# sk: stuck (J.C. Hall) location: 4-?. origin: Spontaneous. references: Beckman, 1970, DIS 45: 36. Hall, Siegel, Tompkins, and Kyriacou, 1980, Stadler Genet. Symp. 12: 43-82. phenotype: Males become stuck in females after copulation; ca. 50% of such matings exhibit this phenotype (data shown in Hall et al., 1980; Beckman, 1970, quoted 100% penetrance origi- nally, which had fallen to 78% by the time of her report); stuck males not infrequently are able to disengage eventually on their own; if so, appendages of their terminalia are held in aberrantly protruding positions (Hall et al., 1980); Beck- man mentions anatomical abnormality in the strain (near time of isolation): affected males showing narrowing of abdomen (not observable in current versions of stock and was never consistent enough to allow discrimination of affected indivi- duals from those who would behave normally); if mutant males are unable to withdraw after copulating, he and the female die within a few days (Beckman 1970, quotes 14% as mortality fre- quency for mated pairs); a stuck vs. non-stuck mating result is stochastic (as opposed to being a pure penetrance problem, as it were), given that (for example) re-testing a non-stuck case can readily lead to stuck outcome in a subsequent mating (Hall et al., 1980); mutant male-female pairs are more diffi- cult to separate (by vortexing) than are normal copulating pairs (Hall et al., 1980); females unaffected by the genetic variant(s). other information: Beckman (1970) reported that sk maps on chromosome 3; Hall et al. (1980) unable to confirm this, but their mapping to 4 was somewhat problematical, in that other factors in the strain seem necessary for full mutant phenotype to be realized. Sk: Streak From Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 216. # Sk: Streak location: 2-16.0. origin: Spontaneous. discoverer: Bridges, 12k27. references: Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 222 (fig.). phenotype: Dark streak extends down middle of thorax from neck to tip of scutellum. Wings may diverge and droop. Overlaps wild type. Enhanced by b or es. Homozygous lethal. RK2. cytology: Salivary chromosomes apparently normal (Bridges). # skd: skuld (J.A. Kennison) location: 3-51. origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1984. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Isolated as a dominant suppressor of Pc mutations. Associated with recessive lethality at the larval-pupal tran- sition. Also interacts with Pcl, Scr, and Ubx mutations. May weakly suppress AntpNs. alleles: skd1 induced by ethyl methanesulfonate and skd2 induced by gamma irradiation. cytology: Proximal to 87B15 on basis of exclusion from Df(3R)ry615 = Df(3R)87B12-15;87E8-11. # Ski: see Si # ski-3: see si-3 # Skilike: see Sil # skuld: see skd # sl: small wing location: 1-53.5. phenotype: Wings about 80% normal length, straight edged, and blunt tipped. Crossveins rather close. Eyes large and slightly rough. alleles: allele origin discoverer ref( comments _____________________________________________________________ sl1 spont Bridges, 15l21 sl2 X ray Dobzhansky, 31b3 2 sl3 X ray Lefevre 1 associated with Tp(1;2)r+75c *sl34 spont Gottschewski, 1934 eyes normal ( 1 = Schalet., 1986, Mutat. Res. 163: 115-44. 2 = Sivertzev-Dobzhansky and Dobzhansky, 1933, Genetics 18: 173-92. cytology: Placed in 14B13 based on probable association of sl3 with distal X break of Tp(1;2)r+75c =Tp(1;2)14B13;15A9;35D-E. sl2/Tp(1;2)r+75c and sl2/Dp(1;2)r+75c have small wings and rough eyes; sl2/Df(1)r75c has very rough eyes. sl2 has a nor- mal phenotype in combination with Dp(1;4)r+ = Dp(1;4)14A1- 2;16A1-2;102F2-3 (Schalet, 1986, Mutat. Res. 163: 115-44). #*Sl: Splotched location: 1-56.9 (to the right of f). origin: X ray induced. discoverer: Muller, 26l11. references: 1935, DIS 3: 30. phenotype: Wing hairs disarranged in small patches. Male infertile. Viability excellent. RK1. # sla: slimma location: 1-48.6. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 74. phenotype: Fly slim with very narrow abdomen. Body length nor- mal. Eclosion delayed slightly. Wings curve slightly. sla/slb and sla/sld wild type. Male fertile and viable. Female sterile; viability about 50% wild type. RK3. other information: Two alleles each induced by CB. 3007 and CB. 3025. # slater: see tkv #*slb: slim body location: 1-45.3. origin: Induced by ethyl methanesulfonate (CB. 1528). discoverer: Fahmy, 1956. references: 1958, DIS 32: 74. phenotype: Body narrow but of normal length. slb/sla and slb/sld wild type. Viability and fertility good in both sexes. RK3. # slc: slim chaetae location: 1-3.6. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1954. references: 1959, DIS 33: 90-91. phenotype: Bristles thin and short. Inner wing margins occa- sionally incised. Both sexes viable and fertile. RK1. # sld: slender location: 1-50.1. origin: Induced by p-N,N-di-(2-chloroethyl)amino- phenylethylamine (CB. 3034). discoverer: Fahmy, 1957. references: 1959, DIS 33: 91. phenotype: Fly rather small and slim with narrow abdomen. sld/sla and sld/slb wild type. Male fertile but shows delayed eclosion and reduced viability. Female very inviable. RK3. other information: One allele induced by CB. 3025. #*sldpta: slender-pointed abdomen origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. synonym: pta. references: 1959, DIS 33: 88. phenotype: Fly small, has narrowed abdomen and slightly altered eye and wing shape. Male sterile; viability about 25% wild type. RK3. # slender chaetae: see sch # slf: schlaff location: 2-15. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Roarke, Mahoney, Graham, and Lengyel, 1985, Dev. Biol. 109: 476-88. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Embryonic lethal. Cuticular differentiation normal but arrangement of cuticle around embryo abnormal. Cuticle is detached from the body. Head skeleton tilted backwards. Pos- terior segments contracted, anterior segments stretched around egg tip. alleles: Two ethyl methanesulfonate-induced alleles retained, slf1 and slf2 (originally designated IG and IJ) plus four dis- carded alleles. # slgA: sluggish-A (J.C. Hall) location: 1- {65}. origin: Induced by ethyl methanesulfonate. discoverer: Eichenberger and Benzer. synonym: EE85. references: Markow and Merriam, 1977, Behav. Genet. 7: 447-55. Hall, 1978, Genetic Mosaics and Cell Differentiation, (W.J. Gehring, ed.). Springer-Verlag, Berlin, pp. 259-305. Miklos, Kelly, Coombe, Leeds, and Lefevre., 1987, J. Neuro- genet. 4: 1-19. phenotype: Isolated as defective in fast phototaxis, using counter-current-distribution (CCD) machine; also turned out to have poor (negative) geotaxis in this machine; yet mutant males showed some positive optomotor responses and had a nor- mal electroretinogram; hence termed sluggish (as opposed to phototaxis-defective per se); Markow and Merriam (1977) con- firmed aberrant CCD phototactic response; in maze tests the mutant was found to be quite photonegative (more so than wild type) and seemingly normal in geotaxis (Markow and Merriam, 1977). slgA causes poor viability, as well as aberrant behavior in hemizygous females (Miklos et al., 1987); in mosa- ics studied for sluggishness, a mutant leg seemed to be debil- itated independently of behavior of other legs, with the six foci for such movement deficits mapping to the ventral blasto- derm (A. Ghysen, cited in Hall, 1978). cytology: Mapped to 19F4, along with sol, these two mutations being flanked by l(1)19Fe and l(1)19Ff; this determination (Miklos et al., 1987) was based on the poor phototaxis of slg in heterozygous combination with Df(1)GA104, but not with Df(1)16-129 or Df(1)JA117, none of which have breakpoints determined cytologically. molecular biology: Gene located in a 25 kb subsegment of 19F. Three transcription units detected by Delaney et al. (unpubl.). other information: Complements sol (Miklos et al., 1987). Also complements PC16, another phototaxis/geotaxis-defective muta- tion in the region, isolated in laboratory of S. Benzer and studied by Markow and Merriam (1977). # slgB (J.C. Hall) location: 1- {1}. origin: / ray induced. references: Sharma, 1977, Experientia 33: 171-77. phenotype: Isolated with regard to poor response to light in fast phototaxis tests; both sexes are sluggish in this regard. Males in this strain do not mate with females in darkness; in the light, males court and mate with females (40-50%, within 10 m) and other males with equal vigor; the latter behavior includes formations of chains and rings of intermale courters, as well as pseudo-copulation attempts; courtees in these cir- cumstances do not exhibit wing-flick repelling responses characteristic of wild-type males. Spectral sensitivity stu- dies of the light-elicited courtship activities showed 420- 515 nm to be effective (thus orange/red range ineffective); yellow light was perhaps the most stimulatory; quick turn-ons and turn-offs of intermale courtships could be effected by intermittent exposures to yellow and red light, respectively. cytology: Associated with a reciprocal T(1;3), whose X break- point is in 2C; appears to cause the aberrant behaviors; the other breakpoint is said to be in 97A10 (but also indicated as being in 3L in Sharma, 1977). other information: fru causes somewhat similar courtship abnor- malities, but its locus (polytene 90-91) is not near the third-chromosome breakpoint in this T(1;3). # sli: slit location: 2-77. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Rothberg, Hartley, Walther, and Artavanis-Tsakonas, 1988, Cell 55: 1047-59. phenotype: Homozygotes die as embryos. Head involution abnor- mal. In the ventral nervous system, transverse commissures lacking entirely. Midline neurons and supportive mesectoder- mal cells missing. Gene expression confined to ectoderm in cellular blastoderm (i.e., no expression in presumptive meso- derm) and to the midline neuroepithelium at gastrulation. Antibodies raised against a TrpE fusion protein fail to stain mutant embryos. More severe abnormality in Df/sli than sli/sli indicates that sli is hypomorphic in nature. In com- bination with Pc-like mutants abdominal transformations occur (Jurgens). alleles: Two ethyl-methanesulfonate-induced alleles, sli1 and sli2 (originally designated IG2 = IG23 and IG7 = IG107); also a P-induced allele mentioned by Rothberg et al. cytology: Localized to 52D by in situ hybridization. molecular biology: Isolated from genomic library using a 7 kb EcoRI fragment from the Notch locus that contains the epidermal-growth-factor-like repeats. A 2.5 kb HindIII genomic fragment sequenced; cDNA sequence indicates presence of 63 base-pair intron. Within exonic sequence a single large ORF can code for six adjacent and one noncontiguous EGF-like repeat separated by 99 amino acids. EGF-like repeats show 59% identity to those of N. # slight: see slt # slim: see slm # slim body: see slb # slim bristle: see smb # slim chaetae: see slc # slimma: see sla # slimmer abdomen: see sln # slip: slipshod (T. Schupbach) location: 2-42. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal. Embryos from homozygous mothers do not hatch; in cuticle preparations they show irreg- ular segmentation and variable segment fusions. alleles: slipPX = slip1. # slit: see sli # slm: slim location: 1-33.7. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1955. references: 1958, DIS 32: 75. phenotype: Small fly with narrow abdomen. Viability and fer- tility good. RK3. other information: One allele induced by CB. 1506. #*sln: slimmer abdomen location: 1-53.5. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1959, DIS 33: 91. phenotype: Rather small fly with narrow abdomen. Occasionally, wings slightly upheld and eyes small or misshapen. Male infertile; viability about 15% wild type. Female sterile. RK3. # slo: slowpoke (J.C. Hall) location: 3-86. origin: Induced by ethyl methanesulfonate. references: Elkins, Ganetzky, and Wu, 1986, Proc. Nat. Acad. Sci. USA 83: 8415-19. Elkins and Ganetzky, 1988, J. Neurosci. 