. First basal wing cell absent because L3 and L4 veins close. Wings narrow and pointed. Viability and fertility low. RK2. other information: On basis of phenotype and position, could be an allele of either ov or shf or both; not tested. # shg: shotgun location: 2-92. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Embryonic lethal. Embryonic cuticle has many small holes with necrotic rims. Head grossly distorted. Weak alleles show head defects and irregular flaws in segmentation pattern. alleles: Two retained alleles, shg1 and shg2 (originally desig- nated IG and IH) plus sixteen discarded alleles. # shi: shibire (C. A. Poodry) location: 1-51.5. discoverer: Grigliatti, 1971. references: Grigliatti, Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-14. phenotype: The shibire locus is characterized by its temperature-sensitive alleles, which are reversibly paralyzed by exposure to 29, but are essentially normal at 22 (Grigli- atti et al.). Exposure of developing animals to the restric- tive temperature for pulses of one to several hours leads to a plethora of developmental defects, which are specific for the stage treated (Poodry, Hall, and Suzuki, 1973, Dev. Biol. 66: 442-56) (see following table). Short exposures to res- trictive temperatures at the time of delamination of the neu- roblasts from the neurogenic ectoderm leads to excess neuro- genesis at the expense of epidermogenesis, as seen in the neu- rogenic mutants (Poodry, 1990, Dev. Biol., in press). Dif- ferentiation of myoblasts and neuroblasts is inhibited in shi1 embryonic cells in vitro at 30 (Buzin, Dewhurst, and Seecof, 1978, Dev. Biol. 66: 442-56). Embryonic neurons cultured at 30 show reduced adhesion to the substrate, retardation of growth cone formation and suppressed neuron formation and elongation; reversed by shift to permissive temperature (Kim and Wu, 1987, J. Neurosci. 7: 3245-55). Lethal embryos disorganized by the restrictive temperature can be cultured in vivo as tumorous masses (Poodry). Eye-antenna discs can also be cultured as tumorous masses for several transfer genera- tions (Williams, 1981, DIS 56: 158-61). Primary in vivo cul- ture of cut leg imaginal discs leads to an exceptionally high rate of transdetermination (Poodry). temperature- sensitive period developmental phenotype _________________________________________________________________________ 1.5-3 hr loss of pole cells 3-4 hr fusion of cell membranes leading to syncytium 5-12 hr disorganized proliferation of cells leading to transplantable tumorous masses late third instar stubby legs; joints missing; 12 hr heat pulse clipped wings 48 hr before pupariation eye scar (loss of pigment cells and cone cells). The later the heat pulse, the more anterior the position of the scar on eye pupariation to pupation animals die and fail to undergo pupation 14-24 hr after pupariation supernumerary microchaetae on head and thorax; the temperature sensitive period for each bristle site precedes the final cell division of bristle precursor; loss of macrochaetae on head and thorax. Disruption of giant- fiber pathway development (Hummon and Costello, 1987, J. Neurosci. 7: 3633-38). Reduced numbers of dorsal-longitudinal flight muscles (Hummon and Costello, 1988, Roux's Arch. Dev. Biol. 197: 383-93) 24-36 hr after pupariation loss of head and thoracic micro- chaetae; supernumerary abdominal macrochaetae and microchaetae 28-42 hr after pupariation loss of abdominal macrochaetae and microchaetae 32-48 hr after pupariation loss of abdominal microchaetae 48 hr after pupariation scimitar-shaped bristles adult eggs fail to mature The temperature-sensitive alleles differ in the severity of their paralysis, recovery period, the restrictive temperature for developmental effects, and in their viability as hemizy- gotes. They are all