# e: ebony location: 3-70.7. discoverer: E. M. Wallace, 12b15. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 50 (fig.). phenotype: Body color varies from shining black to slightly darker than wild type, depending on allele. Puparia much lighter than wild type. Classifiable throughout larva period by darkened color of spiracle sheaths (Brehme, 1941, Proc. Nat. Acad. Sci. USA 27: 254-61). Viability lowered to about 80% wild type. Heterozygotes for dark alleles have slightly darker body color than normal. For interaction with other body color mutants, see Waddington (1941, Proc. Zool. Soc. London, Ser. A 111: 173-80). Postulated to encode |-alanyl dopamine synthetase, a 90-kd enzyme that requires ATP and MgCl2 to catalyze the formation of N-|-alanyl dopamine from | alanine and dopamine; | alanyl dopamine absent from newly eclosed e flies (Wright, 1987, Adv. Genet. 24: 127-222); | alanine and dopamine accumulate in pupae and pharate adults, dopamine to twice normal levels, in e and e11 homozygotes; levels return to normal in older adults (Hodgetts, 1972, J. Insect Physiol. 18: 937-47; Hodgetts and Konopka, 1973, J. Insect Physiol. 19: 1211-20). Unable to utilize | alanine in tanning of puparium. Labeled | alanine or uracil injected into e pupae remains in hemocoel, not incorporated into pupal case as in +; light-colored pupa result; e/+ intermediate in these respects. Only newly emerged + adults incorporate uracil or | alanine into cuticle; e flies and older + flies do not; | alanine toxic to the latter two types (Jacobs, 1968, Biochem. Genet. 1: 267-75). Defect in tanning leads to spongey cuticle which responds to | alanine administration (Jacobs, 1980, Biochem. Genet. 18: 65-76). Phenylthiocarbamide inhibits development of e11 homozygotes more than wild type; reverse is true for inhibition by silver chloride; heterozygotes intermediate in both cases. Mixtures of the two inhibitors affect heterozy- gotes to a greater extent (Kroman and Parsons, 1960, Nature 186: 411-12). Electroretinograms of e flies abnormal; lamina potential reduced or absent (Hotta and Benzer, 1969, Nature 222: 354-56). Threshold for phototaxis 200-fold higher than that for wild type; high sensitivity (retinulae 1-6) optomotor threshold 500 times normal and high acuity (retinulae 7 and 8) optomotor threshold ten times normal [Heisenberg, 1972, Infor- mation Processing in the Visual Systems of Arthropods (R. Wehner, ed.). Springer-Verlag, Berlin, Heidelberg, and New York, pp. 265-68]. e flies more sensitive to polarized light than wild type (Heisenberg, 1972). Abnormal distribu- tion of uptake of 3H-GABA by the lamina ganglionaris described by Campos-Ortega (Cell Tissue Res. 147: 415-31). Reduced mating success compared to wild type (Rendel, 1951, Evolution 5: 226-30). Courtship frequently aborts owing to mismounting by male [Crossley and Zuill, 1970, Nature (London) 225: 1064-65]; relative mating success increased in dark (Kyriacou, 1981, Anim. Behav. 29: 462-71) but not according to Crossley (1970, DIS 45: 170). Courtship shows deficiency in wing vibration; low proportion of sine song and long intra- pulse interval; e/+ outsings +/+ (Kyriacou, Burnet, and Con- nolly, 1978, Anim. Behav. 26: 1195-1206). RK1. alleles: Changes at e not known to be associated with defi- ciency for the locus tabulated below. e1 inseparable from In(3R)C; stocks labeled as carrying e, but not In(3R)C, for the most part carry e4 (Craymer). allele origin ref ( phenotype cytology ___________________________________________________________________ e1 spont 1, 2 dark In(3R)C e4 spont 1, 2 dark e11 spont 2, 5 dark e60h spont 2, 3 intermediate e100.265 X ray 2, 8 dark In(3R)93B5-6;95E *e100.307 X ray 2, 8 *e300.96 X ray 2, 8 dark In(3R)89F-90A;99B2-4 eAFA X ray 4 In(3R)86C;96D1-6 eAT5 EMS 4 eAT8 EMS 4 eD8 X ray 4 T(2;3)40-41;93D1-6 eD12 X ray 4 In(3R)92E12-13;93D1-6 *eF5 X ray 4 eF6 | X ray 4 es spont 1, 2 intermediate *est spont 2, 7, 8 intermediate eUg spont 2, 9 light ex ( 1 = Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. 327: 59, 99, 184; 2 = CP627; 3 = Ives, 1965, DIS 40: 55; 4 = Scalenghe and Ritossa, 1976, Atti Accad. Lincei 13: 439-528; 5 = Stern, 1926, Z. Indukt. Abstamm. Verer- bungsl. 41: 198-215; 6 = Villee, 1941, DIS 14: 40; 7 = Villee, 1942, Univ. Calif. Berkeley, Publ, Zool. 49: 137; 8 = Ward and Alexander, 1957, Genetics 42: 42-54; 9 = Zurcher, 1963, Genetics 34: 1-33 (fig.). | Probably independent of e mutation. cytology: Placed in 93D2-6 by D'Alessandro, Ritossa, and Scalenghe (1977, DIS 52: 46) based on its being the position of the breakpoint common to a number of e rearrangements. Probably at the left end of this region based on Df(3R)e67l = Df(3R)93B5-7;93D3 (Korge, 1972, DIS 48: 20) and Df(3R)e-H5 = Df(3R)93B10-13;93D2-3 (Henikoff, 1980, DIS 55: 61-62). # E74: Ecdysone-inducible gene encoded in region 74 (W.A. Segraves) location: 3-{45}. synonym: Eip74EF. references: Burtis, 1985, PhD Thesis, Stanford University. Janknecht, Taube, Ludecke and Pongs, 1989, Nucleic Acids Res. 17: 4455-64. Burtis, Thummel, Jones, Karim and Hogness, 1990, Cell 61: 85-99. Thummel, Burtis and Hogness, 1990, Cell 61: 101-11. phenotype: Encodes an ecdysone-inducible gene associated with the early puff at 74E-F. Periodic expression of the gene fol- lows, by approximately one hour, pulses of ecdysone occurring during development; two periods of expression occur indepen- dently of ecdysone pulses, one at the end of embryogenesis and one at the end of pupal development. Return to base line lev- els of expression requires protein synthesis and presumably results from repression by ecdysone-induced gene products; in situ hybridization to larvae detects transcription of E74 in most tissues, both imaginal and strictly larval. alleles: Two mutant alleles selected by Burtis (1985); one dies in the pharate-adult stage, whereas the other is a prepupal lethal, showing defects in larval shortening and cuticular tanning; a low frequency of defective prepupae reach the pharate