8: 428-34. phenotype: Isolated in screen for third chromosomal temperature-sensitive paralytic mutants (Elkins et al., 1986); this one is uncoordinated and unable to climb when exposed to 38 but not completely paralyzed; four-minute exposure to that high temperature causes several minutes of motionlessness on return to 22. Legs shake when under ether anesthesia, as in Shaker mutants but less extreme. Unconditionally defective in behavior (e.g., diminished flight ability; tends to walk or fly in anomalous short hops when in large open container). Physiologically, the mutation abolishes Ca2+-dependent potas- sium current (IC), as shown, and analyzed further, in a variety of experiments involving recordings from dorsal longi- tudinal flight muscles (DLMs) of adults (Elkins et al., 1986; Elkins and Ganetzky, 1988): DLM spikes abnormally broadened after stimulation of giant fiber nerve pathway (one of whose endpoints is DLMs) or of motor neurons synapsing on these mus- cles. From voltage clamp analyses, a peak of early outward current following a step pulse from -80 to -40 mV, as revealed by a Sh mutation, is absent in slo, though inward Ca2+ currents in same traces are normal; no early outward current seen when slo is treated with 4-aminopyridine (which pheno- copies Sh) or combined with Sh14. (This double mutant has very low viability and severe impairment in locomotor activity); charybdotoxin, which blocks IC channels in wild- type DLMs, had no effect on outward currents in slo; delayed excitation of DLMs, observed in response to depolarizing currents delivered to wild-type (or Sh), absent in slo, and spike amplitudes increased; these abnormalities phenocopied by reducing IC in normal muscle by injecting EGTA into such cells or using low-Ca2+ saline; the lengthened muscle action poten- tials in slo indicate importance of IC in effecting repolari- zation of such potentials. alleles: Several alleles; slo1 and slo4 have been mentioned (Atkinson, Robertson, and Ganetzky, 1989, Neurosci. Abstr. 15: 541). cytology: Localization defined in part by In(3R)slo4, with one breakpoint in the E(spl) region (in 96F) and the other at or very near slo locus, which is indicated as proximal to E(spl) (Atkinson et al., 1989). # slope wing: see slw # sloppy paired: see slp # slow receptor potential: see slrp # slowpoke: see slo # slp: sloppy paired location: 2-8. 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 parts of naked cuti- cle of T2, A1, A3, A5, and A7 in an irregular fashion. No effect of ftz expression (Carroll and Scott, 1986, Cell 45: 113-26). alleles: Three ethyl methanesulfonate-induced alleles, slp1 (weak) and slp2 and slp3 (both strong) (original designations IIM, L12, and 7L, respectively). cytology: Placed in 24A3-D4 based on its being in the segment deleted by Df(2L)ed1 = Df(2L)24A3-4;24D3-4. # slrp: slow receptor potential (J.C. Hall) location: 1-51.4 (Pak, 1975); 49.7 (Homyk and Pye, 1988). origin: Induced by ethyl methanesulfonate. discoverer: Pak. references: Pak, 1975, Handbook of Genetics (R.C. King, ed.). Plenum Press, New York, Vol. 3, pp. 703-33. Homyk and Sheppard, 1977, Genetics 87: 95-104. Homyk and Pye, 1989, J. Neurogenet. 5: 37-48. phenotype: In electroretinogram recordings, there is an abnor- mally slow return of photoreceptor potential to baseline after stimulus is turned off; also, reduced light-on and light-off transient spikes; these phenotypes reported for the first three alleles isolated (Pak, 1975); action spectrum of mutant ERG (Pak, 1975) same as in wild-type; hence, opsins unlikely to be altered. Intracellular recordings reveal some penetrated photoreceptors to have potentials with abnormally slow decay and others to show normal receptor potentials (Pak, 1975). slrp mutants are generally hypoactive (Homyk, Pye, and Pak, 1981, Genetics 97: s50) and show ether-induced leg shak- ing, cold-induced leg paralysis, and the defects in ERG; slrp4 exhibits, in its permissive temperature range (20-30), the phenotypes just listed; in addition it is difficult to arouse for flight, has abnormally short jumps elicited, and, as a male, shows abnormal courtship wing displays (Homyk and Shep- pard, 1977); in the temperature range noted above, this allele causes ERG phenotypes like those associated with the original mutations (slow rate of repolarization, transient amplitude deficits); as the temperature is lowered from 20 to 15, slrp4 becomes (<17) sensitive to mechanical stress (Homyk and Shep- pard, 1977), and eventually completely paralyzed (Homyk and Pye, 1989); the ERG abnormalities are accentuated at these low temperatures (Homyk and Pye, 1989); for example, the off- transient spike can be completely eliminated in 15 recordings; this effect is reversed on raising the temperature (Homyk and Pye, 1989). alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________ slrp1 EMS Pak slrpP28 p slrp2 EMS Pak slrpP29 p slrp3 EMS Pak slrpP67 p slrp4 EMS hypoD h strongest allele ( h = Homyk and Sheppard, 1977, Genetics 87: 95-104; p = Pak, 1975, Handbook of Genetics (R.C. King, ed.). Plenum Press, New York, Vol. 3, pp. 703-33. cytology: Maps to 13F10-14B1, based on inclusion of slrp4 in both Df(1)sd72b = Df(1)13F1;14B1 and Dp(1;4)r+ = Dp(1;4)13F10;16A1-2;102F2-3 (Homyk and Pye, 1988). # sls: sallimus (J.A. Kennison) location: 3 (unmapped). origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1984. synonym: sam (preoccupied). references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Dominant suppressor of the extra-sex-combs phenotype of heterozygous Pc alleles. Also suppresses the dominant extra-sex-combs phenotype of Pcl alleles. # slt: slight location: 2-106.3. origin: Spontaneous. discoverer: Curry, 39b20. references: 1939, DIS 12: 45. phenotype: Fly small. Bristles short and thin. Enhances px. Viability and fertility good. RK3. # sluggish: see slg # slv: see svr #*slw: slope wing location: 1-51.2. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1958, DIS 32: 75. phenotype: Wings usually slightly upheld or spread. Viability and fertility good. RK3. # sm: smooth location: 2-91.5. origin: Spontaneous. discoverer: Bridges, 35c14. phenotype: Abdomen partially denuded of bristles and shrunken. Wings usually warped and semierect. Acrostichal hairs disar- ranged. Tendency for erect postscutellars. Male genitalia often disturbed. Anal protuberance of female bent down. Via- bility 30% wild type. Both sexes entirely sterile. RK2. # sm2 references: Frankham and Nurthen, 1980, DIS 80: 204. synonym: 2smlab: low abdominal bristle number. phenotype: Reduced numbers of abdominal bristles; alteration of abdominal bristle pattern and a reversal of the sexual dimor- phism for abdominal bristle number. Temperature sensitive with a TSP in the pupal period. Both sexes fertile. # sm: see smk # sma: smaller location: 1-29.9. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 75. phenotype: Body small. Eye color frequently dark. Viability and fertility good. RK2. other information: One allele each induced by CB. 1528, CB. 1540, CB. 2511, CB. 3007, CB. 3025, CB. 3026, CB. 3034. Two alleles induced by CB. 1414. # small: see sml # small body: see sby # small body 62: see srb # small bristles: see sbr # small eye: see oss # small narrow: see smn # small optic lobes: see sol # small pallid: see smp # small round: see srd # small thin: see sth # small thorax: see smt # small tumoroid: see stu # small wing: see sl # smaller: see sma # smaller body: see srb # smaller eye: see sme # smaller thinner: see smh # smalloid: see smd # smb: slim bristle location: 1-23.1. origin: Induced by ethyl methanesulfonate (CB. 1528). discoverer: Fahmy, 1956. phenotype: Bristles thin and rather short. Male viable and fertile; female sterile. RK2. other information: One allele induced by CB. 1540. # smd: smalloid location: 1-61.1. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 75. phenotype: Rather small body. Eyes frequently dark. Viability and fertility good. RK2. cytology: Placed in salivary chromosome region 18A4-18B8 on the basis of its inclusion within the deficiency resulting from recombining left end of In(1)y4 = In(1)1A8-B1;18A3-4 with right end of In(1)sc9 = In(1)1B2-3;18B8-9 (Norton and Valen- cia, 1965, DIS 40: 40). other information: One allele each induced by CB. 1414, CB. 1540, CB. 1592, and CB. 3007. Two alleles each induced by CB. 1506 and CB. 1528. Seven alleles induced by CB. 3025 and 10 by X rays. #*sme: smaller eye location: 1-68.9. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1955. references: 1959, DIS 33: 91. phenotype: Small fly with small, round, and slightly dark eyes. Wings occasionally diverge. Male sterile; viability about 50% wild type. RK2. other information: One allele induced by CB. 3051. # smell blind: see sbl #*smh: smaller thinner location: 1-1.5. origin: Induced by methyl methanesulfonate (CB. 1540). discoverer: Fahmy, 1956. references: 1959, DIS 33: 91. phenotype: Rather small fly with thin bristles. Both sexes viable and fertile. RK2. #*smk: smoky location: 2-58.6. origin: Ultraviolet induced. discoverer: Edmondson and Meyer, 49d. synonym: sm (preoccupied). references: 1949, DIS 23: 61. phenotype: Body color dark, especially along sides of thorax. Similar to es but somewhat lighter. At 27, female sterile and male fertile; at 17, both sexes fertile. Viability and clas- sification good. RK2. #*sml: small location: 1-25. origin: Induced by P32. discoverer: Bateman, 1950. references: 1950, DIS 24: 56. phenotype: Body small; wings short; eyes small, rough, and bulging. Thoracic hairs irregular. Eclosion delayed. Ten percent normal viability. RK3. #*smn: small narrow location: 1-45.7. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1955. references: 1959, DIS 33: 91. phenotype: Fly weak and inviable, usually dies within 48 hr of eclosion. Wings frequently upheld slightly. Abdomen narrow. RK3. # smo: smoothened location: 2-4. 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. All denticles in abdominal seg- ments point posteriorly. At 18 naked cuticle deleted and den- ticle belts of adjacent segments fused and locally arranged as mirror-image duplications. alleles: Three ethyl-methanesulfonate-induced cold-sensitive alleles, smo1, smo2, and smo3 (originally designated IIG, IIX, and Q14). # smoky: see smk # smooth: see sm # smoothened: see smo #*smp: small pallid location: 1-25.6. origin: X ray induced. discoverer: Fahmy, 1954. references: 1959, DIS 33: 91. phenotype: Fly quite small and lightly pigmented. Bristles slightly thin. Occasional eye misshapen. Male viable and fertile. Female sterile. RK2. #*smt: small thorax location: 1-51.9. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 75. phenotype: Thorax and head small. Wings correspondingly short but of normal width and frequently wavy. Both sexes fertile. Viability about 50% wild type. RK2. sn: singed From Mohr, 1922, Z. Indukt. Abstamm. Vererbungsl. 28: 1-22. # sn: singed location: 1-21.0. references: Bender, 1960, Genetics 45: 867-83. phenotype: Macrochaetae deformed, from short and gnarled to wavy, depending on allele. Similarly, microchaetae may be straight or wavy. Electron-microscope examination of develop- ing bristle shaft shows flattened fiber bundles around peri- phery, which occupy but 5% of cross-sectional profile, com- pared to wild type, which have fiber bundles that are circular in cross section and occupy 20% of cross-sectional area [Over- ton, 1967, J. Morph. 122: 367-80 (fig.)]. Females homozygous for the most extreme alleles are completely sterile; vitello- genesis defective. Eggs laid by sn1 homozygotes are normal in number, but are short, blunt, and wrinkled with small blunt dorsal appendages [Mohr, 1922, Z. Indukt. Abstamm. Vererbungsl. 28: 1-22 (fig.)]