hypomorphs, being recessive and having a more extreme expression in combination with a deficiency than when homozygous. A wild-type paternal gene can rescue an egg from a homozygous mother only after 10 hr of development (Swanson and Poodry, 1976, Dev. Biol. 48: 205-11). Of the developmental effects tested, all are autonomous in mosaics generated by somatic recombination or in gynandromorphs (Poo- dry). The developmental effects on bristles is not enhanced or suppressed by the presence of temperature-sensitive alleles of N; shi is epistatic to N (Lujan, 1981, DIS 56: 86). Physiological studies of shi have revealed the loss of tran- sients in electroretinograms (Kelley and Suzuki, 1974, Proc. Nat. Acad. Sci. USA 71: 4906-09) and failure of neuromuscular transmission at the restrictive temperature (Ikeda, Ozawa, and Hagiwara, 1976, Nature 259: 489-91; Siddiqi and Benzer, 1976, Proc Nat. Acad. Sci. USA 73: 3253-57), though axonal conduc- tion and muscle membrane excitability are unimpaired (Ikeda et al.). Exposure of shi1 adults to 29 causes the depletion of synaptic vesicles from the neuromuscular synapse and their replacement with large cisternae (Poodry and Edgar, 1979, J. Cell Biol. 81: 520-27; Koenig, Saito, and Ikeda, 1983, J. Cell Biol. 96: 1517-22). Accumulation of acetyl choline is reduced at the restrictive temperature, not because of reduced synthesis but because of an abnormally rapid rate of release from the cell, which is not reduced by inhibiting tetrodotoxin-sensitive nerve activity (Wu, Merneking, and Barker, 1983, J. Neurochem. 40: 1386-96). Endocytosis is reversibly blocked in the nerve terminus (Kosaka and Ikeda, 1983, Neurobiol. 14: 207-25; Masur, Kim, and Wu, 1990, J. Neurosci.) and may limit the ability of nerves to regenerate synaptic vesicles. Neuromuscular transmission temperature is sensitive in mosaics in which the neuron but not the muscle is mutant, but not in the converse situation (Koenig and Ikeda, 1983, J. Neurobiol. 14: 411-19). During recovery from expo- sure to 30 shits1 muscles display a multimodal distribution of miniature excitatory junction potential amplitudes never seen in wild type (Ikeda and Koenig, 1987, J. Physiol. 406: 215- 23). Further, as the temperature is increased the amplitude of evoked excitatory junction potentials decreases; the numbers of vesicles per synapse displays a correlated decrease (Koenig, Kosaka, and Ikeda, 1989, J. Neurosci. 9: 1937-42). Endocytosis is also blocked in the garland cells (Kosaka and Ikeda, 1983, J. Cell Biol. 97: 499-507). Vesiculation of cell membranes results in fusion of blastoderm cells (Swanson and Poodry, 1981, Dev. Biol. 84: 465-70) and vesiculation of sur- face membranes accompanies secretion of protein epicuticle (Poodry). alleles: The first alleles recovered were recognized as temperature-sensitive paralytic mutations. These show dif- ferent temperature responses as summarized in the second table below. allele origin discoverer synonym ref ( comments ___________________________________________________________________ shi1 EMS Grigliatti 1 temperature sensitive shi2 EMS Grigliatti 1 temperature sensitive shi3 EMS Grigliatti 1 temperature sensitive shi4 EMS Grigliatti 1 temperature sensitive shi5 EMS Grigliatti 1 temperature sensitive shi6 EMS Grigliatti 1 temperature sensitive shi7 EMS Lindsley & 2 temperature sensitive Poodry *shi8 / ray Poodry shi2-11 4 T(1;4)14A1;? shi9 / ray Poodry shi4-14C 4 shi10 / ray Poodry shi4-14D 4 shi11 / ray Poodry shi6-1 4 shi12 / ray Poodry shi6-7 4 shi13 / ray Poodry shi6-13 4 shi14 / ray Poodry shi8-9 4 shi15 / ray Poodry shi8-13 4 shi16 / ray Poodry shi8-18 4 In(1)14A;16A *shi17 / ray Poodry shi12-6 4 In(1)12D-E;14A1 shi18 / ray Poodry shi12-12A 4 shi19 / ray Poodry shi12-13 4 T(1;3)14A1;94D shi20 / ray Poodry shi12-18 4 T(1;2)14A1;24C