# en: engrailed (T.Kornberg) location: 2-62. references: Eker, 1929, Hereditas 12: 217-22. Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801. Kornberg, 1981, Proc. Nat. Acad. Sci. USA 78: 1095-99. Eberlein and Russell, 1983, Dev. Biol. 100: 227-37. phenotype: Four classes of alleles, all recessive. (1) en1. Viable hemizygous and homozygous; fertile. Longi- tudinal cleft extends from rear border of scutellum forward, may be reduced to median nick or posterior flattening of scu- tellum. Wings larger, broader, and thin textured with spatu- late end; venation and distribution of sensilla abnormal in posterior wing compartment. Variable duplication of anterior triple row bristles on posterior margin; alula reduced, with costal-like bristles. In males, extra sex comb often present (Brasted, 1941, Genetics 26: 347-73), smaller than normal, and in mirror-image position in posterior compartment. Dupli- cations of transverse rows in female prothoracic leg, extra bristles in mesothoracic and metathoracic tarsi (Garcia- Bellido, and Santamaria, 1972, Genetics 72: 87-104; Lawrence, Struhl, and Morata, 1979, J. Embryol. Exp. Morph. 51: 195- 208). Action of en1 is autonomous except for scutellar cleft (Tokunaga, 1961, Genetics 46: 157-76; Stern and Tokunaga, 1968, Proc. Nat. Acad. Sci. USA 60: 1252-59; Garcia-Bellido, and Santamaria, 1972, Genetics 72: 87-104). Clones of en cells of posterior compartment origin fail to respect anterior-posterior compartment border in wing disc as do mwh clones in wing discs of en1 homozygotes (Morata and Lawrence, 1975, Nature 255: 614-17; Morata and Lawrence, 1976, Dev. Biol. 50: 321-37). en abnormalities are associated with pos- terior compartment structures only, except for scutellar cleft. Restriction of glucose-6-phosphate dehydrogenase, 6- phosphogluconate dehydrogenase (Cunninghamn, Smith, Makowski, and Kuhn, 1983, Mol. Gen. Genet. 191: 238-43) and of a pro- tein recognized by monoclonal antibody PS2 (Brower, 1984, Nature 310: 496-98; 1987, EMBO J. 5: 2649-56) to posterior compartment of wing disc altered by en1. Interaction with ci, cg, sx (House, 1953, Genetics 38: 200-15; House, 1953, Genetics 38: 309-27; House, 1961, Genetics 46: 871; Mukher- jee, 1965, Genetics 51: 285-304; Datta and Mukherjee, 1971, Genetics 68: 269-86) and fu (Fausto-Sterling and Smith- Schiess, 1982, EMBO J. 1: 827-33) partially increase pheno- type. No suppression by su(Hw). (2) Lethal alleles with normal cytology. Embryonic lethal. Anterior margin of each segment defective. Pair rule defects in naked cuticle of T1, T3, A2, A4, A6, A8 result in pair-wise fusion of adjacent segments. Autonomous effects in adult cuticular clones observed in posterior compartment of pro- boscis, thorax, abdomen, and genitalia. enlethal clones are without effect in anterior compartments and in eye-antennal region (Kornberg, 1981, Proc. Nat. Acad. Sci. USA 78: 1095- 99; Kornberg, 1981, Dev. Biol. 86: 363-72; Lawrence and Struhl, 1982, EMBO J. 1: 827-33). The en1/enlethal heterozy- gote characterized by wing abnormalities only; disruption of anterior crossvein, gap in vein IV, and occasional socketted bristles on posterior margin. In some combinations complemen- tation is complete or nearly so (Condie and Brower, 1989, Dev. Biol. 135: 31-42). No maternal effect (Lawrence, Johnston and Struhl, 1983, Cell 35: 27-34). (3) Deficiencies and lethal alleles with inversion or translocation breakpoints. Embryonic lethal. Embryonic seg- ment defects slight and variable. Alleles of this class in heterozygous combination witn en1 produce adults more extreme than en1. For example, in en1/en2, legs are truncated, the tarsi reduced to densely bristled stumps; wings are greatly enlarged and spatulate with greater disruption of veins IV and V; higher penetrance of socketed bristles along the posterior margin. Extreme scutellar cleft. At 29, duplication of ante- rior compartment bristles in