# se: sepia location: 3-26.0. phenotype: Eye color brown at eclosion, darkening to sepia, and becoming black with age. Thought to be the structural gene for the enzyme PDA synthetase which catalyzes the conversion of 6-pyruvoyltetrahydropterin to 2-amino-4-oxo-6-acetyl-7,8- dihydro-3H,9H-pyrimido [4, 5, 6]-[1, 4] diazepine (=PDA), which is a precursor of the red drosopterin pigments. The enzyme has been partially purified and has a molecular weight of 48,000 daltons (Wiederrecht and Brown, 1984, J. Biol. Chem. 259: 14121-27). Pigment of ocelli normal. Chromatographi- cally, se eyes characterized by having no red pigment [e.g. drosopterin and isodrosopterin (McKay, 1972, DIS 48: 62)] and an accumulation of yellow pigment (Hadorn and Mitchell, 1951, Proc. Nat. Acad. Sci. USA 37: 650-65; Ziegler-Gunder and Hadorn, 1958, Z. Vererbungsl. 89: 235-45). Three yellow pig- ments identified are 6- derivatives of 2-amino-4-hydroxy-7,8- dihydropteridine; the most abundant is sepiapterin, the 6- lactyl derivative; minor species are isosepiapterin (Viscon- tini and Mohlmann, 1959, Helv. Chim. Acta 42: 836-41; Forrest, VanBaalen, and Myers, 1959, Arch. Biochem. Biophys. 83: 508-20) and neosepiapterin (Takikawa, 1973, DIS 50: 158; Sugiura, Takikawa, Tsusue, and Goto, 1973, Bull. Chem. Soc. Jpn. 46: 3312-13), which are the 6-proprionyl and 6-acetyl derivatives respectively; the latter compound shown to be D- erythro-neopterin by Katoh and Arai (1974, DIS 51: 70). Other pteridines present in greater-than-normal amounts [e.g. isoxanthopterin II, xanthopterin I, and biopterin (McKay)]. Eye color autonomous in se eye disks transplanted into wild- type hosts (Beadle and Ephrussi, 1936, Genetics 21: 230). pn se flies have 10% amount of sepiapterin of se alone (Lifschytz and Falk, 1969, Genet. Res. 14: 53-61); dor se displays reduced viability (Lucchesi, 1968, Genetics 59: 37-44). RK1. alleles: allele origin discoverer ref ( comments __________________________________________________________________ se1 spont E. M. Wallace, 13e10 3 se51j spont Hungerford, 51j 10 *se51k spont Clark, 51k 5 *se58 spont Andrew, 58k 1 se61 spont Clancy, 61c 4 se72 spont Anxolabehre, 72l 2 se79 spont Najera, 79i 7, 8 se80i spont Najera, 80i 9 se81 spont Najera, 81d 7 *sev X ray 6 T(Y;3) variegated ( 1 = Andrew, 1959, DIS 33: 82; 2 = Anxolabehre and Periquet, 1973, DIS 50: 21; 3 = Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 86 (fig); 4 = Clancy, 1964, DIS 39: 65; 5 = Clark, 1952, DIS 26: 60; 6 = Jeffery, Stephans, and Giddings, 1974, Genetics 77: s32; 7 = Najera, 1984, DIS 60: 241; 8 = Najera, 1985, DIS 61: 215; 9 = Najera, 1986, DIS 63: 167; 10 = Redfield, 1952, DIS 26: 68. # se-like 62: see pn2 # sed: see Hnr3 # Segregation distorter: see Sd # seg: short egg location: 1- (proximal to B). synonym: l(1)SE. references: Wieschaus, 1978, Symp. Soc. Dev. Biol. 36: 23-43. phenotype: Eggs of homozygous females 20% shorter and 10% wider than normal; volume and density of blastoderm nuclei unchanged. Defect in somatic tissue inferred from normal phenotype of germ-line clones (Wieschaus). # sei: seizure (J.C. Hall) location: 2-106 [Ganetzky; probably a short distance (<1 m.u.) distal to this, as inferred from cytology]. origin: Induced by ethyl methanesulfonate. discoverers: Wu and Ganetzky. references: Jackson, Wilson, Strichartz, and Hall, 1984, Nature 308: 189-91. Jackson, Gitschier, Strichartz, and Hall, 1985, J. Neurosci. 5: 1144-51. Kasbekar, Nelson, and Hall, 1987, Genetics 116: 423-31. phenotype: Paralyzed fairly rapidly at temperatures above 38; adults seem to have a fit before becoming immobile, as opposed to immediately ceasing their movements; increasing times of exposure to high temperature leads to progressively longer times necessary for recovery when temperature is lowered (Jackson et al., 1985); sei1 is recessive for heat-sensitive paralysis (Jackson et al., 1985); sei2 is semi-dominant in this respect, and behavior of hyperploid adults exhibits dose dependence: sei2/sei2/+ flies become paralyzed, at 40, slightly less rapidly than homozygous mutants; sei2/+/+ paralyzed more slowly than sei2/+ but faster than wild-type (Jackson et al., 1985); biochemically, head membrane extracts from sei2 adults exhibit anomalously high Kd of saxitoxin (STX) binding activity, and a different pH dependence of this activity from wild-type; these abnormalities observed when the incubations done at high, but not low, temperatures (Jackson et al., 1984); in flies carrying three sei alleles, apparent reductions in the amounts of STX bound are observed, which are proportional to the relative number of mutant alleles (Jackson et al., 1985); when these kinds of biochemical experiments are performed on head extracts from sei1, Kd values are not appre- ciably different from wild-type at all assay temperatures, but the concentrations of STX binding activity are lower than wild-type under the influence of this allele, with such reduc- tions being more marked at higher assay temperatures; recovery times, after exposure to high temperature and subsequent return to mild conditions, are shortened when sei2 is combined with napts (Jackson et al., 1985). Recordings of action potentials in the adult giant-fiber pathway reveal no decre- ment in sei2 at 40 (Nelson and Baird, 1985, Neurosci. Abstr. 