adult stage. allele origin discoverer synonym comments __________________________________________________________________ E741 X ray Burtis, 1985 E74x1001 pharate adult lethal; T(2;3)29A-C;74E-F ( E742 EMS Burtis, 1985 E74e3109 prepupal lethal ( Broken in first intron of the long transcript. cytology: Placed in early ecdysone-inducible puff at 74E-F by in situ hybridization. molecular biology: The gene is 6 kb in length; three different transcripts produced by transcription from right to left. The long transcript comprises eight exons and is dispersed over all 6 kb; the mature message encodes a protein of 829 amino- acids and 87.1 kd. The other two transcripts are shorter and are initiated from promoters 300 base pairs apart in the fifth of seven introns of the long transcript; they have four exons, the last three being the same as those of the long transcript; thus the proteins share their C-terminal sequences but have different N-terminal ends; both short transcripts encode the same polypeptide of 833 amino acids and 94.7 kd. The sequences indicate a polypeptide with an acidic N terminus and a basic C terminus separated by a region of homopolymeric repeats. A segment of 84 amino acids in the C-terminal end shows 50% identity with a similarly situated sequence in the protein encoded by the human c-ets-2 oncogene. Thummel et al. demonstrate that E74 is transcribed at 1.1 kb per minute such that an hour is required from the time of ecdysone stimulation until the first mature transcripts are produced. # E75 (W.A. Segraves) location: 3-{46}. synonym: Eip75. references: Segraves, 1988, PhD Thesis, Stanford University. Feigl, Gram, and Pongs, 1989, Nucleic Acids Res. 17: 7167-78. Segraves and Hogness, 1990, Genes Dev. 4: 204-19. phenotype: Encodes an ecdysone-inducible gene associated with the early puff at polytene position 75B. Periodic expression occurs in response to ecdysone pulses occurring at specific times during development; regression of puff and reduction of E75 expression in third instar does not occur in the presence of cycloheximide, and presumably depends on ecdysone-induced gene products. alleles: 28 alleles recovered by Segraves (1988), falling into two groups, one displaying early lethality (early larval for the combinations examined) and one displaying pharate-adult lethality. allele origin synonym comments ________________________________________________________ E751 X ray E75x37 pharate-adult lethal over E754; 60 kb deletion ( E752 X ray E75x44 early lethal; In(3L)75B3-5;75F3-5 | E753 X ray E75x46 early lethal E754 X ray E75x48 105-kb deletion / E755 X ray E75x51 larval-pupal lethal E756 EMS E75e101 early lethal E757 EMS E75e102 pupal lethal E758 EMS E75e109 early lethal E759 EMS E75e149 early lethal ` E7510 EMS E75e165 early lethal E7511 EMS E75e172 early lethal E7512 EMS E75e174 pharate-adult lethal E7513 EMS E75e197 pharate-adult lethal E7514 EMS E75e198 early lethal ` E7515 EMS E75e202 early lethal E7516 EMS E75e203 early lethal E7517 EMS E75e207 early lethal E7518 EMS E75e213 early lethal E7519 EMS E75e264 early lethal E7520 EMS E75e273 pharate-adult lethal E7521 EMS E75e281 early lethal E7522 EMS E75e283 pharate-adult lethal E7523 EMS E75e295 early lethal ` E7524 EMS E75e304 early lethal E7525 EMS E75e316 early lethal E7526 EMS E75e341 early lethal E7527 EMS E75e355 early lethal E7528 EMS E75e397 early lethal ( Breaks in the long transcription unit immediately downstream from the first exon. | Breaks immediately downstream from the first exon of the E75 A transcription unit; chromosome has an associated, possibly complex, inversion from 67B to the base of 3R. / Removes the entire E75 gene and eliminates the 75B puff. ` Lost. cytology: Placed in early ecdysone-inducible puff at 75B by in situ hybridization. molecular biology: 350 kb from 75B region cloned and used to identify two overlapping ecdysone-responsive transcription units; E75 A and E75 B. The E75 A unit contains six exons spread over 50 kb, and gives rise to mRNA's of 4.9 or 5.7 kb by use of alternate polyadenylation sites within the final exon. The E75 B unit begins within the second intron of E75 A and contains five exons, the final four of which are shared with E75 A, and produces mRNA's of 5.2 and 6.0 kb. The polypeptides encoded by the two thus contain different N ter- mini and a common C terminus. The E75 A polypeptide contains 266 unique and 971 shared amino acids for a molecular weight of 132 kd; the E75 B polypeptide contains 422 + 971 amino acids and has a molecular weight of 151 kd. The conceptual amino acid sequence exhibits striking homology to the steroid receptor superfamily of proteins. The homology is restricted to the DNA-binding and hormone-binding domains of the pro- teins. The two polypeptides differ most significantly in that the E75 A protein contains both of the characteristic zinc fingers of the steroid-receptor-like DNA-binding domain, whereas the E75 B protein contains only one. A third type of E75 cDNA has been reported, which closely resembles the E75 A mRNA except for the substitution of novel sequences for the first E75 A exon (Feigl et al., 1989). This would result in the production of an E75 protein with the same DNA-binding and hormone-binding domains as the E75 A protein, but with a dif- ferent amino terminus. These novel sequences are transcribed from an exon 50 kb upstream of the E75 A promoter, which defines the > 100 kb E75 C transcription unit (Segraves, unpublished). # E(2)Bic: see E(Bic) # E(A53g): Enhancer of abnormal abdomen-53g location: 2-6 (between al and dp). origin: Spontaneous. references: Thalmann, 1974, DIS 51: 22. phenotype: Extreme intensification of A53g phenotype; flies nearly denuded of tergites. Does not enhance S, and E(S), which maps in same region, does not enhance A53g. # E(Arp): see Ba10 # E(B): Enhancer of Bar location: 1-57.3. origin: Spontaneous. discoverer: Bonnier and Nordenskiold. synonym: i; I: Intensifier of Bar; Eb: Exaggeration of Bar. references: 1942, DIS 16: 47. Bonnier, Nordenskiold, and Bagman, 1943, Hereditas 29: 113-33 (fig.). Rasmuson, 1948, Proc. Intern. Congr. Genet., 8th. pp. 645-46. phenotype: E(B) heterozygous with any B allele, including B+, produces flies similar in phenotype to homozygotes for that allele. B +/+ E(B) eyes have 80-90 facets, but B E(B)/++ eyes have only 40. Homozygous lethal. RK2(A). cytology: Salivary chromosomes appear normal, but there is occasional indication of deficiency for faint bands 16A5 and 6. other information: Reduces B-fu crossing over about 40%. # E(Bic) location: 2-64.0. origin: Induced by ethyl methanesulfonate. synonym: E(2)Bic. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Roux's Arch. Dev. Biol. 193: 267-82. Mohler and Wieschaus, 1986, Genetics 112: 803-22. phenotype: An incompletely penetrant dominant female-sterile mutation; heterozygous females produce 60% apparently unfertilized eggs. In heterozygotes with Bic-C or Bic-D, E(Bic) causes a substantial increase in the incidence of double-abdomen embryos, but E(Bic)/+ females produce normal embryos. # e(bx): see zebx # E(bx): Enhancer of bithorax location: 3- (to the left of R). origin: X ray induced. discoverer: E. B. Lewis. synonym: En-bx. phenotype: Enhances expression of bx34e, bx3, and Ubx/+. Lethal homozygous. RK2. # E(da): Enhancer of daughterless location: 2-55 (inferred from rearrangement breakpoint). origin: X ray induced. references: Mange and Sandler, 1973, Genetics 73: 73-86. phenotype: One dose of E(da) in da/+ females, in either cou- pling or repulsion with da, reduces the number of daughters among their progeny; without effect in da/+ males. da E(da)/SM1 females are daughterless. Effect enhanced by reduced heterochromatic content of progeny (Mange and Sandler, 1973). Maternal effect of E(da) strong at 29 but absent at 17 (Cline 1980, Genetics 96: 903-26). Sxlf1/+;da E(da)/+ females produce no Sxlf1/+ daughters at 29 (Cline, 1980). E(da)/abo females produce normal sex ratios; show zygotic suppression of the maternal effect of homozygous abo (Mange and Sandler, 1973). cytology: Associated with T(2;3)E(da) = T(2;3)41;66C. Sandler and Mange (1973) suppose E(da) to be a consequence of the break in 2R. # e(dpv): enhancer of dumpy-vortex location: 3-40.4. origin: Spontaneous. discoverer: Bridges, 16h7. synonym: vo-3: vortex in chromosome 3. references: 1919, Bridges and Mohr, Genetics 4: 283-306 (fig.). 1923, Bridges and Morgan, Carnegie Inst. Washington Publ. No. 327: 168. 1925, Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 41-43 (fig.). phenotype: Normal. In combination with dpv, produces one or two pairs of pits or volcano-like protrusions on thorax; hairs and bristles arranged in whorls. RK3. #*E(f): Enhancer of forked location: 2-86.5. origin: X ray induced. discoverer: Belgovsky, 37c4. synonym: I-f: Intensifier of forked. references: 1937, DIS 8: 7. 1938, Izv. Akad. Nauk SSSR, Ser. Biol. 1017-36. 1940, DIS 13: 52. 1944, Zh. Obshch. Biol. 5: 325-56. phenotype: Homozygote has short, twisted bristles intermediate between f and Bl; postscutellars often pale; viability and fertility reduced. Heterozygote is wild type. f/+; E(f)/+ slightly more extreme than f. f/f; E(f)/+ has an extreme forked phenotype and hairs are forked. f/f; E(f)/E(f) rarely survives. RK3. cytology: Salivary chromosomes normal. # e(faswb): enhancer of facet-strawberry location: 1-1.5 (no recombination with wa). origin: Spontaneous. discoverer: Keppy. synonym: e(faswb) faswb which was originally designated faswb- h: facet-strawberry-hairy. references: Welshons and Welsons, 1986, Genetics 113: 337-54. phenotype: By itself e(faswb) is wild type in phenotype; when in cis with faswb, either in homozygous or hemizygous condi- tion, it produces narrow, rough, glossy eyes, bowed tibiae on the metathoracic legs, and a proliferation of microchaetae. e(faswb) faswb/fag have glossy phenotype; faswb/fag have facet phenotype. cytology: Postulated to be an inversion of bands 3C2 and 3 on the basis of its elimination of wa-rst recombination and its normal appearing polytene banding pattern. #*e(g): enhancer of garnet location: 1-5.9. discoverer: Payne and Denny, 1921. synonym: m(g): modifier of garnet. references: 1921, Am. Naturalist 55: 377-81. phenotype: Apparently wild type but, in combination with g, produces a more orange eye than g alone. RK3. # E(H): see Su(H) # E(lz): Enhancer of lozenge location: 3-64.0 (between sr and Dl). origin: Induced by ethyl methanesulfonate. discoverer: Grell. phentotype: Dominant enhancer of lozenge; no effect observed in absence of lz. Homozygous viable. #*E(M99E): Enhancer of Minute (3) 99E location: 3- (near spindle attachment). origin: Spontaneous. discoverer: Bridges. synonym: E(M3g). phenotype: Specific intensifier of shortness of bristles of M(3)99E. RK3. #*e(N8): enhancer of Notch-8 location: 3- (not located). origin: Spontaneous. discoverer: Mohr, 181. references: 1923, Z. Indukt. Abstamm. Vererbungsl. 32: 108-232 (fig.). phenotype: Produces slight nicking of wings. Enhances N8. RK3. # E(Pc): Enhancer of Polycomb (R. Denell) location: 2-61.9 (0.1 cM to the left of en). origin: Induced by ethyl methanesulfonate. synonym: l(2)28-28-12. references: Russel and Eberlein, 1979, Genetics 91: s109. Sato, Russel, and Denell, 1983, Genetics 105: 357-70. Sato, Hayes, and Denell, 1984, Dev. Genet. 