shi21 Siddiqi & shiST139 3 Benzer shi22 EMS Katzen ( 1 = Grigliatti, Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-14; 2 = Dale Lindsley and Poodry, Dev. Biol. 56: 213-18; 3 = Siddiqi and Benzer, 1976, Proc Nat. Acad. Sci. USA 73: 3253-57; 4 = Poodry. temperature temperature temperature viability of of adult of larval causing develop- allele over allele paralysis paralysis mental defects deficiency ________________________________________________________________________ shi1 29 29 29 weak shi2 29 31 31 strong shi3 29 29 29 very weak shi4 29 none lethal shi5 29 shi6 29 31 31 strong shi7 29 31 31 strong shi21 29 29 29 cytology: Located in 13F to 14A (Austin and Poodry, 1991; Mor- gan, 1991). molecular biology: Cloned and sequenced by van der Bliek and Meyerowitz (1991, Nature 351: 411-14); homologous to rat dynamin. # shifted genitals: see sge #*shl: shorter legs location: 1-36.3. origin: Induced by 2-fluoroethyl methanesulfonate (CB. 1522). discoverer: Fahmy, 1957. references: 1959, DIS 33: 90. phenotype: Small fly with short legs. Male viability and fer- tility low. RK3. # shm: short macros location: 1-22.4. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1953. references: 1959, DIS 33: 90. phenotype: Bristles short and stiff. Eclosion delayed. Male sterile and viability reduced. RK2. # shn: schnurri location: 2-62. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Embryonic lethal. Embryos lack dorsal hypoderm. Internal organs appear normal and extruded through the open dorsal side of the embryo. Ventral hypoderm contracted. alleles: Two ethyl-methanesulfonate-induced alleles shn1 and shn2 (formerly designated IB and IM), the latter being heat sensitive, and one hybrid-dysgenesis-induced allele, shn3, (formerly TD5) isolated by Gergen. In addition fifteen dis- carded alleles. cytology: Placed in 47E3-48A6 based on its location to the area of overlap between Df(2R)en-A = Df(2R)47D3; 48A5-6 and Df(2R)en-B = Df(2R)47E3;48B2. #*sho: shovel location: 2- (not located). origin: Spontaneous in In(2L)t. discoverer: GoodSmith, 49k. references: Ives, 1952, DIS 26: 65. phenotype: Wings short and rounded. Viability good. RK2A. # short bristle: see stb # short egg: see seq # short macros: see shm # short tarsi: see sht # short vein: see shv under dpp # short wing: see sw # short winged: see sh # short-5: see sh-5 # short-bristle: see ml # shortened wing: see sg # shortened bristles: see shb # shortened veins: see svs # shorter bristles: see sbt # shorter legs: see shl # shotgun: see shg # shovel: see sho #*shp: shrimp location: 1-47.5. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1955. references: 1958, DIS 32: 74. phenotype: Small fly. Eclosion delayed. Male viability about 30% wild type. Both sexes fertile. RK3. # shr: shrunken location: 2-2.3. discoverer: Bridges. phenotype: Body small and dark. Viability and fertility good. Overlaps wild type unless combined with abb, where mutual enhancement occurs. RK3. cytology: Placed between 22A3 and 22B1 on the basis of its inclusion in Df(2L)S2 = Df(2L)21C6-D1;22A6-B1 but not in Df(2L)S5 = Df(2L)21C2-3;22A3-4 (Lewis, 1945, Genetics 30: 137-66). # shrew: see srw # shrimp: see shp # shroud: see sro # shrunken: see shr # Shrunken thorax: see Sht # shrunken-3: see wz #*sht: short tarsi location: 1-20.9. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1953. references: 1959, DIS 33: 90. phenotype: Legs extremely short; reduction in length most pro- nounced in metatarsal and tarsal regions. Some tarsi fused, others absent. Bristles thin and short. Adult short lived. RK3. # Sht: Shrunken thorax location: 2-54.7 (2.8_0.4 map units to the left of cn). origin: Induced by ethyl methanesulfonate. references: Kulkarni and Babu, 1981, DIS 56: 192. phenotype: Heterozygotes exhibit an indentation across the dor- sal mesothorax giving the appearance of shrunken thorax. Typ- ically a groove runs across the thorax in a V shape. There is some variability in the expressivity; a small fraction of flies have only a marginal phenotype, but the penetrance is nearly complete. Newly emerged flies do not often show the phenotype or have only a faint line on the thorax; the groove becomes visible as the cuticle hardens. Mutant flies have good viability and fertility. Homozygous lethal. other information: Possibly an allele of Mhc. # shu: shut down (T. Schupbach) location: 2-105. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female sterile; homozygous females contain few developing egg chambers in their ovaries, which may contain abnormal numbers of nurse cells and usually degenerate before yolk uptake begins. Rarely a few very small and abnormal eggs are produced. alleles: shu1 and shu2 recovered as WQ and WM respectively. cytology: Placed in 59D8-60A2, since uncovered by both Df(2R)bw-S46 = Df(2R)59D8-11;60A7 and Df(2R)bw-D23 = Df(2R)59D4-5;60A1-2. # Shu: Shudderer (J.C. Hall) location: 1-55.1. origin: Induced by ethyl methanesulfonate. discoverer: R.L. Williamson. references: Williamson, 1982, Psychopharmacology 76: 265-68. phenotype: Sudden leg jerks are frequent and enough to topple the fly; negative geotaxis is sluggish and seemingly not a consequence of shuddering bouts during climbing toward top of glass vials; neither of these behavioral abnormalities is pro- nounced in young adults, but they become maximal after about a week of adult life; lithium or ammonium ions placed in medium on which the mutant is grown reduce the severities of the eventual adult phenotypes. Homozygous females are not observed. # shut down: see shu # shv: see under dpp # shv: see svs # Shw: see Sh4 # shy: shy (T. Schupbach) location: 2-62. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal effect lethal. Embryos from homozygous mothers develop into larvae with no visible cuticular abnor- malities, but which do not hatch out of the egg case. alleles: shyRU = shy1. #*Si: Ski location: 2-36. discoverer: Clausen, 15l1. references: Clausen and Collins, 1922, Genetics 7: 385-426. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 149 (fig.). phenotype: Homozygous or heterozygous Si combined with homozy- gous si-3 produces wings with turned up tips. Double homozy- gote also has a crimped costal vein. Other genotypes wild type. RK3. #*si-3: ski-3 location: 3-46.5. discoverer: Clausen, 15l1. references: Clausen and Collins, 1922, Genetics 7: 385-426. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 149. phenotype: si-3/si-3 fly has upturned wing tips when homozygous or heterozygous for Si, otherwise normal. RK3. # sic: sichel location: 3-48.8. references: Mayer and Nusslein-Volhard, 1988, Genes Dev. 2: 1496-1511 (fig.). Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal effect lethal; embryos produced by homozy- gous mothers show narrow dentical bands and head skeleton with fused ventral arms. Embryos may also be normal and hatch or die early with irregular cell cleavage patterns. Distribution of syncytial blastoderm nuclei normal in some embryos and irregular in others. Germ line dependent but may also have a somatic component. Mutant expression autonomous in mutant pole cells transplanted into wild type recipients. Embryonic phenotypes of progeny of sic/sic and sic/Df(3R)by10 are simi- lar indicating null alleles. alleles: Four ethyl methanesulfonate-induced alleles; all cold sensitive: sic1 (weak allele), sic2, sic3, and sic4 (origi- nally designated 215, 256, 371, and 612). cytology: Placed in 85D8-12 based on its inclusion in the region of overlap of the synthetic deficiency for 84F2-85E in In(3R)ScrMscLAntpBR and Df(3R)by10 = Df(3R)85D8-12;85E7-F1. # side wings: see siw # sie: sieve (T. Schupbach) location: 2-68. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal. Embryos from homozygous females show variable defects and irregularities at cellulari- zation; at final differentiation embryos form only fragmented pieces of cuticle. alleles: sie1, sie2, and sie3 recovered as HA, RF, and IIIE respectively. cytology: Placed in 49E7-50A3, since uncovered by Df(2R)vgB = Df(2R)49D3-4;49F15-50A3, but not by Df(2R)vgC = Df(2R)49B2- 3;49E7-F1. other information: sie3 has a semi-dominant effect, causing 60-80% embryonic lethality when mother heterozygous. #*Sil: Skilike location: 2- (not located). discoverer: Goldschmidt. references: 1947, J. Exptl. Zool. 104: 216. phenotype: Wings turned up at tips. Semidominant. Poor via- bility. RK3. other information: Not an allele of Si. # silver: see svr # silver tips: see stp # sim: single minded location: 3-52.2 (just distal to pic). synonym: l(3)S8; schm; l(3)87Ea. references: Hilliker, Clark, Gelbart, and Chovnick, l981, DIS 56: 65-72. Thomas, Crews, and Goodman, 1988, Cell 52: 133-41 (Fig.). Crews, Thomas, and Goodman, 1988, Cell 52: 143-51 (Fig.). Mayer and Nusslein-Volhard, 1988, Genes Dev. 2: 1496-1511 (Fig.). phenotype: Embryonic lethal. Denticle bands of all segments narrow. Both head skeleton ventral arms and anal plates fused. In the ventral nervous system, transverse commissures lacking entirely. Midline neurons and supportive mesectoder- mal cells missing. Germline viable with no maternal com- ponent. Deficiency test indicates that sim1 is amorphic. In normal genotypes, transcript first noted at cellular blasto- derm in a pair of longitudinal rows of cells at the interface between the presumptive mesoderm and the neurogenic ectoderm. At the end of gastrulation, the mesoderm has invaginated into the ventral furrow and the two rows of expressing cells have come together in the ventral midline and both transcript and protein expressed in a row of cells in the midline and in an annulus around the presumptive anterior midgut. By eleven hours of development, protein is found in the cell types miss- ing in the midline of the central nervous system of mutant embryos, more in mesectodermal cells than neuronal elements, and in a subset of cells of the foregut. Antibody staining confined to nuclei. alleles: allele origin discoverer synonym ref ( __________________________________________________________ sim1 X ray Schalet l(3)S8 3 sim2 EMS Hilliker, Clark l(3)H9 1, 2 sim3 EMS Hilliker, Clark l(3)H66 1, 2 sim4 EMS Hilliker, Clark l(3)H79 1, 2 sim5 EMS Hilliker, Clark l(3)B13-4 1, 2 sim6 EMS Hilliker, Clark l(3)B21-2 1, 2 sim7 EMS Hilliker, Clark l(3)B30-1 1, 2 sim8 EMS Nusslein-Volhard E320 sim9 EMS Nusslein-Volhard RD ( 1 = Hilliker, Clark, and Chovnick, l980, Genetics 95: 95- 110; 2 = Hilliker, Clark, Gelbart, and Chovnick, l981, DIS 56: 65-72; 3 = Schalet, Kernaghan, and Chovnick, l964, Genetics 50: 1261-68. cytology: Placed in 87E1 based on its being between Df(3R)ry75 = Df(3R)87D1-2;87D14-E1 and Df(3R)l26c = Df(3R)87D14-E1;87E3- 5. molecular biology: The 3' end of the gene has been cloned, a cDNA containing the 3' end sequence, and the conceptual sequence of 655 C-terminal amino acids determined. The only identity encountered in protein-sequence data bases is to the Drosophila per gene; a 239-amino-acid sequence exhibits 23% identity and contains two 51-amino-acid repeats separated by 115 amino acids in sim and 99 amino acids in per. The sequence contains no transmembrane, homeobox, or zinc-finger motifs. A transcript of 3.0 kb is present from 0-3 hr post fertilization, increases in 3-6 hr and then disappears; a 3.5 kb transcript appears strongly from 3-6 hr, declining over the next six hours, and then persisting at low levels throughout embryogenesis. # sina: seven in absentia (R. Carthew) location: 3-45.5. origin: Induced with ethyl methanesulfonate. discoverer: Carthew, 1988. phenotype: Photoreceptor cell R7 of eye transformed into a cone cell, resulting in the absence of R7 in adult ommatidia. In amorphic alleles, 40% of ommatidia also missing an additional photoreceptor cell and 10% of ommatidia also missing two pho- toreceptor cells. Eyes weakly rough; ocelli appear normal. Adult bristles sometimes missing and sometimes duplicated, arising from a common socket; occasionally three bristles arise from a common socket. Wings sometimes held outstretched. Adults eclose normally but fail to survive after 24 h; display lethargic behavior and are not fertile, though mature sperm and ova are produced. alleles: Six, designated sina1 through sina6. sina1, sina4, sina5, and sina6 hypomorphic; sina2 and sina3 amorphic based on the phenotypes of hemizygous [sina/Df(3L)st-g18] versus that of homozygous flies. cytology: Located in 73D1-7 by deficiency mapping. # sine oculis: see so # singed: see sn # singed wing: see l(1)nfw # single minded: see sim # sis-a: sisterless a (T.W. Cline) location: 1-34.3 (based on 4496 v-m recombinants). origin: Induced by ethyl methanesulfonate. references: Cline, 1986, Genetics 113: 641-63, corregendum 114: 345. Cline, 1988, Genetics 119: 829-62. phenotype: Homozygous females die but hemizygous males and heterozygous females fully viable; females die as embryos and larvae; rare morphologically normal and fertile escapers observed at lower temperatures. Single extant allele hypo- morphic; locus also defined by dominant behavior of deficien- cies and duplications. Dominant lethal for females simultane- ously heterozygous for sis-b- or Sxl- or whose mothers are heterozygous for da-. Magnitude of female-lethal dominant synergism sensitive to genetic background, but can be very high. Lethal interactions are generally less severe at lower culture temperatures. Constitutive allele, SxlM1, suppresses female lethality of sis-a homozygote or of any heterozygous combination of mutant alleles or deficiencies of these four genes. Duplication of Sxl+ also suppresses, but less effec- tively. Female-lethal interactions between sis-a and Sxl mutations display remarkably similar Sxl allele specificity to those between maternal da and zygotic Sxl mutations, indicat- ing that da and sis-a disrupt the same aspect of Sxl regula- tion. Oogenesis normal for homozygous sis-a germ-line clones induced by mitotic recombination; no maternal effect. Sexual phenotype of 2X:3A animals extremely sensitive to sis-a+ dose (more male at lower temperatures), and like da and Sxl-, shows masculinizing interaction with autosomal male-specific lethal mutations but no increase in viability of escapers; neverthe- less, sexual phenotype of homozygous sis-a clones generated by mitotic recombination normal. Female-lethal effects caused by decrease in sis-a function have their complement in male- lethal interactions caused by increase in sis-a function (duplications). Male lethality is increased as Sxl+ dose or sis-b+ dose is increased, and is suppressed by loss-of- function Sxl mutations. The dose-dependent interactions of this gene with Sxl+ identify it as part of the numerator of what has been called the X/A balance, the primary sex- determination signal--a character it shares with sis-b. cytology: Placed in extreme distal position in 10B4-9 based on its failure to complement Df(1)N71 = Df(1)10B4-5;10D4 and its genetic position distal to l(1)10Bb and within <0.004 cM of l(1)10Ba. # sis-b: see under Asc #*siw: side wings location: 1-58.5. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1955. references: 1958, DIS 32: 74. phenotype: Wings rotated on long axis so that inner margin is higher than costal margin. Male sterile; viability about 50% wild type. jK2.