11: 313); at temperatures >40, sei2 causes spontaneous activity in recordings from dorsal longitudinal flight mus- cles, to appear coincidentally with the heat-induced paralysis (Kasbekar et al., 1989); from "tight-seal whole-cell" record- ings, using cultured neurons from sei1 embryos, this mutation found to cause sodium current density to be about half-normal; yet, voltage dependence and channel-gating properties were not different from wild type (O'Dowd and Aldrich, 1988); for other aspects of sei-associated defects in physiology, see enhancer of seizure. alleles: Two temperature sensitive alleles; sei1 and sei2. Some new ones recently isolated (Deak and Hall, 1989, Neu- rosci. Abstr. 15: 196), but not specified as to how many, the mutagenizing agent, or the allele names; certain of these, however, were found to be small deletions of the locus, which were used to generate apparently viable overlapping, Df/Df genotypes; these adults are paralyzed at 38, suggesting that the null phenotype is temperature-sensitive paralytic (Deak and Hall, 1989). cytology: Placed in 60A7-B10 based on its position between Df(2R)bw-S46 = Df(2R)59D8-11;60A7 and Df(2R)Px = Df(2R)60B8- 10;60D1-2 (Jackson et al., 1986; L.M. Hall, unpublished). other information: Though some of the data mentioned above sug- gest sei might code for a voltage-sensitve sodium-channel com- ponent, this gene could not be co-localized with a known sodium-channel-encoding factor in 2R, which on the basis of clone and sequence plus in situ hybridization, maps within 60D-E (Salkoff, Butler, Wei, Scavarda, Griffen, Ifune, Good- man, and Mandel, 1987, Science 237: 744-749); see NaCP. #*semi-f: semiforked location: 3- (not located). origin: Spontaneous. discoverer: Lancefield, 18b. references: 1918, Am. Naturalist 52: 462-64. phenotype: Homozygotes that are also heterozygous for f have slightly forked bristles. RK3. # sens(3)str: sensitivity (3) streptomycin location: 3-. origin: Spontaneous. synonym: strs. references: Duke and Glassman, 1968, Nature (London) 220: 588-89. phenotype: Homozygous larvae, but not adults, show 96% lethal- ity when cultured on media containing 1% streptomycin, a con- centration tolerated by wild type. Development of homozygotes arrested in early larval stages. # sep: separated location: 3- (rearrangement). discoverer: Muller. phenotype: Most of posterior crossvein absent, one-third usu- ally remaining attached to vein L5. RK2A. cytology: Associated with In(3LR)sep = In(3LR)65D2-3;85F2-4 (Craymer, 1981, Genetics 99: 75-97). # sepia: see se # sepiaoid: see Hnr3 # sepiapterin synthetase: see pr # Ser: see BdS # Ser1: Serine protease 1 location: 3-{101}. references: Yun and Davis, 1989, Mol. Cell. Biol. 9: 692-700. phenotype: Expressed abundantly in larval gut. Mutants dncM11 and dncM14 show lower levels of Ser1 RNA than normal flies; levels of cAMP, however, are elevated in the mutants. The Ser1-related genes Ser2 and Ser3 (with same location and cytology) are not expressed differentially in dnc mutants. cytology: Located in 99C-D by in situ hybridization to salivaries. molecular biology: Ser1, Ser2, and Ser3 cloned and their nucleotide and putative amino acid sequences determined (Yun and Davis, 1989); amino acid sequences homologous to serine protease enzyme family. # Serendipity: see Sry # Serendipity cognate: see Sryc # Serine protease 1: see Ser1 # serpent: see srp # Serrate: see BdS # sesA: stress-sensitive: A (J.C. Hall) location: 1-23.3 (Homyk). origin: Induced by ethyl methanesulfonate. discoverer: Homyk. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. phenotype: Paralyzed briefly by mechanical shock, effected by banging a container of the flies (this barely, or not at all, stuns wild-type flies); mutant's paralysis is accompanied by wing beating and followed by erratic movements; when stimu- lated to jump and fly, does so abnormally for short distances. Lethal when raised at 29. # sesB (J.C. Hall) location: 1-32.4 (Homyk). origin: Induced by ethyl methanesulfonate. discoverer: Homyk. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. phenotype: sesB1 causes adults to be extremely sensitive to mechanical shock (Homyk and Sheppard, 1977); paralysis lasts many seconds, and recovery is slow; the mutant is also gen- erally inactive and uncoordinated; when stimulated to jump and fly, does so abnormally for short distances; when reared at 29, after being raised at 22, sesB2 is not only stress- sensitive, but it also becomes debilitated after several bouts of induced to hopping and flying; in addition, sesB2 is heat sensitive for female sterility (after rearing at low tempera- ture). alleles: Lack of complementation of lethal alleles and sesB alleles reported by Zhimulev, Pokholkova, Bgatov, Umbetova, Solovjeva, Khudyakov, and Belyaeva (1987, Biol. Zentralbl. 106: 699-720). Janca, Woloshyn, and Nash (1986, Genetics 112: 43-64) report lack of full complementation between sesB3 and l(1)9Ed alleles. allele origin discoverer synonym ref ( comments ___________________________________________________________________ sesB1 EMS Homyk 1,2 viable allele sesB2 EMS Homyk 1,2 viable allele sesB3 X ray Schalet l(1)S12 3 lethal allele sesB4 X ray Lefevre l(1)HF380 4 lethal allele; In(1)9E-F;20A4-5 sesB5 EMS Lefevre l(1)EA79 5 lethal allele ( 1 = Homyk and Sheppard, 1977, Genetics 87: 95-104; 2 = Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65; 3 = Lefevre, 1971, Genetics 67: 497-513; 4 = Lefevre, 1981, Genetics 99: 461-80; 5 = Lefevre and Wat- kins, 1986, Genetics 113: 869-95. cytology: Placed in 9E7-F4 based on its inclusion in the region of overlap between Df(1)ras-P14 = Df(1)9E1-2;9F3-4 and Df(1)v64f = Df(1)9E7-8;10A1-2 (Zhimulev et al.). # sesC: see stn # sesD (J.C. Hall) location: 1-23.8 (Homyk and Pye, 1989). origin: Induced by ethyl methanesulfonate. references: Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65; Homyk and Pye, 1989, J. Neurogenet. 