4: 185-98. phenotype: Although E(Pc) heterozygotes are cuticularly normal as larvae and adults, the mutation acts zygotically as a dom- inant enhancer of the adult homoeotic syndrome of flies heterozygous for Polycomb mutations or Df(3L)Pc-MK. The locus is haplo-abnormal, as heterozygous deficiencies of the E(Pc) locus have an equivalent effect. Heterozygosity for E(Pc) or a deficiency also enhances the adult homoeotic syndrome of Polycomblike mutation or deficiency heterozygotes, and renders the normally recessive mutations esc and l(4)29 slightly pseu- dodominant, but has no effect on phenotypes associated with AntpNs, Antp73b, AntpScx, AntpEfW15, ScrMsc, Cbx, Ubx, bx34e or abx bx3 pbx heterozygotes. E(Pc) is a recessive lethal mutation; homozygotes and hemizygotes die as late embryos or larvae, which appear cuticularly normal. E(Pc) has dominant maternal as well as zygotic effect on the severity of the embryonic homoeotic syndrome of Pc3 or Df(3L)Pc-MK homozy- gotes. Zygotic homozygosity for E(Pc) also enhances the embryonic effects of PclW4, PclW5, and PclW6, and E(Pc); l(4)29 doubly homozygous embryos from heterozygous mothers show incomplete head involution, presumably due to a cryptic homoeotic effect. cytology: Placed in 48A3-6 based on its inclusion in Df(2R)en30 = Df(2R)48A3-4;48C6-8 and Df(2R)en-A = Df(2R)47D3-4;48A5-6. # E(Pc)-a location: 3- (near Dl). discoverer: E.B. Lewis and Chang. references: Eberlein, 1984, Genetics 107: s26. phenotype: Homozygous lethal; heterozygotes show partial transformation of legs 2 and 3 to first leg and occasionally of first and fourth abnominal segments to second and fifth, respectively. Phenotype enhanced by combination with Pc or E(Pc). #*e(S): enhancer of Star location: 3- (between 0 and 10; perhaps an allele of ru or R). origin: Spontaneous. discoverer: Bridges, 16k18. synonym: S-i: intensifier of Star. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 175 (fig.). phenotype: By itself, homozygous e(S) has normal eyes. S/+; e(S)/e(S) has eyes smaller and rougher than S/+, although overlapping somewhat; abdomen bulbous; body color darkish. RK3. # E(S): Enhancer of Star location: 2-6 [claimed to lie between left break of In(2L)Cy and locus of Cy]. discoverer: Bridges, 30a27. phenotype: E(S)/+ normal, E(S)/E(S) gives slight roughening of eye. E(S)/+ strongly reduces size and increases roughness of S/+ and S2/+ eyes; imparts dominance to ast/+, ast2/+, ast3/+, and ast4/+ (Lewis, 1945, Genetics 30: 137-66). S +/+ E(S) occasionally emerges as a late-eclosing giant. RK3A. cytology: Arose in In(2L)Cy = In(2L)22D1-2;33F5-34A1. Placed in 22D3-E1 on the basis of enhancement of S by a duplication for the interval (Gelbart). # E(sd): Enhancer of scalloped location: Autosomal. origin: Spontaneous. discoverer: R. M. Valencia, 1963. references: 1965, DIS 40: 37. phenotype: Almost completely removes wings of sdsp; not tested with other alleles of sd. No interaction wth Bx or Bxr. RK2. # E(Sd): Enhancer of Segregation Distorter location: 2-55. origin: Found on SD chromosomes. references: Ganetzky, 1977, Genetics 86: 321-55. phenotype: In the presence of E(SD), either in coupling or repulsion, Sd characterized by k values of > .95. Deletion of E(SD) reduces k values to .65-.75. Non-SD chromosomes carry either no allele or a nonenhancing allele. E(Sd) in the absence of Sd able to cause differential recovery of Rsp+ and Rsp- chromosomes (Sharp; Temin). cytology: Located in proximal heterochromatin of 2L. Deleted by three deficiencies for lt, Df(2L)ESD1, Df(2L)ESD3, and Df(2L)ESD36. # e(sei): enhancer of seizure location: 3-39.0. origin: Spontaneous. references: Kasbekar, Nelson, and Hall, 1987, Genetics 116: 423-31. phenotype: In the homozygous condition, it lowers the tempera- ture threshold of two temperature-sensitive alleles of sei. seits2, which is a dominant paralytic at 40, a recessive para- lytic at 38 and nonparalytic at 35, becomes a dominant para- lytic at 38 and displays a recessive hyperactive uncoordinated phenotype at 35 in the presence of homozygous, but not heterozygous e(sei). Homozygous seits1 which is normal at 35 becomes paralyzed at that temperature in the presence of homozygous e(sei). Flies homozygous for e(sei) by itself, when their container is tapped lightly, become hyperactive and unable to crawl up the sides of the container to the top. e(sei) flies exhibit spontaneous neuronally stimulated firing of the dorsal longitudinal muscle and greatly enhances such firing of seits2. Also e(sei) does not affect saxitoxin bind- ing by membrane extracts as do sei mutations. cytology: Placed in 69A4-B5 based on its inclusion in Df(3L)vin7 = Df(3L)68C8-11;69B4-5 but not Df(3L)vin6 = Df(3L)68C8-11;69A4-5 or Df(3L)vin5 = Df(3L)68A2-3;69A1-3. # E(spl): Enhancer of split location: 3-89. references: Welshons, 1956, DIS 30: 157-58. Von Halle, 1965, DIS 40: 60. Lehmann, Jimenez, Dietrich, and Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 62-74 (fig.). Vassin, Wielmetter, and Campos-Ortega, 1985, J. Neurogenet. 2: 291-308. Knust, Bremer, Vassin, Ziemer, Tepass, and Campos-Ortega, 1987, Dev. Biol. 122: 262-73 (fig.). de la Concha, Dietrich, Weigel, and Campos-Ortega, 1988, Genetics 118: 499-508. Ziemer, Tietze, Knust, and Campos-Ortega, 1988, Genetics 119: 63-74. phenotype: Locus involved in the differentiation of the neural ectoderm into neuroblasts and epidermoblasts. Increased lev- els of gene product favor epidermal differentiation, whereas decreased levels favor neuronal differentiation. Locus origi- nally identified by the split-enhancing feature of a dominant gain-of-function mutation. Loss of function mutations are lethals and are described separately. A weak hypomorphic allele described as gro (groucho) is also described below. E(spl) causes spl/+ to display a split phenotype and elicits a more extreme phenotype in spl/spl and spl/Y. The spl- enhancing effect of E(spl)1 is suppressed in flies heterozy- gous for Dl (Shepard, Boverman, and Muskavitch, 1989, Genetics 122: 429-38). With respect to enhancement, +/+/+ < +/E(spl) < E(spl)/+/+ < E(spl)/E(spl), in accord with expectations from a hypermorphic allele; duplication for E(spl)+ achieved with Dp(3;3)M95A+16. In the absence of spl, E(spl) causes slight roughening of the eyes; furthermore, depending on parental constitution, varying percentages of embryos display defects in central- and peripheral-nervous-system development and irregular cuticular defects. A fraction of these fail to develop; percentages vary from 25% neural hypoplasia and 8% embryonic mortality in crosses between homozygous E(spl) parents to 100% death and 78% neural hypoplasia when both parents are