. Sterility autonomous in transplants (sn1; Clancy and Beadle, 1937, Biol. Bull. 72: 47-56; Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). Heterozygotes between female-sterile and fertile alleles are fertile, between female sterile alleles are sterile. alleles: The sn locus seems to be a very favorable site for P- element insertion; a number of the alleles listed below were isolated from natural populations in the USSR or are deriva- tives thereof. These alleles are highly mutable, generating innumerable derivative mutable normal-appearing and extreme singed alleles; some have been shown to carry P-element sequences at sn (Golubovsky, Ivanov, and Green, 1977, Proc. Nat. Acad. Sci. USA 74: 2973-75; Green, 1977, Proc. Nat. Acad. Sci. USA 74: 3490-93). Also some display slight increases in the rate of nondisjunction from Basc (Golubovsky, 1983, DIS 59: 40-42). Bender has classified sn alleles into four classes: class 1 = female sterile with gnarled macrochae- tae and kinky microchaetae; class 2 = female fertile with kinky macrochaetae only; class 3 = female fertile with gnarled macrochaetae and kinky microchaetae; class 4 = female sterile with gnarled macrochaetae only. To these Golubovsky and Kozlovskaya (1978, DIS 53: 141-42) have added class 5 = kinky microchaetae only. Derivative alleles have sometimes been designated generically as snf, snm, sns, and snex, for faint, moderate, strong, and extreme phenotypes; these symbols do not specify particular alleles (e.g., Zakharov and Golubovsky, 1984, Genetika 20: 1117-24). Unstable alleles also classed as snA and snB, snA alleles mutating to normal and back to the original phenotype only and snB alleles mutating to an array of intermediate states as well as to normal. allele origin discoverer ref ( comments | __________________________________________________________________________________________________________________________________ sn(+) / P Engels 11, 12, 43 0.95 kb P insert at -0.589 to 0.582; snw derivative; unstable sn1 spont Mohr, 18j25 7, 35, 43 class 1; sequence normal sn2 spont Bridges, 1912 7, 37, 43 class 2; lesion at 8.0 to 10.5 kb sn2-2 spont 17 class 1 sn3 spont Mohr, 22f11 7, 36, 43 class 3; 0.3 kb deletion in -0.9 to 0.0 kb sn4 spont Bridges, 30126 7, 43 class 2; sequence normal sn4 spont 17 class 3 sn5 spont Bridges 30b5 7 class 1 sn5S spont Skinner, 42c18 26, 43 class 1; 2 kb insert in -0.9 to 0.0 kb sn7 spont Berg 8, 17 class 3; unstable sn7-27 spont 17 class 5 sn7-55 spont 17 class 3 sn8 spont Berg 8, 17 class 3; stable sn9 spont 17 class 2 sn9-152 spont 17 class 3, unstable sn9e P Green 20 functional P element insert sn11 spont Berg 8, 17 class 2; unstable sn13a1 X ray, R(1)2 Hannah, 1947 45 Tp(1;3)6C;7C9-10;79E; breakpoint at 0.0 to 5.5 kb sn14e P Green 20 functional P element insert sn15 P Green 20 functional P element insert sn17 spont 13 P sequences at 7D sn19Bb5 X ray Valencia 45 Tp(1;3)3C1-2;7C9-10;72A-B sn26-7 spont 16, 17, 24, 47 class 3; unstable sn27-10 mustard Sobels, 57j 44 sn27-49 mustard Sobels, 57j 44 sn29-1 X ray Sobels, 57l 44 sn29-11 spont 17 class 3; in Basc sn31f X ray Patterson 39 class 1 sn33-13 spont 16, 17, 47 class 2, unstable sn33-13a spont 17 class 5 sn34e Duncan, 34e20 10, 43 class 2; complex lesion 2.4 to 4.3 kb sn34p HD 12a sn36a spont Spencer, 36a21 7, 43 class 4; 5.5 kb insert in -1.2 to 0.0 kb sn37b spont Poulson, 37b 40, 41 class 1 sn39k Buzzati-Traverso, 9 class 1 39k19 sn41i spont Oliver, 41i25 38 class 1 sn42 spont 17 class 5 sn42-5 spont 16, 17 class 3; unstable sn44-12 spont 17 class 1 sn45-7 spont Ivanov, 73j 23 stable; in Basc sn46a X ray Belgovsky 6 class 2 sn48h X ray Lindsley, 48h11 31 class 2 sn49 / spont 18, 25, 46 unstable; also clw mutant sn49h 32P King, 49h 42 class 1 sn49-5 spont 17, 24 class 1; unstable sn50-18 spont 16, 17, 24 class 2; unstable sn50k Ives 7, 27 class 1; sequence normal sn55a spont Hillman, 55a 22 class 3 sn57c spont Kadel 28 class 1 sn61k / ray Mickey, 61k 33 class 1 sn61k2 / ray Mickey, 61k 33 class 3 sn63-15 / spont Ivanov 16, 17, 23, 24, 47 class 5; unstable sn63-15a spont 17 class 5 sn63a radio waves Mickey, 63a 32 class 1 sn63b radio waves Mickey, 63b19 32 sn65a X ray Becker 5 class 4 sn68 NNG Kaufman 29 class 1 sn73-8 spont 17, 24 class 1; in Basc sn77-27 / spont Ivanov, 73j 17, 23, 24, 47 class 1; unstable sn78 spont Anxolabehere, 73b 3 synonym: frise sn79-15 spont 16, 17, 47 class 2; stable sn79-22 spont 17, 47 class 1 sn79b10 P Green 43 class 1; 1 kb P insert at -0.667 to - 0.660 kb sn79f22 P Green 43 class 1; 1 kb P insert at -.667 to - .660 kb sn79h2 P Green 43 class 1; 1 kb P insert at -.667 to - .660 kb sn83i7(1) P Green 43 class 1; 2.9 kb P insert at -.667 to - .660 kb sn83i7(2) P Green 43 class 1; 2.9 kb P insert at - 0.667 to - 0.660 kb sn83i7(3) P Green 43 class 1; 2.9 kb P insert at - 0.667 to - 0.660 kb sn83i7(15) P Green 43 2.9 kb P insert sn83i7(17) P Green 43 class1; 2.9 kb P insert at - 0.667 to - 0.660 kb sn84-6 spont 16, 17, 24, 47 class 3; unstable sn84-6a spont 17 class 5 sn88-9 spont 16, 17, 47 class 5; stable sn90-9 spont 24, 16, 17, 47 class 2; unstable sn110 spont 13 P element insert at 7D sn633-45 snA spont Golubovsky 14, 15 a class of mutable alleles; e.g., sn77-27 snA1 EMS 4 class 1 snA2.4 P Engels 43 class 1; 1.2 kb insert at -0.684 to -0.677 kb snB spont Golubovsky 14, 15 a class of mutable alleles; e.g., sn63-15 snB332.1 In(1)7D1-2;17C; breakpoint at -0.6. snB337.2 In(1)7D1-2;17C; breakpoint at -0.6. snc spont Muller 7 class 1 snCFL3 P Osgood 43 class 1; 2.9 kb P insert at - 0.667 to - 0.660 kb snCFL5 P Osgood 43 1.3 kb P insert sncm / P Hawley 21 class 3; 628 base pair P insert at -0.667 kb sne / 11, 12, 43 1.3 kb P insert at -0.589 to 0.582; snw derivative; unstable snext / P 21 derivative of sncm snh12-1 spont, MR Green 19 unstable snh12-2 spont, MR Green 19 unstable snh12-3 spont, MR Green 19 unstable snh12-4 spont, MR Green 19 unstable snh12-5 spont, MR Green 19 unstable snh12-6 spont, MR Green 19 unstable snK Krivshenko 1 class 1 snK1 EMS 30 class 1 snK2 EMS 30 class 1 snK3 EMS 30 class 1 snK4 EMS 30 class 1 snKH36 P Osgood 43 0.4 kb P insert snKH40 P Osgood 43 1.0 kb P insert snKHL1 P