5: 37-48. phenotype: Paralyzed by mechanical shock; one allele (sesD2) causes constitutive inactivity, poor jumping and flying abil- ity, abnormal landing responses, and feeble male courtship (Homyk et al., 1980); this allele also leads to longer stress-induced paralysis than does sesD1; the latter is a heat-sensitive developmental lethal. In addition, sesD1 is reversibly temperature sensitive for the following visual phenotype, shown by electroretinogram recordings (Homyk and Pye, 1989): at temperatures <30, orange-light-elicited recovery from blue-induced prolonged depolarizing after poten- tial (PDA) is slow, and orange responses induced after recovery are aberrantly low-amplitude; at higher temperatures, orange-induced recovery from PDA involves incomplete repolari- zation, so that potential levels off below baseline extant before exposure to blue light; this persists even after con- tinued orange stimulation or in the dark; under these condi- tions, orange light also leads to light-on and light-off ERG transient spikes with anomalously low amplitudes; these heat- induced effects are quickly reversible (to normal ERG/PDA- associated potentials) when temperature lowered to 25. alleles: Two alleles, sesD1 and sesD2. cytology: Maps within 7D13-14, based on assessment of ERG abnormalities of heterozygotes between sesD1 and Df(1)HA11 = Df(1)7D13-14;7D22, which uncovers the defects and Df(1)/a2 = Df(1)7D14;8A3, which does not (Homyk and Pye, 1989). other information: Complements adult-lethal-1, which maps nearby; rapid exhaustion does, too, but it maps to 7C1-3 (Homyk and Pye, 1989); mosaic analysis suggests stress-induced paralysis of legs associated with sesD maps to separate foci, since the individual appendages can be paralyzed independently in such gynandromorphs (Homyk, unpublished); sesD1's develop- mental temperature-sensitive lethality originally said (Homyk et al., 1980) to be caused by separate mutation on the X chro- mosome, but turned out not to be the case (Homyk, unpub- lished). # sesE (J.C. Hall) location: 1-29.8 (Homyk). origin: Induced by ethyl methanesulfonate. discoverer: Homyk. references: Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. Homyk, Sinclair, Wong, and Grigliatti, 1986, Genetics 113: 367-89. phenotype: Severely paralyzed by mechanical shock and also con- stitutively inactive; adults become hyperactive under crowded conditions (Homyk et al., 1980). A heat-sensitive developmen- tal lethal, with two temperature-sensitive periods, one pri- marily during second larval instar and another ranging from late third instar to early pupation (Homyk et al., 1986); also an adult lethal, such that about half the flies are dead after five days exposure to 29 (Homyk et al., 1986). From analysis of high-temperature-induced adult death and leg paralysis in mosaics, the foci of the former concluded to be diffuse, "dom- ineering," and near posterior region of ventral blastoderm; regarding the behavioral phenotype, individual legs observed to be paralyzed, or not, in these gynandromorphs, and from these data it was also inferred that the paralysis foci are rather near that for lethality. # sesF (J.C. Hall) location: 1-49.6 (Homyk). origin: Induced by ethyl methanesulfonate. discoverer: Homyk. references: Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. phenotype: Adults have small bristles and are heat-sensitive for death during development; temperature-sensitive period for lethality includes at least larval stages (Homyk); when cul- tures shifted to 29 after pupariation, adults eclose but are very uncoordinated (Homyk); the originally stress-sensitive character seems to have vanished from the strain, though jump- ing ability of adults may still be impaired. cytology: Placed in 12E1-13A5, on the basis of its inclusion in Df(1)KA9 = Df(1)12E1;13A5 (Homyk, unpublished). other information: Complements nearby sesG and sesH mutations. # sesG (J.C. Hall) location: 1-50.8 (Homyk). origin: Induced by ethyl methanesulfonate. discoverer: Homyk. references: Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. phenotype: Flies become hyperactive when mechanically shocked, especially in crowded conditions; when in uncrowded con- tainers, the adults tend to be inactive after coming to rest from flight. other information: Complements the nearby sesF and sesH muta- tions. # sesH (J.C. Hall) location: 1-51.7 (Homyk). origin: Induced by ethyl methanesulfonate. discoverer: Homyk. references: Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. phenotype: Briefly paralyzed after mechanical shock; during tethered flight, wing beating anomalously stops and starts again spontaneously; adults become hyperactive during various kinds of behavioral testings (e.g., assessments of flying, climbing, running abilities; ability to hop when wings removed; landing responses; male tracking of, and vibration at, females). other information: Complements the nearby sesF and sesG muta- tions. # sev: sevenless location: 1-33.38. references: Harris, Stark, and Walker, 1976, J. Physiol. 