mirror-image symmetry in poste- rior compartment of second antennal segment (Morata, Kornberg, and Lawrence, 1983, Dev. Biol. 99: 27-33). (4) Non-lethal alleles with breakpoints. Hemizygous viable, embryos normal. Heterozygous with other allele classes, vari- able gaps in wing veins IV and V. Variable reductions or deletions in male and female genitalia (Epper and Sanchez, 1983, Dev. Biol. 100: 387-98). Scutellum may also be affected. allele origin discoverer synonym ref ( comments | ________________________________________________________________________ en1 spont Evang 26k7 1, 3 viable; 7 kb insert at 0 kb en2 EMS Kornberg enC2 2, 3 lethal; In(2R)47A;48A; breakpoint at -0.0 to 2.7 kb en3 EMS Kornberg enLA3 2, 3 viable; T(2;3)48A;96C; breakpoint at 25.3 to 34.2 kb en4 EMS Kornberg enLA4 2, 3 lethal en5 EMS Kornberg enLA5 2 en6 EMS Kornberg enLA7 2 en7 EMS Kornberg enLA9 2 en8 EMS Kornberg enLA10 2 en9 EMS Kornberg enLA11 2 en10 EMS Kornberg enLA12 2 en11 EMS Kornberg enLA13 2 en12 EMS Kornberg enLA14 2 en13 EMS Kornberg enLA15 2 en14 EMS Kornberg enLA16 2 en15 EMS Kornberg enLA17 2 en16 EMS Kornberg enLA18 2 en17 / ray Kornberg enSF/1 2 en18 HOOH Kornberg enSFH1 2 en19 HOOH Kornberg enSFH2 2 en20 HOOH Kornberg enSFH3 2 en21 HOOH Kornberg enSFH4 2 en22 HOOH Kornberg enSFH5 2 en23 HOOH Kornberg enSFH6 2 en24 HOOH Kornberg enSFH7 2 en25 HOOH Kornberg enSFH8 2 en26 HOOH Kornberg enSFH9 2 en27 HOOH Kornberg enSFH10 2 en28 HOOH Kornberg enSFH11 2 en29 HOOH Kornberg enSFH12 2 en30 HOOH Kornberg enSFH13 2 en31 HOOH Kornberg enSFH14 2 lethal en32 X ray Kornberg enSFX1 2 lethal en33 X ray Kornberg enSFX12 2 en34 X ray Kornberg enSFX24 2, 3 lethal; T(2;3)48A;90C; breakpoint at 2.7 to 12.0 kb en35 X ray Kornberg enSFX26 2 en36 X ray Kornberg enSFX29 2 en37 X ray Kornberg enSFX30 2 lethal en38 X ray Kornberg enSFX32 2, 3 T(Y;2)48A; breakpoint at -4.2 to -1.0 kb en39 X ray Kornberg enSFX33 2 en40 X ray Kornberg enSFX34 2 en41 X ray Kornberg enSFX35 2 en42 X ray Kornberg enSFX36 2 en43 X ray Kornberg enSFX37 2, 3 Tp(2;3)46C;48A;80-81; breakpoints at -33.9 to -28.0 kb and 2.7 to 12.0 kb en44 X ray Kornberg enSFX38 2 en45 X ray Kornberg enSFX39 2 en46 X ray Kornberg enSFX40 2 en47 X ray Kornberg enSFX42 3 lethal; T(2;3)48A;65F; breakpoint at -15.2 to -10.6 kb en48 X ray Kornberg enSFX49 3 lethal; In(2R)47F;48A3-4; breakpoint at -15.2 to -10.6 kb en49 X ray Kornberg enSFX50 3 lethal; T(2;3)48A;57A;81A breakpoint at -4.7 to -1.0 kb en50 X ray Kornberg enSFX52 3 lethal; T(2;3)48A;57B;88F; breakpoint at -33.9 to -28.0 kb en51 X ray Kornberg enSFX61 3 lethal; T(2;3)48A;89A3;96B; breakpoint atl 13 to 20.5 kb en52 X ray Kornberg enSFX62 3 viable; T(2;3)48A;84D; breakpoint at -15.2 to -10.6 kb en53 X ray Kornberg enSFX63 3 breakpoint at -10.6 to -5.4 kb en54 EMS enIIB 5, 6 en55 EMS enIIIB 5, 6 en56 EMS enIIT 5, 6 en57 EMS enIK 5, 6 en58 EMS enIM 5, 6 en59 EMS enIO 5, 6 enEs X ray Baker 3, 4 viable; T(2;3)48A;84D; breakpoint at 25.3 to 34.2 kb ( 1 = Eker, 1929, Hereditas 12: 217-22; 2 = Kornberg, 1981, Proc. Nat. Acad. Sci. USA 78: 1095-99; 3 = Kuner, Nakan- ishi, Ali, Drees, Gustavson, Theis, Kornberg, and O'Farrell , 1985, Cell 42: 309-16; 4 = Lindsley, Sandler, Baker, Car- penter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero, 1972, Genetics 71: 157-84; 5 = Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801; 6 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. | Origin of molecular coordinates defined as the insertion site in en1; minus values to the left. cytology: Placed in 48A3-4, based on two inversion and eleven translocation breakpoints. molecular biology: 225 kb of genomic DNA proximal to tRNA-Met2 at 48B5-7 (Poole, Kauver, Drees, and Kornberg, 1985, Cell 40: 37-43) was used to locate en rearrangements. Gene also isolated directly from genomic library using Ubx homeobox probe (Fjose, McGinnis, Gehring, 1985, Nature 313: 284-89). en1 is associated with a 7-kb