E(spl)/Dp(3;3)M95A+. Both of these effects are sensitive to maternal genotype. That E(spl) is not simply a hypermorph is indicated by the fact that although +/Df(3R)Espl is viable, E(spl)/Df(3R)Espl is virtually lethal, especially when the deficiency is maternally inherited. Embryos homozy- gous for loss-of-function alleles vary in phenotype from weak to very strong neural hyperplasia, with concomitant aplasia of the epidermal sheath. Heterozygotes for stronger hypomorphic alleles may show terminal thickening of wing veins L4 and L5, and may have adventitious vein segments in the posterior wing membrane. Double heterozygotes for E(spl) loss-of-function alleles and either N or Dl are lethal. In the adult, increas- ing levels of E(spl) function result in increasing levels of split enhancement and in decreased numbers of sensilla as measured by the number of costal bristles on the wing. Con- versely, decreased E(spl) function results in larger eyes and more sensilla plus ectopic sensory neurons appearing in the wing blade, especially along the posterior margin. Hemizygos- ity for E(spl)+ completely suppresses spl. Three doses of E(spl)+ increase the severity of the effects of the absence of function of Dl, reduce the severity of the absence of function of N, neu and mam and are without effect on the phenotype of bib-; conversely, absence of function of E(spl) is not affected by hyperploidy for any of the neurogenic loci or by loss of H function; from this De la Concha et al. infer that E(spl) is positively controlled by N and negatively controlled by H and Dl. Unlike the results using other neurogenic mutants, single vitally stained cells taken from the neuro- genic ectoderm of E(spl)- embryos and transplanted into wild- type host embryos fail to give rise to clones containing epi- dermal cells; only neuronal elements are produced. This observation is interpreted to indicate that the E(spl)+ pro- duct serves a receptor rather than a signalling function (Technau and Campos-Ortega, 1987, Proc. Nat. Acad. Sci. USA 84: 4500-04). alleles: One true mutant allele is the original dominant E(spl) and it is likely a double mutant; a number of recessive lethals recovered either as reversions of E(spl), designated E(spl)rv and mostly associated with chromosome rearrangements, or as mutations designated E(spl)r that fail to complement Df(3R)Espl-3, a cytologically visible deficiency that contains more than eleven transcription units. These lethals display variable levels of neural hyperplasia and are treated as alleles in the literature; however interactions among them in trans heterozygotes lead to complex complementation patterns, and in general, the mutations have not been associated with particular transcription units. allele origin discoverer synonym ref ( comments __________________________________________________________________________________ E(spl)1 spont Green E(spl)D 1, 4, 5 unique dominant allele; 0.7-kb deletion in 12 to 14 kb; 5-kb insertion at 16.5 kb E(spl)2 spont Grell,64k gro: groucho viable hypomorphic allele? E(spl)r3 EMS E(spl)A4 5 E(spl)r4 EMS E(spl)B7 5 E(spl)r5 EMS E(spl)B12 5 E(spl)r6 EMS E(spl)B37 5 E(spl)r7 EMS E(spl)B48 5 E(spl)r8 EMS E(spl)B88 5 E(spl)r9 EMS E(spl)B93 5 E(spl)r10 EMS E(spl)B94 5 E(spl)r11 EMS E(spl)B95 5 E(spl)r12 EMS E(spl)B102 5 E(spl)r13 EMS E(spl)B115 5 E(spl)r14 EMS E(spl)B128 5 E(spl)r15 X ray Muskavitch E(spl)BX21 3 T(2;3)40-41;96F9-10 E(spl)r16 X ray Muskavitch E(spl)BX22 3 ~14-kb deletion; 4 to 17.5 kb ~14-kb inversion; breaks in -10.5 to -7.6 and 4 kb E(spl)r17 EMS Preiss E(spl)E28 3 E(spl)r18 EMS Preiss E(spl)E48 3 E(spl)r19 EMS Preiss E(spl)E73 3 E(spl)r20 EMS Preiss E(spl)E75 3 E(spl)r21 EMS Preiss E(spl)E77 3 E(spl)r22 EMS Preiss E(spl)E107 3 E(spl)r23 X ray E(spl)L5 2, 5 E(spl)r24 X ray E(spl)L9 5 E(spl)r25 X ray Tietz E(spl)L11 2, 5 T(3;4)96F7-11;102B-C; breakpoint in -7 to -5 kb E(spl)r26 X ray l(gro)X115 3 E(spl)rv27 X ray Knust and E(spl)R-A7.1 1, 2, 5 34-kb deletion; Ziemer -15 to +19 kb E(spl)rv28 X ray Knust and E(spl)R-C1.4 1, 2, 5 T(3;4)96F12-14;102E-F; Ziemer breakpoint in m3 at -5 to -6 kb E(spl)rv29 X ray E(spl)R-F4.4 2, 5 lesion in -15.5 to -11.5 kb E(spl)rv30 X ray E(spl)R-F6.2 2, 5 lesion in 19 to 20.5 kb E(spl)rv31 X ray E(spl)R-H2.1 5 E(spl)rv32 X ray Bremer E(spl)R14.8 1, 2, 5 T(3;4)96F8-9; 100F5;102B-D breakpoint at ~ -65 kb ( 1 = Knust, Bremer, Vassin, Ziemer, Tepass and Campos- Ortega, 1987, Dev. Biol. 122: 262-73; 2 = Knust, Tietze and Campos-Ortega, 1987, EMBO J. 6: 4113-23; 3 = Preiss, Hartley and Artavanis-Tsakonas, 1988, EMBO J. 7: 3917-27; 4 = Welshons, 1956, DIS 30: 157-58; 5 = Ziemer, Tietze, Knust and Campos-Ortega, 1988, Genetics 119: 63-74. cytology: Placed in 96F11-14 based on its inclusion in Df(3R)ro82b = Df(3R)96F11-14;97F3-11 but not Df(3R)Tl-Q = Df(3R)97A1;97D (Preiss et al.). molecular biology: Region isolated in two independent walks both initiated from the some cloned sequence: a 150-kb walk (Knust, Tietze and Campos-Ortega, 1987, EMBO J. 6: 4113-23) with an EcoRI site just to the right of the initiating clone designated as coordinate 0 and positive values to the right and an 80-kb walk (Preiss, Hartley and Artavanis-Tsakonas, 1988, EMBO J. 7: 3917-27) with a Xho site just to the right of the initiating clone designated as the 0 coordinate and positive values to the left. The Xho site appears to be approximately 2.5 kb to the left of the EcoRI site; accord- ingly changing the sign and subtracting 2.5 kb from the Preiss et al. coordinates approximates the Knust et al. coordinates which are used here. Lesions of twelve different mutations identified within 36 kb from -15 to +21 kb of the walk. At least 11 transcripts detected in this region; they are num- bered m1 through m11 in order from proximal to distal; coordi- nate 0 is between transcription units m4 and m5. All of these transcription units are expressed at some level during embryo- genesis and several are expressed maternally as well. In situ hybridization of cDNA or genomic