256: 127-62. Tomlinson and Ready, 1986, Science 231: 400-02. Banerjee, Renfranz, Hinton, Rabin, and Benzer, 1987a, Cell 51: 151-58. Banerjee, Renfranz, Pollock, and Benzer, 1987b, Cell 49: 281-91. Hafen, Basler, Edstrom, and Rubin, 1987, Science 236: 55-63. Tomlinson, Bowtell, Hafen, and Rubin, 1987, Cell 51: 143-50. Tomlinson and Ready, 1987, Dev. Biol. 123: 264-75. Basler and Hafen, 1988, Cell 54: 299-311. Bowtell and Rubin, 1988, Genes Dev. 2: 620-34. Tomlinson, Kimmel, and Rubin, 1988, Cell 55: 771-84. Bowtell, Simon, and Rubin, 1989, Cell 56: 931-36. Bowtell, Kimmel, Simon, and Rubin, 1989, Proc. Nat. Acad. Sci. USA 86: 6245-49. Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29. Rubin, 1989, Cell 57: 519-20. phenotype: Homozygotes and hemizygotes lack the R7 rhabdomere in all ommatidia; the R7 photoreceptor cell instead develops as an accessory lens-secreting cell, the equatorial cone cell (Tomlinson and Ready, 1986, 1987). Cell autonomous in mosaics (Harris et al.). Mosaic analysis demonstrates that sev+ pro- duct is required only in the presumptive photoreceptor 7 cell and is therefore involved in receiving signals from neighbor- ing cells. Electroretinograms normal; defective in response to ultraviolet; in T-maze tests sev flies prefer visible to ultraviolet wavelengths and green light to darkness; slight preference for blue wavelengths over ultraviolet used in selecting mutant alleles (Gerresheim, 1988, Behav. Genet. 18: 227-46). In the presence of Phb the preference of green light to darkness is reversed for sev1 and sev10 but not for six other unspecified alleles; the absence of R7 is unaffected by Phb (Ballinger and Benzer, 1988, Proc. Nat. Acad. Sci. 85: 3960-64). Gene expression demonstrated by in situ hybridization and immune staining to take place in developing eye imaginal disc, near and posterior to the morphogenetic furrow, during ommatidial differentiation. Protein present transiently in at least nine cells in each developing omma- tidium and is detectable before any overt differentiation of R7 observed (Tomlinson et al., 1987; Banerjee et al., 1987a). Transient expression of sev+ by means of a transformed con- struct under control of the Hsp70 promoter in a sev background results in a narrow stripe of ommatidia that contain photore- ceptor cell 7 in eyes that are otherwise sevenless; the posi- tion and time of expression required for normal function are highly restricted (Bowtell, Simon, and Rubin, 1989, Cell 56: 931-36). alleles: allele origin discoverer synonym ref ( comments _________________________________________________________________ sev1 EMS Harris sevLy3 3 sev2 EMS sevdr1 1 sev3 EMS sevE1 1 sev4 EMS sevE2 1 sev5 EMS sevE3 1 sev6 EMS sevE4 1 sev7 EMS sevE5 1 sev8 EMS Ready sevelm 1 sev9 EMS Ready sevfig 1 sev10 EMS Ready 1 sev11 EMS Gerresheim, 1988 seva27 2 sev12 EMS Gerresheim, 1988 seva32 2 4.3kb insertion sev13 EMS Gerresheim, 1988 sevb8 2 sev14 EMS Gerresheim, 1988 sevd2 2 sev15 EMS Gerresheim, 1988 sevf1 2 sev16 EMS Gerresheim, 1988 sevf3 2 sev17 EMS Gerresheim, 1988 sevi3 2 sev18 P sevP1 1 53kb deletion; female sterile sev19 P sevP2 1 sev20 P sevP3 1 11kb deletion ( 1 = Banerjee, Renfranz, Pollock, and Benzer, 1987, Cell 49: 281-91; 2 = Gerresheim, 1988, Behav. Genet. 18: 227- 46; 3 = Harris, Stark, and Walker, 1976, J. Physiol. 256: 127-62. cytology: Placed in the right edge of the 10A1-2 doublet on the basis of its inclusion in Df(1)ras-vCc8 = Df(1)9D1-2;10A2-3 but not Df(1)sbr-K8 = Df(1)9B1-2;10A1-2 or Df(1)v64f = Df(1)9E7-8;10A1-2 (Zhimulev, Semeshin, and Belyaeva, 1981, Chromosoma 82: 9-23). molecular biology: Locus cloned by transposon tagging (Banerjee et al., 1987b) and by microdissection followed by chromosome walking (Hafen et al., 1987). cDNA sequencing (Hafen et al., 1987; Basler and Hafen, 1988) reveals a gene with twelve exons, the first four of which are separated by long introns; exons 4-7 are short and separated by short introns; exon 8 contains the majority of the gene; exons 9-12 are again short and separated from exon 8 and from each other by short introns. The conceptual amino-acid sequence indicates a pro- tein of 2554 amino acids of calculated molecular weight 290 kd. Two putative membrane-spanning domains indicated-22 and 24 amino acids, beginning with residues 102 and 2124, respectively. These hydrophobic domains flank closely two short hydrophilic stretches (Basler and Hafen, 1988). The 2000 residues between the membrane-spanning domains are the extracellular domain (Bowtell, Simon, and Rubin, 1988). Tran- scription from right to left; produces an 8.2 kb mRNA, which is found in isolated third-instar imaginal eye discs, but not in wing discs or pre-third-instar discs, at low levels in adult heads, but not bodies, and in 5-12 h, but not 22-30 h pupae. The carboxy-terminal cytoplasmic domain shows homology with the tyrosine kinase domains of such proteins as c-ras, v-src, and the EGF receptor (Hafen et al.). A single amino acid substitution in the ATP-binding site of the putative kinase inactivates the gene as determined in transformation experiments (Basler and Hafen). Expression of sev+-|- galactosidase fusion protein confined to the apical surface of developing retina; expression not restricted to R7 cell; expressed in presumptive photoreceptor cells, cone cells, and possibly others. Protein localizes to all membrane of the apical tips and their microvilli, away from the bulk of the cell-cell contacts (Banerjee et al., 1987a). 