Osgood 43 0.4 kb P insert snKHL3 P Osgood 43 0.4 kb P insert snKHL4 P Osgood 43 0.6 kb P insert snKHL5 P Osgood 43 0.4 kb P insert snM1 EMS Mohler 34 class 1 snM2 EMS Mohler 34 class 1 snM3 EMS Mohler 34 class 1 snM4 EMS Mohler 34 class 1 snMJ19.3 P Engels 43 0.5 kb P insert snMK7 P Engels 43 2.9 kb P insert at -0.589 to - 0.582 snMH18.2 P Engels 43 1.0 kb P insert snMH26.5 P Engels 43 class 1; 2.9 kb P insert at -0.667 to -0.660 snMI17 P Engels 43 0.5 kb P insert snMR2 spont 13 P element at 7D snqr spont Mensua 2 class 3; to the right of sn1; qr = quetas recordatas snw / P Engels 11, 12, 43 class 3; hypermutable; 2.25 kb P insert at -0.589 to 0.582 snX2 X ray Muller 7, 43 class 1; 0.1 kb insert in -1.9 to -1.2 same insert present in parental chromosome ( 1 = Agol, 1936, DIS 5: 7; 2 = Alvarez, 1980, DIS 55: 193; 3 = Anxolabehere and Periquet, 1973, DIS 50: 21; 4 = Gans, Audit, and Masson, 1975, Genetics 81: 683-704; 5 = Becker, 1967, DIS 42: 40; 6 = Belgovsky, 1946, DIS 20: 63; 7 = Bender, 1960, Genetics 45: 867-83 (fig.); 8 = Berg, 1974, DIS 51: 100; 9 = Buzzati-Traverso, 1940, DIS 13: 49; 10 = Duncan, 1935, DIS 4: 10; 11 = Engels, 1979, Proc. Nat. Acad. Sci. USA 76: 4011-15; 12 = Engles, 1981, Genetics 98: 565-87; 12a = Furman and Zabanov, 1988, DIS 67: 37; 13 = Gerasimova and Ilyn, 1984, DIS 60: 111-12; 14 = Golu- bovsky, 1978, DIS 53: 171; 15 = Golubovsky, 1977, Genetika 16: 1605-11; 16 = Golubovsky, Ivanov, and Green, 1977, Proc. Nat. Acad. Sci. USA 74: 2973-75; 17 = Golubovsky and Kozlovskaya, 1978, DIS 53: 141-42; 18 = Golubovsky and Zakharov, 1980, DIS 55: 49-51; 19 = Green, 1977, Proc. Nat. Acad. Sci. USA 74: 3490-93; 20 = Green, 1986, Proc. Nat. Acad. Sci. USA 83: 1036-40; 21 = Hawley, Steuber, Marcus, Sohn, Baronas, Cameron, Zitron, and Chase, 1988, Genetics 119: 85-94; 22 = Hillman, 1957, DIS 31: 82; 23 = Ivanov, 1974, DIS 51: 71; 24 = Ivanov, 1978, DIS 53: 119; 25 = Ivanov and Golubovsky, 1977, Genetika 13: 655-66; 26 = Ives, 1943, DIS 17: 50; 27 = Ives and Noyes, 1951, Anat. Rec. 111: 565; 28 = Kadel, 1957, DIS 37: 83; 29 = Kaufman, 1969, DIS 44: 44; 30 = Komitopoulou, Gans, Margaritis, Kafatos, and Masson, 1983, Genetics 105: 897- 920; 31 = Lindsley, 1949, DIS 23: 60; 32 = Mickey, 1963, DIS 38: 29; 33 = Mickey, 1963, DIS 38: 31; 34 = Mohler and Carrol, 1984, DIS 60: 236-41; 35 = Mohr, 1922, Z. Indukt. Abstammungs. Vererbungsl. 28: 1-22 (fig); 36 = Mohr, 1923, Hereditas 4: 142-60 (fig.); 37 = Morgan, Bridges, and Stur- tevant, 1925, Bibliog. Genet. 2: 235; 38 = Oliver, 1942, DIS 16: 53; 39 = Patterson, 1934, DIS 2: 59; 40 = Poulson, 1938, DIS 10: 55; 41 = Poulson, 1939, DIS 12: 49; 42 = Poulson and King, 1949, DIS 23: 63; 43 = Roiha, Rubin, and O'Hare, 1988, Genetics 119: 75-83; 44 = Sobels, 1958, DIS 32: 85; 45 = Valencia, 1966, DIS 41: 58; 46 = Yur- chenko, Zakharov, and Golubovsky, 1984, Mol. Gen. Genet. 194: 279-85; 47 = Zakharov and Golubovsky, 1984, Genetika, 20: 1117-24. | Class according to Bender (1960); coordinates according to Roiha, Rubin, and O'Hare (1988). / More detailed information given below. cytology: Placed in 7D1-2 by in situ hybridization (Spradling; Engels). molecular biology: 40 kb cloned; from coordinates -15 to +25 with the origin at an arbitrary EcoRI site and positive values to the right. Six out of nine alleles tested have lesions between -1.9 and +10.5 kb. Three breakpoints [Dp(1;2)sn13a, In(1)snB332.1 and In(1)snB337.2 (Roiha, Rubin, and O'Hare, 1988, Genetics 119: 75-83)] between -0.6 and +5.5; P element hotspot at -0.7 to 0.0 with at least four different insertion sites. Gene consists of six exons with three polyadenylation sites resulting in three sizes for the 3' exon and three sizes of RNA, 3.6, 3.3, and 3.0 kb. Structure of gene-exon 1 from -0.7 to 0.0 kb; exon 2 from 11.0 to 11.3 kb; exon 3 from 12.3 to 12.7 kb; exon 4 from 12.8 to 13.3 kb; exon 5 from 13.4 to 13.6 kb; exon 6 from 13.7 to 14.4 or 14.7 or 15.0 kb. A sin- gle 59-kd protein predicted. other information: Locus divided into three recombinationally different sites from distal to proximal: (sn3 and sn36a) (sn2 and sn4) (sn1, sn5 and sn50k) (Ives and Noyes, 1951, Anat. Rec. 111: 565; Hexter, 1955, Proc. Nat. Acad. Sci. USA 41: 921-25; Genetics 42: 376). Of these, sn3 and sn36a show lesions between -0.9 and 0.0 kb, whereas sn2 has a lesion between 8.0 and 10.5. The others show no detectable molecular lesions, and are presumed to be point mutations within the coding region between 11.1 and 13.8 kb. # sn36a phenotype: Macrochaetae gnarled in a fairly extreme manner. Microchaetae wild type. sn36a is only allele to cause pro- nounced reduction in replication of oocyte nurse cell DNA [King and Burnett, 1957, Growth 21: 263-80 (fig.)]. Also causes more extreme retardation of vitellogenesis than other female-sterile sn alleles (Bender). sn36a sn4 homozygote has nearly normal bristles and is sterile. RK1. # sn49 phenotype: A strong allele of sn recovered from a natural popu- lation. Associated with simultaneous mutation to club wing, clw, a defect in wing expansion with low penetrance. sn49 is unstable, producing an array of derivatives that are in turn stable or unstable. and the expression of clw differs among them. It mutates to sn+ and back at a rate of approximately 10-3; a rare moderate singed derivative exhibits an approxi- mately ten-fold elevation in mutation frequency, mutating either back to the strong allele or to an unstable normal allele; a single extreme singed derivative of a normal deriva- tive of the moderate allele produces strong-singed and non- singed derivatives, which can in turn revert to the extreme allele and in the case of the strong derivative to non singed (Yurchenko, Zakharov, and Golubovsky, 1984, Mol. Gen. Genet. 