probes for nine of the eleven transcribed regions to developing embryos reveal complex tem- poral and spatial patterns of expression; four of the tran- scripts m4, m5, m7 and m8 exhibit virtually identical expres- sion patterns, which accord with expectation for neurogenic genes; transcript first appears in late blastoderm, most intensely the neurogenic ectoderm, a ventrolateral stripe several cells wide on either side of the embryo. They are also expressed in several other neural primordia such as the stomatogastric nervous system and the optic lobes; transcripts subsequently become restricted to epidermal primordia; m9 and m10 are strongly and ubiquitously expressed in the embryo as well as maternally. Among the mutants with lesions within the 36-kb region are gro which appears to be an allele of E(spl), and Pr alleles which do not. Sequence determined for m4, m5, m7 and m8 (Klambt, Knust, Tietze and Campos-Ortega, 1989, EMBO J. 8: 203-10); m5, m7 and m8 are highly homologous to one another and share significant homology with proteins of the helix-loop-helix variety such as those encoded by da, emc, T3, T4, T5 and T8 of ASC and vertebrate myc; m4 is completely dif- ferent from the other three and from known sequences in data- bases. The genomic sequences of all four lack introns and all encode hydrophilic polypeptides; specific information on each is as follows: m4 is a 1.1-kd mRNA that encodes a 152 (or 141 depending on start codon) amino-acid, 19-kd hydrophilic polypeptide with pI = 5.5; m5 is 1.0 kb and encodes a 19.9-kd polypeptide of 178 amino- acids, pI = 10.16; m7 is an 1.5 kb mRNA encoding a 186 amino-acid, 20.5-kd polypeptide, pI = 10.2 and m8, which is 1.0 kd in length, encodes a polypeptide of 179 amino acids and molecular weight of 19.7 kd, pI approxi- mately equal to 10. The genomic sequence of m8 is modified in E(spl); there is an 84-nucleotide deletion upstream from the putative m8 promoter plus a 483-nucleotide deletion that removes the last 56 codons from the message; the next 27 base pairs are in frame and append nine ectopic amino-acids to the truncated polypeptide; these are followed by a 60-base-pair insertion the first three nucleotides of which are a stop codon; then there is a ten-nucleotide deletion followed by wild-type sequence. Klambt et al. have shown that the abnor- mal m8 region is responsible for the E(spl) phenotype; transformation with a genomic segment containing m8 and little else leads to genotypes with strong split suppressing effects. Transformation with a segment including the transcription unit for m9 and m10 is able to rescue lethality of seven presumed lethal point mutations of E(spl), of E(spl)/Df(3R)Espl and the phenotype of Df(3R)Espl/gro; it does not, however, fully res- cue the neural hyperplasia associated with some molecular deficiencies (Preiss et al., 1989). The genomic sequence corresponding to the transcription unit has been sequenced; the two transcripts share a common uninterrupted open reading frame, differing only in the length of their 3 untranslated region. The conceptual amino-acid sequence contains 719 resi- dues with predicted molecular weight of 78,928 daltons; there is no evidence of either a signal sequence or transmembrane regions; three clusters of residues rich in proline seen in the amino-terminal half of the molecule in residues 3-19, 120-208 and 273-421, the carboxy-terminal half contains four or five repeating motifs of 43 to 47 residues. In database searches, the 340 carboxy-terminal amino-acids display 39% homology and 21% identity to | transducin, the G protein involved in signal transduction in the retina; homology is also detected to several other |-G proteins and to the yeast cell-cycle gene, CDC4. # E(spl)2 synonym: gro: groucho. phenotype: Homozygotes have clumps of extra bristles above each eye which give impression of bushy eyebrows; also extra bris- tles on the humerus. Top of head tends to be malformed; ocelli often enlarged and run together. In selected stocks, penetrance approaches 100%, but is low in unselected stocks. Concluded to be an allele of E(spl) on the basis of the visi- ble phenotype of heterozygotes with lethal presumed point mutations at E(spl); however, it does not cause neural hyper- trophy and is wild type in combination with E(spl)1. molecular biology: The chromosome containing the gro mutation contains two inserts, one of ~4 kb between coordinates -4.8 and -3.8 kb and a much smaller one at approximately +11.5 detected by Preiss et al.. The larger of the two is indepen- dent of the gro mutation since Df(3R)Pr4, which deletes the region into which the segment is inserted, does not uncover gro; a similar argument for the independence of the insert at 11.5 can be made since gro is rescued by transformation with a segment from 12.7 to 23.1 (Preiss et al.). # e(tu-K): enhancer of tumor K location: 3- (not located). origin: Spontaneous. discoverer: Burnet and Sang. references: 1964, Genetics 49: 223-35. phenotype: Homozygote produces a significant increase in the penetrance of tu-K in both untreated flies and those treated in ways known to increase tumor incidence in tu-K. RK3. # E(tuh-1): Enhancer of tumorous head-1 location: 3- (not mapped; near BXC). references: Kuhn and Dorgan, 1974, Genetics 77: s37. phenotype: Increases penetrance by 8% and expressivity by 91% for the tumorous-head trait. Acts in trans to iab8,9tuh3 to increase maternal effect of tuh1 on transformation of head to abdominal structures (Kuhn, and Packert, 1988, Dev. Biol. 125: 8-18). # E(var)7: Enhancer of variegation location: 2- (not located). origin: X ray induced. discoverer: Schultz. phenotype: E(var)7/+ has no phenotype of its own but enhances variegation, e.g., wm4 is made much lighter and variegation for rst appears in males. Variegated position effects do not respond uniformly to E(var)7. RK2(A). cytology: May be small abnormality in 25A (Schultz). # E(var)21 discoverer: Schultz. references: Hadorn, Gsell, and Schultz, 1970, Proc. Nat. Acad. Sci. USA 