967 nucleotides of 5' promoter region capable of conferring the correct pat- tern but not level of sev expression on a lacZ reporter gene in some transformants. Enhancer sequences in the genomic seg- ment comprising exons 2-7 able to confer both correct pattern and level of sevenless expression on either sev or heterolo- gous promoters (Bowtell, Kimmel, Simon, and Rubin, 1989, Proc. Nat. Acad. Sci. USA 86: 6245-49). sev minigenes lacking introns expressed at low levels but in correct pattern (Bow- tell et al., 1988). # seven up: see svp # seven-in-absentia: see sina # sex comb distal: see scd # Sex combs extra: see Sce # Sex combs on midleg: see Scm # Sex combs reduced: see Scr under ANTC # Sex lethal: see Sxl # sexcombless: see sx # sey: scratched eyes location: 3-17.0 (to the left of Me). origin: Spontaneous. discoverer: Grell. phenotype: At 25 homozygotes have patches of eroded and black- ened eye tissue; phenotype normal at 18. # sf: safranin location: 2-71.5. phenotype: Eye color soft dark brown. More easily classified in male and in aged fly. Eye color autonomous in larval optic disks transplanted into wild-type host (Beadle and Ephrussi, 1936, Genetics 21: 230). Larval Malpighian tubes of sf1 pale yellow; classifiable (Brehme and Demerec, 1942, Growth 6: 351-56); those of sf2 bright yellow like wild type (Bea- dle, 1937, Genetics 22: 587-611). RK2. alleles: allele origin discoverer synonym ref ( ___________________________________________________ sf1 spont Bridges 16a6 3 sf2 spont Spencer, 25k bronze 7, 8, 9 *sf3 spont Ives, 39c dark eye 1 *sf32e heat Ives, 32e28 2, 6 sf79 spont Najera 4 sf80d spont Najera 5 sf80i spont Najera 5 sf81 spont Najera 4 ( 1 = Curry, 1939, DIS 12: 45; 2 = Plough and Ives, 1934, DIS 1: 33; 3 = Morgan, Bridges, and Sturtevant, 1925, Bibliogr. Genet. 2: 235; 4 = Najera, 1985, DIS 61: 215; 5 = Najera, 1986, DIS 63: 167; 6 = Plough and Ives, 1935, Genetics 20: 42-69; 7 = Spencer, 1934, DIS 1: 35; 8 = Spencer, 1935, Am. Nat. 69: 223-38; 9 = Spencer, 1937, DIS 7: 21. #*sf-3: safranin in chromosome 3 location: 3- (not located). discoverer: Bridges, 15a15. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 126. phenotype: Eye color dull brown. RK3. #*sfc: stiff chaetae location: 1-3.2. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1955. references: 1958, DIS 32: 74. phenotype: Bristles short and stiff; occasionally one missing. Fertility and viability good. RK2. alleles: One allele induced by CB. 1592. #*sg: shortened wing location: 3- (left arm). origin: Spontaneous. discoverer: Herskowitz, 47l18. references: 1949, DIS 23: 57. phenotype: Wings abnormal at base; veins interrupted, missing, or thickened. Many flies have short, rounded wings that curve upward slightly. RK3. # SGA62: see iab7SGA under BXC #*sge: shifted genitals location: 1-48.4. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1958, DIS 32: 74. phenotype: Male gentialia and anal plates rotated to various degrees (up to 90). Wings slightly divergent and drooping, occasionally one outheld. Eyes slightly dark. Male sterile. Viability about 70% normal. RK2. # sgg: shaggy location: 1-1.32. synonym: l(1)zw3. references: Simpson, El Messal, Moscoso del Prado, and Ripoll, 1988, Development 103: 391-401. Ripoll, El Messal, Laran, and Simpson, 1988, Development 103: 757-67. Simpson and Carteret, 1989, Development 106: 57-66. Bourouis, Heitzler, El Messal, and Simpson, 1989, Nature 341: 442-44 (fig.). phenotype: Larval growth protracted, ceasing in the first [sgg2, sgg9], second [sgg5], or third [sgg3 and sgg10] larval instar; death follows. sgg10 may survive to puparium forma- tion. Mutant cuticle tissue survives only in tergites; lacks bristles and appears etched; some deformed mutant wing tissue also observed in sgg3. sgg3, but no other allele produces viable and fertile males in combination with Dp(1;4)wm65g (Shannon, Kaufman, Shen, and Judd, 1972, Genetics 72: 615- 38). sgg1 and sgg10 males exhibiting maternal-zygotic interaction with Dp(1;4)mg display deletion-mirror-image duplication homeotic transformation (eye-antenna, wing, and leg discs) (Robbins, 1983, Genetics 103: 633-48). Same noted in male tissue of gynandromorphs (Kaufman), sgg9, and sgg10 (Garcia-Bellido and Robbins, 1983, Genetics 103: 235-47). More recent studies with sgg32, an amorphic allele, (Bourouis et al.; Ripoll et al.; Simpson et al.; Simpson and Carteret) indicate that sgg is involved in the developmental choice between the epidermal pathway and that of the nervous system. In homozygous clones of sgg32 formed 48 h or more before puparium formation all trichomes are replaced by chaetae in the ratio of one chaeta to four trichomes reflecting the number of cells involved in the elaboration of each structure; chaetae formed conform to positional information and genotype; e.g., wing clones resemble dorsal or ventral costal bristles or triple or double row bristles depending on their position; clones are linear when near the margins and form clumps of chaetae when distant from the margins; adventitious veins often formed in association with wing clones. In the notum scutellar clones form macrochaetae in + but not sc genotypes and microchaetae in h but not + genotypes. Clones formed later than 48 h before puparium formation form trichomes, either more densely than normal (10-21 trichomes) or in normal density (up to 10 trichomes). sgg embryos from homozygous sgg female germ line cells exhibit delayed and disordered cellu- larization at blastoderm; gastrulation does not occur; no dif- ferentiation of ectoderm, mesoderm, or endoderm occurs; cell division continues and the embryo becomes filled with small round cells, most or all of which stain with neuronal-specific antibodies. sgg+ embryos from sgg female germinal