194: 279-85). # sn63-15 phenotype: Moderate sn phenotype. Prototype type B mutable allele; mutation rate 0.1 to 1.2%. Produces both extreme singed and normal-appearing derivatives as well as an array of intermediate phenotypes. In addition strongly reversible alleles (25-50 x more mutable than parental allele) are pro- duced. This allele also associated with increased rate of mutation to fw. # sn77-27 phenotype: Extreme sn phenotype. Prototype type A mutable allele; mutates to an unstable sn+, which mutates back to extreme alleles; no intermediate alleles recovered. # sncm phenotype: An allele of sn that is mutable in dysgenic but not in non-dysgenic genotypes. Mutation takes place in two direc- tions; one is to apparent stable reversions and the other to a more extreme phenotype, snex, which is in turn unstable. molecular biology: Contains a 628-bp defective P element inserted at coordinate -.667. sn+ derivatives characterized by precise or nearly precise excision of the element. snex derivatives contain duplications of the defective P element located close to the right of the original P in inverted orientation. # snw: singed-weak phenotype: Weak singed phenotype, probably class 2. Highly mutable in dysgenic genotypes; 40% to 60% of offspring are either normal (sn(+)) or extreme singed (sne) in phenotype. These derivatives are in turn mutable, but at much lower lev- els. Completely stable in non-dysgenic genotypes. molecular biology: Contains a pair of adjacent defective P ele- ments of 0.95 kb and 1.15 kb inserted in head-to-head orienta- tion between -0.589 and -0.582 kb. All sne derivatives tested retain only the 1.15 kb element and all normal-appearing derivatives retain only the 0.95 kb element, thus the symbol sn(+). # sna: snail location: 2-51. synonym: l(2)br28 = l(2)35Db. references: Simpson, 1983, Genetics 105: 615-32. Grau, Carteret, and Simpson, 1984, Genetics 108: 347-60. phenotype: Embryonic lethal. Partially dorsalized. In homozy- gotes for strong alleles, ventral furrow not formed at gastru- lation; however, endoderm invaginates, cephalic furrow formed, and germ-band elongation takes place. Embryo has few if any mesodermally derived internal tissues. Homozygotes for weak alleles gastrulate normally, but die as late embryos without differentiating normal internal tissues. Many embryos make normal ectodermal derivatives: larval hypoderm with normal or reduced denticle belts, mouth hooks, and spiracles, but tra- cheae seen only in weaker alleles. Head involution abnormal and anterior end of embryo twisted in the egg owing to extra length. Some embryos fail to make normal cuticle and resemble long folded tubes filled with yolk. sna heterozygotes pro- duced from mothers heterozygous for dl or a deficiency for dl show reduced viability; this effect is more extreme at elevated temperatures. Defect in sna embryos enhanced by heterozygosity for Df(2L)75c or Df(2L)fn2. No maternal effect in germ-line clones. No effect on pattern of ftz expression (Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32). sna/+ embryos have delayed ventral furrow for- mation. alleles: Alleles of varying strengths reported. Weak alleles appear to be hypomorphic based on their phenotypes over defi- ciencies versus in homozygotes. Strong alleles behave as amorphs. Trans heterozygotes of weak alleles produce few escapers, which may exhibit missing halteres or more rarely hemithorax. allele origin discoverer synonym ref ( comments ___________________________________________________________________ sna1 EMS Harrington HG31 1, 3, 5 strong allele sna2 EMS Grau EY1 3 strong allele sna3 EMS Grau EY2 3 sna4 EMS Grau EY3 3 weak allele sna5 X ray Simpson R1 3, 5 weak allele sna6 X ray Simpson RY1 2, 3, 5 strong allele; 1.6 kb deletion sna7 X ray Simpson RY2 T(2;3)24B-C; 35C-D;41;81 *sna8 X ray Simpson RY3 sna9 EMS Simpson V1 sna10 EMS Simpson V2 sna11 EMS Simpson V3 sna12 EMS Simpson V4 sna13 EMS Simpson V5 sna14 EMS Simpson V6 sna15 EMS Simpson V7 sna16 EMS El Messal VD1 sna17 EMS El Messal VD2 sna18 EMS Nusslein-Volhard IIG05 3, 4, 5 strong allele sna19 X ray Nusslein-Volhard 4.26 sna20 X ray Nusslein-Volhard 18.19 ( 1 = Ashburner, Tsubota, and Woodruff, 1982, Genetics 102: 401-20; 2 = Boulay, Dennefeld, and Alberga, 1987, Nature (London) 330: 395-98; 3 = Grau, Carteret, and Simp- son, l984, Genetics 108: 347-60; 4 = Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82; 5 = Simpson, 1983, Genetics 105: 615- 32. cytology: Placed in 35C4-D2 based on its inclusion in Df(2L)b80e4 = Df(2L)35C4;35D1-2 but not in Df(2L)osp18 = Df(2L)35B1-2;35C4-5. molecular biology: Gene isolated from walk on the basis of DNA lesions identified in five independent sna alleles. Sequences from the region identify a 1.7 mRNA on Northern blots. A 1.7 kb cDNA of nearly full length cloned and sequenced; injection of antisense RNA into early embryos promotes phenocopy of sna development. Transcription from proximal to distal on 2L. cDNA contains a single open reading frame of 1,170 nucleo- tides, corresponding to 390 amino-acid residues with a calcu- lated relative molecular mass of 43,000. The carboxy terminus of the conceptual polypeptide contains five zinc-finger motifs (Boulay, Dennefeld, and Alberga, 1987, Nature (London) 330: 395-98). other information: The Sco transposition brings a portion of the noc gene into juxtaposition with sna; subsequent rear- rangements with breakpoints within the sna gene are able to revert the Sco phenotype (McGill, Chia, Karp, and Ashburner, 1988, Genetics 119: 647-61). # snake: see snk # snap: see snp # snb: see psnb # Snb: Snow blind (B. Ondek) location: 3-104.7. origin: Induced by ethyl methanesulfonate. discoverer: Ondek and Hardy. phenotype: Deep pseudopupil absent in white-eyed flies raised in either light or dark. Electroretinogram displays no recep- tor potential. Light and electron microscopy reveal no organ- ized ommitidial structure; widespread degeneration and no apparent photoreceptor cells. # snf: see fs(1)A1621 # snk: snake location: 3-52.1. references: Anderson and Nusslein-Volhard, 1984, Nature 311: 223-27. Anderson and Nusslein-Volhard, 1986, Gametogenesis and the Early Embryo, Alan R. Liss, Inc., pp. 177-94. phenotype: Maternal effect