65: 633-37. phenotype: Produces large patches of yellow bristles in combi- nation with E(var)7 in y/y+Y males. # E(var)25F to 100C-F A series of enhancers of variegation inferred from the effects of segmental deficiencies and duplications on the phenotype of In(1)wm4. All but E(var)33A-D, which is a triplo enhancer, are haplo enhancers. Three other triplo enhancers have been associated with haplo suppressors of variegation: Su(var)2-5 = Su(var)205, Su(var)7 and Su(var)9. genetic cytological locus location location included in excluded from ref ( comments __________________________________________________________________________________ E(var)25F 2-{17} 25F2-4 Df(2L)cl2 Df(2L)cl-h1 2, 3, 5 E(var)26A 2-21 25F4-26A1 Df(2L)Gpdh78 2, 3, 5 E(var)28A-B 2-{22} 28E5-28B1 Df(2L)TE28A-1 Df(2L)Gpdh75w 5 E(var)29B-D 2-{30} 29A2-D1 Df(2L)TE29Aa36 5 E(var)33A-D 2-{45} 33A1-D5 5 triplo enhancer; adjacent to Su(var) E(var)36A-E 2-{52} 36A8-E1 Df(2L)H20 Df(2L)M36F-S5 5 E(var)43A 2-{56} 43A2-B1 Df(2R)43A 5 E(var)55 2-{86} 55A-F Df(2R)PC4 5 E(var)87F 3-{54} 87E11-F14 Df(3R)GE41 Df(3R)lC4a 5 = e(var)3-3 Df(3L)red41 E(var)100C-F 3-103.6 100C5-F5 Df(3R)E45 1, 4 ( 1 = Locke, Kotarski, and Tartof, 1988, Genetics 120: 818- 98; 2 = Szidonya and Reuter, 1988, DIS 67: 77-79; 3 = Szi- donya and Reuter, 1988, Genet. Res. 51: 197-208; 4 = Tar- tof, Bishop, Jones, Hobbs, and Locke, 1989, Dev. Genet. 10: 162-76; 5 = Wustmann, Szidonya, Taubert, and Reuter, 1989, Mol. Gen. Genet. 217: 520-27. # E(var)300 series Three ethyl-methanesulfonate-induced dominant enhancers of variegation (Sinclair, Mottus, and Grigliatti, 1983, Mol. Gen. Genet. 191: 326-33). Cause substantial reduction in eye pig- ment of In(1)wm4-bearing flies; less to no effect on wm51b, wmJ, and wmMc; all three enhance bwVDe2 and SbV (Sinclair, Lloyd, and Grigliatti, 1989, Mol. Gen. Genet. 216: 328-33). locus location ____________________ E(var)301 3-49.3 E(var)302 3-36.6 E(var)303 3-34.7 # E(var)c101 location: 3-54 [based on 3.7% recombination with 89C2-3 break- point of T(2;3)apXa (Reuter, Werner and Hoffmann, 1982, Chro- mosoma 85: 539-51)]. origin: Spontaneous in T(2;3)apXa. references: Reuter and Wolff, 1981, Mol. Gen. Genet. 182: 516-19. phenotype: Produces white eyes with occasional single red facets in combination with wm4h. # E(wa): Enhancer of white-apricot location: 2-105.1 (4.6 units to the right of px; to the left of sp). origin: Spontaneous. discoverer: Scandlyn. references: Von Halle, 1969, DIS 44: 119. phenotype: Heterozygote dilutes wa to pale yellow. Homozygote with wa is white. Enhances wa1 and wa4. Also enhances wSp55 and wh (Birchler, 1986, Genetics 113: s47) but not wa2, wa3, wbf, wBwx, wcf, wch, wco, wcol, we, or wsp; enhances phenotype of wa1/wbf. No effect on eye color in presence of w+; and no interaction with other eye-color mutants. Enhancement dominant to two doses of the normal allele in wa/bw+Y;E(wa)/+. Homozy- gous males sterile; homozygous females partially fertile. RK3. cytology: Placed to the left of 60B10 based on the E(wa)/+-like phenotype of E(wa)/Df(2l)Px [= Df(2R)60B8-10:60D1-2]. #*e(we): enhancer of white-eosin location: 1-32. origin: Spontaneous. discoverer: Green, 55b21. synonym: en-we. references: 1957, DIS 31: 81. 1959, Heredity 13: 303-15. phenotype: Enhances certain intermediate alleles of w; e.g., waE, we, we2, wh, and wX16; three of these shown to have tran- sposable element DOC inserted at the same place; two have pogo (we and we2) and one has roo (wh) inserted in the DOC element. Produces a nearly white eye color. No effect on wa, wa2, wa3, wa4, wbf, wch2, wco, wcol, or wsat. Suppresses lzK and gypsy containing mutants lz1, f1, f5, and bx34e (Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97). e(we) flies occasionally have px-like venation or shortened wings, or both. Homozygous females sterile. RK2. alleles: A second spontaneous allele with similar phenotype and map position recovered by Schalet. # e(wgd): see su(f) # e(y): enhancer of yellow A series of sex-linked recessive mutations that modify the expression of y2, a gypsy-induced allele; these mutations do not modify the expression of other gypsy-induced mutations. Recovered from hybrid dysgenic crosses in which the transpos- able element, Stalker plus, in some cases, P were mobilized. The new mutations fall into six complementation groups; they were localized by recombinational analysis and by in situ hybridization using the transposable sequences as probes; (Georgiev and Gerasimova, 1989, Mol. Gen. Genet. 220: 121- 26). y2 suppressed by su(Hw)2; however, the effects of all e(y) mutations on bristle color persist in the presence of su(Hw)2. genetic cytological locus location location comments ( _________________________________________________________________________ e(y)1 1-57.9 16B head and thorax bristles yellow; microchaetae yellow; female sterile e(y)2 1-36.2 10C head and thorax bristles yellow; microchaetae yellow; short stocky body; wings separated; eyes small; facets altered; bristles shortened e(y)3 1-62.2 18C-D head and thorax bristles yellow; microchaetae yellow; thin bristles; female sterile; reduced viability e(y)4 1-58.1 16B thorax macro- and microchaetae yellow; causes yellow bristles on y+ flies; males but not females have short thin bristles e(y)5 1-59.2 17C y+ flies have shortened, thin, yellow, transparent macro- and microchaetae on thorax and abdomen; female sterile e(y)6 1-37.2 10F y+ flies have pale yellow body, wings, and bristles; male sterile; reduced viability ( Effect on phenotype of y2 unless otherwise indicated; no effect on phenotype of y+ unless so indicated. alleles: Independent recovery of mutations at several of the loci recorded; those with P-element inserts generally unstable, reverting to wild type or in some cases generating novel alleles; those with Stalker inserts stable. allele origin ____________________ e(y)11 Stalker e(y)12 Stalker e(y)21 Stalker e(y)31 P e(y)32 P e(y)33 P e(y)34 Stalker e(y)41 P e(y)51 P e(y)52 P e(y)53 P e(y)61 P e(y)62 P e(y)63 P # E(z): Enhancer of zeste location: 3-34.0. synonym: l(3)1902; pco; polycombeotic. references: Kalisch and Rasmuson, 1974, Hereditas 78: 97-104. Shearn, Hersperger, and Hersperger, l978, Genetics 89: 341- 53. Shearn, Hersperger, Hersperger, Pentz, and Denker, 1978, Genetics 89: 355-70. Wu, Jones, Lasko, and Gelbart, 1989, Mol. Gen. Genet. 