tissue show nearly normal blastoderm formation and gastrulation; however they are short with complete cuticles and neural hyperplasia as seen in neurogenic mutants; a lawn of hairs is seen dor- sally, and ventrally most of the denticle belts are lacking. Two doses of sgg+ in such embryos lead to more nearly normal cuticular development, but with odd-numbered denticle bands appearing before even-numbered ones. sgg progeny of females that carry sgg+ in their germ lines die as defective larvae with underdeveloped central nervous systems; the degree of CNS development is positively correlated with the number of mater- nal doses of sgg+. alleles: allele origin discoverer synonym ref ( comments | _______________________________________________________________ sgg1 X ray Judd l(1)zw3b12 1, 2 In(1)b12,MZI sgg2 " Elequin l(1)zw3b24 2 sgg3 " Elequin l(1)zw3b25 2 sgg4 " Judd l(1)zw3d13 2 with l(1)3Ac14 sgg5 X ray+EI Alexander l(1)zw3g5 2 sgg6 EI Alexander l(1)zw3g13 2 sgg7 EMS Judd l(1)zw3h2 2 sgg8 X ray Judd l(1)zw3h15 2 sgg9 X ray Judd l(1)zw3h22 2 MZI sgg10 EI Alexander l(1)zw3k22 1, 2 MZI sgg11 EMS l(1)zw3e6 5 sgg12 EMS l(1)zw3e28 5 sgg13 EMS l(1)zw3e29 5 sgg14 EMS l(1)zw3e56 5 sgg15 EMS l(1)zw3e60 5 sgg16 MMS l(1)zw3m9 6 sgg17 MMS l(1)zw3m17 6 sgg18 MMS l(1)zw3m41 6 sgg19 MMS l(1)zw3m62 6 sgg20 MMS l(1)zw3m69 6 with l(1)3Ag65 sgg21 MMS l(1)zw3m72 6 sgg22 MMS l(1)zw3m80 6 sgg23 MMS l(1)zw3m98 6 sgg24 X ray Lefevre l(1)GE228 3 In(1)3B;20A sgg25 X ray Lefevre l(1)GE257 3 In(1)3B3;20F sgg26 X ray Lefevre l(1)HA41 3 sgg27 X ray Lefevre l(1)JA131 3 sgg28 X ray Lefevre l(1)KA22 3 sgg29 EMS Lefevre l(1)VE762 4 sgg30 EMS Lefevre l(1)VE805 4 sgg31 mei9 / Schalet l(1)zw3S1M sgg32 EMS Ripoll l(1)zw3sgg 1, 7, sggD127 8, 9 ( 1 = Bourouis, Heitzler, El Messal, and Simpson, 1989, Nature (London) 341: 442-44 (fig.); 2 = Judd, Shen, and Kaufman, 1972, Genetics 71: 139-56; 3 = Lefevre, 1981, Genetics 99: 461-80; 4 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 5 = Lim and Snyder, 1974, Genet. Res. 24: 1- 10; 6 = Liu and Lim, 1975, Genetics 79: 601-11; 7 = Ripoll, El Messal, Laran, and Simpson, 1988, Development 103: 757- 67; 8 = Simpson and Carteret, 1989, Development 106: 57-66; 9 = Simpson, El Messal, Moscoso del Prado, and Ripoll, 1988, Development 103: 391-401. | MZI = maternal-zygotic interaction; demonstrated in males carrying mutant allele from heterozygous mother and variegating allele on a paternally derived duplication (Rob- bins, 1983, Genetics 103: 663-48). / Spontaneous in the paternal X chromosome of a cross between wild-type males and mei9 females, such that the F1 females were sgg/mei9. cytology: Placed in 3B1 based on its inclusion in Df(1)64f1 = Df(1)3A9-B1;3B2-3 but not Df(1)62d18 = Df(1)3B1-2;3C6-7. molecular biology: Cloning and sequencing indicates gene pro- duct to be homologous to serine-threonine proteases (Sieg- fried, Perkins, Capaci, and Perrimon, 1990, Nature 345: 825- 29). # Sgs: Salivary gland secretion proteins A group of seven genes encoding proteins that are components of the secretion produced by the larval salivary glands during the third instar for the purpose of attaching the larva to the substrate preparative to pupariation. Initiation of tran- scription of these genes is coincident with the formation of the intermolt puffs in early to mid third instar (Korge, 1975, Proc. Nat. Acad. Sci. USA 72: 4550-54). The genes colocalize with the most prominent intermolt puffs. Synthesis of the glue proteins begins about 106 h after egg deposition and ceases abruptly within a few minutes after the glue is released 14 h later (Beckendorf and Kafatos, 1976, Cell 9: 365-73). Initiation of transcription, but not of intermolt-puff formation seems to depend on the presence of suitable levels of ecdysterone in early third instar larvae (Hansson and Lambertsson, 1983, Mol. Gen. Genet. 192: 395- 401). The subsequent cessation of transcription and puff regression also ecdysterone dependent (Crowley and Meyerowitz, 1984, Dev. Biol. 102: 110-21). Loci designated Sgs1 and Sgs3 through Sgs8 in order of increasing electrophoretic mobility, except that Sgs6 is out of order. # Sgs1 location: 2-13.9 (based on 64 dp-cl recombinants). references: Velissariou and Ashburner, 1980, Chromosoma 77: 13-27. phenotype: Structural gene for the most slowly migrating of the salivary-gland glue proteins, SGS1 (Zhimulev and Kolesnikov, 1975, Wilhelm Roux's Arch. Entwickslungmech. Org. 178: 15- 28). alleles: Nine electrophoretic variants designated Sgs1a through Sgs1i; no naturally occurring null alleles recorded. cytology: Placed in region 25A2-D2 based on increased product in salivary glands of larvae carrying the duplication produced by combining elements of T(Y;2;4)J96 = T(Y;2;4)25A2-3 and T(Y;2)D110 = T(Y;2)25D1-2. Associated with the intermolt puff in 25B3-7, which comes up coincidentally with the other glue- protein puffs. # Sgs3 location: 3-35.0 (based on 100 se-ri recombinants; Kokoza, Kazakova, Karakin, 1982, DIS 58: 94-95). references: Korge, 1975, Proc. Nat. Acad. Sci. USA 72: 4550- 54. Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215- 25. Meyerowitz and Hogness, 1982, Cell 28: 165-76. Garfinkle, Pruitt, and Meyerowitz, 1983, J. Mol. Biol. 168: 765-89. phenotype: The structural gene for glue protein, SGS3. Depen- dence of initiation and cessation of Sgs3 expression on ecdys- terone levels studied by Crowley and Meyerowitz (1984, Dev. Biol. 102: 110-21). Expression of Sgs3 as well as Sgs7 and Sgs8 does not take place in the presence of the nonpupariating lethal mutation, npr, which is a member of the Broad Complex, BRC; expression cannot be rescued by the administration of ecdysterone; npr does not inhibit formation of intermolt puff 67C, thus dissociating transcription from puff formation (Crowley, Mathers, and Meyerowitz, 1984, Cell 39: 149-56). alleles: Four electrophoretic variants designated Sgs3a through Sgs3d identified by Akam et al.. In addition the allele from the Formosa wild strain produces a smaller polypeptide than other alleles. cytology: Placed in 68C3-5 by in situ hybridization; associated with intermolt puff at 68C (Korge; Akam et al.). molecular biology: Sequence recovered as a third-instar- salivary-gland-specific cDNA (Wolfner, 1980, PhD thesis, Stan- ford University). Hybridizes to an mRNA 1120 nucleotides in length (in Oregon R; smaller in some other strains; e.g., For- mosa). Nucleotide sequence and conceptual amino acid sequence of translation product of cDNA clone determined by Garfinkle et al.; 6751 nucleotides of genomic DNA, containing the coding sequences of the cluster, Sgs3, Sgs7, and Sgs8, were sequenced; The sequence encoding Sgs3 extends from approxi- mately nucleotide 4457 to 5646, with an intervening sequence of 73 nucleotides from nucleotides 4514 to 4586, between the first and second nucleotides of codon 10. The conceptual amino-acid sequence comprises three domains; the first 23 amino acids are rich in hydrophobic residues and constitute a signal peptide which is removed from the mature polypeptide; the next 234 amino acids contain an amino terminal 49 amino acids of threonine-rich sequences followed by 185 amino acids that are composed entirely of 37 tandem repeats of minor vari- ants of a five amino acid unit (basic unit = Pro-Thr-Thr-Thr- Lys); twenty of these repeats are deleted in the Formosa wild-type allele (Mettling, Bourouis, and Richards, 1985, Mol. Gen. Genet. 201: 265-68); the carboxy-terminal fifty amino acids of SGS3 are similar to those found in SGS7 and SGS8. i.e., 19 identities including eight cysteines. The SGS3 polypeptide is heavily glycosylated (Beckendorf and Kafatos, 1976, Cell 9: 365-73), probably on the threonine residues (Garfinkle et.al.). Transformation experiments show that as little as 2.3 kb of 5' plus 1.1 kb of 3' sequence is suffi- cient for normal regulation of Sgs3 expression (Crosby and Meyerowitz, 1986, Dev. Biol. 118: 593-607); 980 base pairs of 5' sequence allow for appropriate stage and tissue specificity of expression, but the levels of expression are greatly reduced; 27 5' base pairs are insufficient for Sgs3 expres- sion (Bourouis and Richards, 1985, Cell 40: 349-57). Finally, functional Sgs7 Sgs8 Sgs3 inserts may form ectopic intermolt puffs, but they need not, thus separating puff for- mation from Sgs expression (Crosby and Meyerowitz). # Sgs4 location: 1-3.0 (based on 97 wa-rb recombinants; Kokoza, Kaza- kova, and Karakin, 1982, DIS 58: 94-95). references: Korge, 1977, Chromosoma 62: 155-74. phenotype: Encodes the salivary-gland glue protein, SGS4; this protein not required for viability, since non producers eclose normally; it varies in size owing to a variable number of copies of a heptapeptide repeat in an N-terminal tandem array. Expression of the virtually inactive allele, Sgs4H increased four fold in trans heterozygotes with the normally active allele, Sgs4OR, and nine fold with a tandem duplication [Dp(1;1)Co] containing two copies of a normally active allele; neither Sgs4H/Sgs4Ber nor Sgs4Ber/Sgs4OR exhibits enhanced activity; enhancement decreased by disruption in pairing, e.g., in Sgs4H/FM6 (Kornher and Brutlag, 1986, Cell 44: 879-83). alleles: So-called electrophoretic alleles, which are probably size variants, have been designated Sgs4a, Sgs4b, Sgs4c, and Sgs4d (see Korge, 1977); the correspondence between these designations and those tabulated below is not available. allele origin ref ( express- repeat 5' sequences ` ion (%) | number / ____________________________________________________________________ Sgs4Ber Berkeley 1, 2 0 22 -486 to -444 and -440 to -392 deleted Sgs4Ch Chieti 2 100 22 Sgs4CS Canton-S 1, 2 40 21 C->T at -344 Sgs4D232 Davis 1, 2 40 34 C->T at -344 Sgs4Dk Daekwan- 1 <1 9 single base-pair ryeong alterations Sgs4H Hikone 2 ~2 31 -356 to -305 deleted Sgs4K Kochi 2 ~2 101 Sgs4OR Oregon-R 2 100 19 Sgs4S Seto 2 ~2 28 -356 to -305 deleted Sgs4U Urbana 2 100 27 ( 1 = McGinnis, Shermoen, Heemskirk, and Beckendorf, 1983, Proc. Nat. Acad. Sci. USA 80: 1063-67; 2 = Muskavitch and Hogness, 1980, Cell 29: 1041-51. | mRNA level compared to Oregon-R. / The number of 21-base-pair repeats about 100 nucleotides downstream from the 5' end of coding sequence = seven- amino-acid tandem repeats near the amino-terminal end of polypeptide. ` Comparison of upstream sequences with those of Oregon R; nucleotide 1 is the first base transcribed, the first T of an EcoRI restriction site. cytology: Placed in 3C11-12 based on its inclusion in Df(1)N- 69h9 = Df(1)3C6;3D1 but not Df(1)N-54l9 = Df(1)3C5-6;3C10-11; activity associated with formation of intermolt puff in same bands (Korge, 1977, Chromosoma 62: 155-74). molecular biology: Sgs4 resides within the first intron of dnc (Chen, Malone, Beckendorf, and Davis, 1984, Nature 329: 721- 24). Transcription is from left to right. The entire Sgs4 region cloned and the gene and its flanking regions sequenced (Muskavitch and Hogness, 1980, Proc. Nat. Acad. Sci. USA 77: 7362-66; 1982, Cell 29: 1041-51); gene