lethal. Embryos produced by homozy- gous mothers show extreme dorsalized phenotype; only dorsally derived cuticle remains, resulting in a hollow tube of dorsal ectoderm. No paternal rescue, even by two doses of snk+; dor- salizes the expression of ftz such that entire ftz stripes in the blastoderm exhibit the wide dorsal conformation and do not narrow ventrally as is normal (Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32). Responds most strongly of all maternal dorsalized mutants to rescue by injection of cytoplasm and poly A+ RNA from wild-type embryos. Injection of wild-type cytoplasm or cytoplasm from other dorsalizing maternal-effect mutants into pre-pole-cell snake embryos fully restores the normal dorsal-ventral pattern, and more than 20% can develop into normal adults; the site of injection appears to be unimportant. Partial rescue also achieved by the injec- tion of poly A+ but not poly A- RNA isolated from cleaving embryos. alleles: allele origin discoverer synonym ______________________________________________ snk1 EMS Rice mel(3)4, snk073 snk2 EMS snk229 snk3 EMS snk233 snk4 EMS snkrm4 cytology: Placed in 87D6-13 on the basis of the molecular observation that the right breakpoint of Df(3R)ry36 interrupts the gene and it is to the right of the molecular deficiency associated with ry506. Df(3R)ry36 is not detectable cytologi- cally, but it includes ry but not Hsc2 or pic. molecular biology: Gene identified by finding a DNA segment capable of rescuing snk by germ-line transformation. This 13.5 kb segment begins and ends in the loci of ry and Hsc2, respectively. Northern blots of embryonic RNA probed with a 2.4 kb EcoRI internal fragment from the above segment reveal a 1.65 kb transcript; a slightly smaller pupal transcript that differs from the embryonic transcript at its N and C termini is recognized by the same probe. Transcription is from right to left, and the cDNA sequence predicts a protein of 430 resi- dues. The conceptual sequence reveals homology to several known serine proteases over its 246 C-terminal amino acids; may also have a Ca2+ binding site near its amino-terminus (DeLotto and Spierer, 1986, Nature (London) 323: 688-92). # snl: sonless location: 1-56.3. discoverer: Pare, 1964. references: Colaianne and Bell, 1970, Genetics 65: 619-25. Colaianne and Bell, 1972, Genetics 72: 293-96. Colaianne and Bell, 1972, DIS 48: 20. phenotype: Maternal-effect recessive lethal or semilethal. snl/snl females crossed to normal males produce fewer that 10% of the expected number of sons. Lethality can be rescued by a paternally derived snl+ allele as demonstrated by the survival of exceptional sons but not daughters (i.e., snl+/0 but not snl/snl/Y) of the above mating. Lethality occurs during embryonic or early larval stages. snl/+ females crossed to snl/Y males produce normal offspring in a 1:1 sex ratio. Crosses between snl males and females are nearly sterile, pro- ducing extreme sex ratios favoring females among surviving offspring. Data indicate that homozygosity for tra enhances and for dsx reduces the lethality of sons of snl mothers. other information: Complements both r and fu, nearby genes that also act as maternal-effect lethals. # sno: strawberry notch location: 1-41.8 (based on mapping of sno4). synonym: g-l: glossy like. references: Lefevre and Peterson, 1972, DIS 48: 126-27. Lefevre and Wright, 1976, Genetics 83: s44-45. phenotype: Males and females homozygous for viable alleles have notched wings, thickened, Confluens-like wing veins with del- tas at the junctions of the longitudinal veins and the mar- gins, extra hairs on thorax and wings, shortened tarsal seg- ments, and roughened, shiny bright, somewhat mottled eyes, closely resembling fag. All macrochaetae thin and delicate. Phenotype almost completely suppressed by euchromatic duplica- tions of the Notch locus, e.g., Dp(1;2)51b = Dp(1;2)3C1- 2;3D6-7;52E. Insertions into heterochromatin, e.g., w+Y, are less effective in suppression. fa sno males and fa sno/+ sno females have exaggerated phenotypes and are semilethal; spl sno less extreme. sno1 does not survive when raised at 29 or in RpII215Ubl/+ genotypes; exhibits slight dominance in trans heterozygotes with RpII215Ubl (Mortin and Lefevre, 1981, Chro- mosoma 82: 237-47). alleles: allele origin discoverer synonym ref ( comments _________________________________________________________________________ sno1 EMS Lefevre, 71e sno71e 2, 3, 5 heat-sensitive lethal; sno2 EMS Lefevre 2 Tp(1;3)C92 sno3 | EMS Mayoh l(1)HM16 4 cold-sensitive lethal sno4 | EMS Mayoh l(1)HM23 4 cold-sensitive lethal sno5 EMS Lefevre, 75b sno75b 3 heat-sensitive sno6 | EMS Falke l(1)TW2 1 cold-sensitive lethal sno7 EMS Lefevre, 76a sno76a 5 sno8 EMS Lefevre l snoDC800 5 lethal; lethal in heterozygotes with Rpll215Ubl sno9 ENU Scott 6 lethal sno10 ENU Scott 6 lethal ( 1 = Falke and Wright, 1975, Genetics 81: 655-82; 2 = Lefevre and Peterson, 1972, DIS 48: 126-27; 3 = Lefevre and Wright, 1976, Genetics 83: s44-45; 4 = Mayoh and Suzuki, 1973, Can. J. Genet. Cytol. 15: 237-54; 5 = Mortin and Lefevre, 1981, Chromosoma 82: 237-47; 6 = Scott, 1987, Ph.D. thesis, University of California, San Diego. | Further phenotypic description below. cytology: Placed in 11D9-10 based on its inclusion in Df(1)N12 = Df(1)11D1-2;11F1-2 and the breakpoint in 11D of Tp(1;3)C92 = Tp(1;3)6E1-2;11D9-10. # sno3 phenotype: No survivors at 17; short fine bristles at 25. Females become sterile when held at 17. # sno4 phenotype: No survivors at 17; normal at 25. Females become sterile when held at 17. # sno6 phenotype: Survivors of development at 17 have, in addition to the phenotype described above, reduced or absent ocelli, dark head, small trident, and underdeveloped legs; phenotype normal when raised at 25. Females become sterile when held at 17. # snp: snap location: 3-50. references: Glover. # snRNA: see under RNA # snw: stonewall location: 3-{41}. references: Yu, Berg, and Spradling. cytology: Located in 70D-E.