218: 559-64. Phillips and Shearn, 1990, Genetics 125: 91-101. Jones and Gelbart, 1990, in press. phenotype: Locus named after original gain-of-function allele E(z)1 (Kalisch and Rasmuson); subsequently designated polycom- beotic (pco) (by Phillips and Shearn) based on phenotype of lethal homozygotes. Loss of function alleles recovered as (a) recessive lethal mutations (b) reversions of E(z)1 and (c) reversions of the antimorphic allele, E(z)59. Reduction of E(z)+ activity leads to suppression of the z eye color, whereas gain-of-function alleles are dominant enhancers of zeste eye color [i.e., z w+/Y; E(z)1/+ males have brownish eyes as do z w+/z+ w+; E(z)1/+ females]. E(z)59 an antimorphic allele, is a dominant suppressor of z [i.e. z w+; E(z)59/+ females have orange eyes]. Hemizygosity for E(z)+ produces a very mild suppression of the z eye color. No effects on eye color in z+ or za backgrounds, and effects on eye color not specific to a particular w allele. Reduction of E(z)+ activity also allows ectopic expression of the segment identity genes of the Antennapedia and bithorax gene com- plexes, resulting in homeotic transformations. This latter effect defines E(z) as a Polycomb-group locus. E(z)61 displays temperature-sensititive suppression of z eye color and homeotic phenotypes. At 22, z wis/Y; E(z)61/Df(3L)E(z)- males have orange eyes and no homeotic transformations. At 29, such males have wild-type red eyes and die as pharate adults with strong homeotic transformations of the mesothora- cic and metathoracic legs toward the prothoracic state. Embryos produced by E(z)61 homozygous females at 29C die with homeotic transformations of most segments toward the eighth abdominal segment. Even two copies of paternally contributed E(z)+ does not rescue viability of these embryos. Complete lack of zygotically produced E(z)+ results in early pupal lethality and small imaginal disks. Larval brain squashes from individuals homozygous for an amorphic allele reveal a very low mitotic index; metaphase chromosomes irregularly condensed and fragmented (Gatti and Baker, 1989, Genes Dev. 3: 438-53). alleles: With the exception of the first four alleles, which are gain-of-function dominant suppressors of zeste, and E(z)60, which is an antimorphic dominant suppressor of zeste, all alleles listed below are presumably hypomorphic and amorphic alleles, which can act as dominant suppressors of zeste and are homozygous lethal. allele origin synonym ref ( comments ______________________________________________________________________ E(z)1 EMS 2, 5 gain-of-function allele E(z)2 EMS 2 gain-of-function allele E(z)3 EMS 2 gain-of-function allele E(z)4 EMS 2 gain-of-function allele E(z)5 NNG l(3)1902 3, 4 E(z)6 EMS l(3)GST311 3 E(z)7 EMS l(3)MK436 3 E(z)8 EMS l(3)MM130 3 E(z)9 EMS l(3)MM634 3 E(z)10 EMS l(3)MM701 3 E(z)11 | EMS l(3)MR127 3, 4 unconditional female sterile E(z)12 EMS l(3)MY939 3, 4 E(z)13 EMS l(3)MZ1007 3, 4 E(z)14 EMS l(3)NH006 3, 4 E(z)15 EMS l(3)NU808 3, 4 E(z)16 EMS l(3)NV931 3, 4 E(z)17 EMS l(3)NW522 3, 4 E(z)18 EMS l(3)NY721 3 E(z)19 EMS l(3)OA001 3 E(z)20 EMS l(3)OD522 3 E(z)21 EMS l(3)OP813 3 E(z)22 EMS l(3)OQ626 3 E(z)23 EMS l(3)OR030 3 E(z)24 EMS l(3)OS628 3 E(z)25 EMS l(3)OT502 3 E(z)26 EMS l(3)OU511 3 E(z)27 EMS l(3)OW105 3 E(z)28 | EMS l(3)OX736 3 E(z)29 EMS l(3)OZ440 3 E(z)30 EMS l(3)OZ1340 3 E(z)31 EMS l(3)PB901 3 E(z)32 EMS l(3)PC025 3 E(z)33 EMS l(3)PI1517 3 E(z)34 EMS l(3)PK911 3 E(z)35 EMS l(3)PQ1129 3 E(z)36 EMS l(3)PU620 3 E(z)37 EMS l(3)PW111 3 E(z)38 EMS l(3)PX338 3 E(z)39 EMS l(3)PX811 3 E(z)40 EMS l(3)QH527 3 E(z)41 EMS l(3)QN916 3 E(z)42 EMS l(3)QO703 3 E(z)43 EMS l(3)QO1407 3 E(z)44 EMS l(3)QW206 3 E(z)45 EMS l(3)RC318 3 E(z)46 EMS l(3)RF306 3 E(z)47 EMS l(3)SD121 3 E(z)48 EMS l(3)SO230 3 E(z)49 EMS l(3)UO573 3 E(z)50 EMS l(3)US53 3 E(z)51 EMS l(3)VL151 3 E(z)52 EMS l(3)VM7 3 E(z)53 EMS l(3)VS528 3 E(z)54 EMS l(3)VT244 3 E(z)55 EMS l(3)VT329 3 E(z)56 EMS l(3)VY141 3 E(z)57 EMS l(3)VZ416 3 E(z)58 EMS l(3)WA86 3 E(z)59 EMS l(3)WB68 3 E(z)60 EMS E(z)S1 5 antimorphic allele Su(z)301 E(z)61 EMS E(z)S2 1, 5 cytology normal E(z)62 EMS E(z)S3 1 cytology normal E(z)63 EMS E(z)S4 1 cytology normal E(z)64 EMS E(z)S5 1 cytology normal E(z)65 / ray of E(z)1 E(z)1R1 1 T(2;3)21C1-2;67E3-4 E(z)66 / ray of E(z)1 E(z)1R4 1 cytology normal E(z)67 / ray of E(z)1 E(z)1R5 1 cytology normal E(z)68 / ray of E(z)1 E(z)1R6 1 In(3L)64E-F;75C-76B E(z)69 / ray of E(z)1 E(z)1R7 1 cytology normal E(z)70 / ray of E(z)1 E(z)1R8 1 cytology normal E(z)71 / ray of E(z)1 E(z)1R10 1 cytology normal E(z)72 / ray of E(z)1 E(z)1R11 1 cytology normal E(z)73 / ray of E(z)1 E(z)1R14 1 cytology normal E(z)74 / ray of E(z)60 E(z)S1R2 1 cytology normal E(z)75 / ray of E(z)60 E(z)S1R3 1 cytology normal ( 1 = Jones and Gelbart, 1990, in press. 2 = Kalisch and Rasmuson, 1974, Hereditas 78: 97-103. 3 = Shearn, Her- sperger, and Hersperger, l978, Genetics 89: 341-53. 4 = Shearn, Hersperger, Hersperger, Pentz, and Denker, 1978, Genetics 89: 355-70. 5 = Wu, Jones, Lasko, and Gelbart, 1989, Mol. Gen. Genet. 218: 559-64. | Heat sensitive alleles. cytology: Placed in 67E3-4 based on its inclusion in the region of overlap of Df(3L)Ez6 = Df(3L)67E1-2;67E3-5 and Df(3L)Ez3 = Df(3L)67E3-4;67E6-7, as well as on the breakpoint to T(2;3)E(z)65 = T(2;3)21C1-2;67E3-4. molecular biology: Region cloned by Jones. P-element mediated germline transformation of 9 kb fragment of DNA rescues all mutant phenotypes. Single 2.5-kb transcript expressed throughout development but most abundant in maternal mRNA. Approximately 1 kb proximal and in opposite transcriptional orientation to hay transcription unit.