contains no introns and is characterized by a tandem array of 21-base-pair repeats occupying the 5' 45% of the sequence. The repeating unit appears to be (Arg or Thr)-Cys-(Glu, Lys, or Arg)- Thr- Glu-Pro-Pro. The number of repeats is uncorrelated with gene activity; rather regions some 300 to 500 base pairs upstream of the start of transcription are abnormal or deleted in alleles with little or no activity. Fifteen transpositions of Sgs4 with 2.6 kb of 5' and 1.3 kb of 3' sequences display nor- mal expression with respect to quantity, stage and tissue specificity, and dosage compensation but not puff formation (Krumm, Roth, and Korge, 1985, Proc. Nat. Acad. Sci. USA 82: 5055-59); reduction of the 5' flanking sequences to -840 but not to -392 retains normal regulation (McNabb and Becken- dorf, 1986, EMBO J. 5: 2331-40). # Sgs5 location: 3- {60}. references: Guild, 1984, Dev. Biol. 102: 462-70. Guild and Shore, 1984, J. Mol. Biol. 179: 289-314. Shore and Guild, 1986, J. Mol. Biol. 190: 149-58. Shore and Guild, 1987 Genes Dev. 1: 829-39. phenotype: The structural gene for the salivary-gland glue pro- tein, SGS5, a polypeptide of 163 amino-acid residues, 13% of which are serine and threonine. SGS5 lightly glycosylated (Beckendorf and Kafatos, 1976, Cell 9: 365-73). The first 18 amino acids are highly hydrophobic as expected for a signal peptide. cytology: Located in 90B3-8 by in situ hybridization; associ- ated with the intermolt puff at 90B (Wolfner.1980, PhD Thesis, Stanford University, Stanford, CA). alleles: One null allele, Sgs5n1, found in a strain designated C2 from Wallace. molecular biology: Genomic clone isolated; 1 kb including the Sgs5 transcription unit sequenced; extends from nucleotide -173 to +839, with the transcribed region beginning at +1 and ending at the site of poly(A) addition at +769. Upstream sequences resemble those of other Sgs genes; information necessary for Sgs5 expression contained within 109 base pairs upstream and 69 base pairs downstream of the transcribed region. Two introns, one extending from +302 to +357 and the other from +547 to +605; both introns interrupt a proline codon after the first nucleotide. Sgs5n1 differs from wild type in seven base-pair substitutions between nucleotides -84 and +75. # Sgs6 location: 3-42.0 (based on 42 h-th recombinants). references: Velissariou and Ashburner, 1981, Chromosoma 84: 173-85. phenotype: A component of the glue-protein mixture that is not present in all stocks. Electrophoretic mobility between that of SGS1 and SGS3, close to SGS3. cytology: Placed in 71C1-F5 based on dosage studies with seg- mental aneuploids involving T(Y;3)A60 = T(Y;3)71C1-2 and T(Y;3)B99 = T(Y;3)71F3-5. Associated with intermolt puff at 71C3-4, which is absent in flies lacking SGS6. # Sgs7 location: 3-35.0. references: Crowley, Bond, and Meyerowitz, 1983, Mol. Cell. Biol. 3: 623-34. phenotype: Encodes the 5481 kd salivary-gland glue protein, SGS7; the protein contains, in common with SGS3 and SGS8, a 23-residue amino-terminal signal peptide and a carboxy- terminal region of about 50 amino acids that shows consider- able homology with that of SGS3 and SGS8; it is not glycosylated. Expressed coordinately with Sgs3 and Sgs8. cytology: Placed in 68E3-5 by in situ hybridization. molecular biology: Cloned by Meyerowitz and Hogness (1982, Cell 28: 165-76); located approximately 2 kb distal to Sgs3 and 500 base pairs to the right of Sgs8; transcribed from left to right, as is Sgs3. Has a small intervening sequence between the first and second bases of the tenth codon; mRNA contains 320 nucleotides. Expression absent in su(f)ts67g (rescuable by administration of ecdysterone) (Hansson and Lambertsson, 1983, Mol. Gen. Genet. 192: 395-401) and in npr flies (not rescued by ecdysterone) (Crowley, Mathers, and Meyerowitz, 1984, Cell 39: 149-56). # Sgs8 location: 3-35.0. references: Crowley, Bond, and Meyerowitz, 1983, Mol. Cell. Biol. 3: 623-34. phenotype: Encodes the 5592 kd salivary-gland glue protein, SGS7; the protein contains, in common with SGS3 and SGS7, a 23-residue amino-terminal signal peptide and a carboxy- terminal region of about 50 amino acids that shows consider- able homology with that of SGS3 and SGS8; it is not glycosylated. Expressed coordinately with Sgs3 and Sgs7. cytology: Placed in 68E3-5 by in situ hybridization. molecular biology: Cloned by Meyerowitz and Hogness (1982, Cell 28: 165-76); located approximately 500 base pairs to the left of Sgs7; transcribed from right to left from the opposite strand transcribed by Sgs7. Has a small intervening sequence between the first and second bases of the tenth codon; mRNA contains 360 nucleotides. Expression absent in su(f)ts67g (rescuable by administration of ecdysterone) (Hansson and Lam- bertsson, 1983, Mol. Gen. Genet. 192: 395-401) and in npr flies (not rescued by ecdysterone) (Crowley, Mathers, and Mey- erowitz, 1984, Cell 39: 149-56). # Sgs9 location: 3-60.8 (based on eight bx-sr recombinants). synonym: GP5. references: Hoshizaki, Dlott, Joslyn, and Beckendorf, 1987, Genet. Res. 49: 111-19. phenotype: Controls the quantity of SGS9 (P5 of Beckendorf and Kafatos, 1976, Cell 9: 365-73), which migrates ahead of SGS5 in SDS polyacrylamide gel electrophoresis. Not demonstrated to encode SGS9. Protein levels inordinately sensitive to background genotype. alleles: A null allele exists in a stock labeled Stromsvreten 10; used in mapping experiments. cytology: Genetic mapping places it close to Sgs5 and the intermolt puff at 90 B-C.