insertion of a middle-repetitive DNA element (defined as molecular coordinate 0 with negative values to the left). Lethal breakpoints span the en1 inser- tion from -35 kb proximally to +10 kb distally; non-lethal breakpoints are at +15 to +35 (Kunner, Nakanishi, Ali, Drees, Gustavson, Theis, Kauvar, Kornberg and O'Farrell, 1985, Cell 42: 309-16). Subclones from -20 to -12 detect transcripts of 1.4, 2.7 and 3.6 kb on Northern blots of RNA from embryos (high abundance), larvae, and pupae (low abundance), but not from adults; the abundance of the 2.7-kb species is ten times that of the other two in all stages investigated. Sequence determinations reveal a 1700-nucleotide open reading frame within which a polypeptide of 562 amino-acids and approxi- mately 60 kd is encoded. The initial transcript contains introns of 1.1 and 0.28 kb, the latter one being 3 to the first and interrupting a homeobox encoding domain. The homeo- box sequence diverges significantly from those at ftz, Antp, and Ubx, the latter displaying closer homology to human homeo- box sequences than they do to the en homeo domain. In addi- tion, in the 5 end of the gene there is a concentration of the repeating CAA and CAG as well as other single-amino-acid runs throughout the sequence (Poole, Kauvar, Drees, and Korn- berg, 1985, Cell 40: 37-43). Transcription occurs from the right to left (Drees, Ali, Soeller, Coleman, Poole, and Korn- berg, 1987, EMBO J. 6: 2803-09). en protein binds to clus- ters of sequences located upstream from the en transcription- start site; both en and ftz gene products compete for the con- sensus sequence TCAATTAAAT (Desplan, Theis, and O'Farrell, 1985, Nature 318: 630-35; Jaynes and O'Farrell, 1988, Nature 336: 744-49; Desplan, Theis, and O'Farrell, 1988, Cell 54: 1081-90). Shown to form stable polyprotein DNA-binding complex with other soluble proteins in the nucleus (Gay, Poole, and Kornberg, 1988, EMBO J. 4291-97). The developmental and spatial program of en expression determined by immunolo- calization of its protein product (DiNardo, Kuner, Theis, and O'Farrell, 1985, Cell 43: 59-69; Karr, Weir, Ali, and Korn- berg, 1989, Development 105: 605-12). Engrailed protein is first detectable in Western blots in the precellular blasto- derm; at the initiation of cellularization a low level of pro- tein distributed uniformly in embryo; as cellularization proceeds, the protein becomes concentrated in the second and fifth sixths of the egg length; subsequently stripes become more numerous and narrower, filling the central third of the embryo with stripes, first in even-numbered segments and then in every segment. At the onset of gastrulation; the cellular blastoderm exhibits fourteen one-cell-wide stripes of en expression; each stripe defines the anlagen of the posterior compartment of a metameric segment and the anterior paraseg- ment boundary. At full germ-band extension en expressed in labial, maxillary, mandibular primordia, in three thoracic, and nine abdominal segments. Cell movements in head and tail regions lead to complex distributions of expressing cells. Subsets of cells in the ventral nervous system also seen to be expressing en at ten hours of development. As expected for a DNA-binding protein, en antigen accumulates in nuclei. In third-instar larvae en expression observed in presumptive pos- terior compartments of imaginal discs and in discrete cells in the ventral ganglion of the larval brain (Brower, 1987, EMBO J. 5: 2649-56). Expression of en positively controlled by ftz, eve, and prd; modulated by h, odd, opa, and run (Weir, and Kornberg, 1985, Nature 318: 433-39; Harding, Rushlow, Doyle, Hoey, and Levine, 1986, Science 233: 953-59; Howard, and Ingham, 1986, Cell 44: 947-57; DiNardo, and O'Farrell, 1987, Genes Dev. 1: 1212-25; Ingham, Baker, and Martinez- Arias, 1988, Nature 331: 73-75; Martinez-Arias, and White, 1988, Development 102: 325-28). # en-we: see e(we) # En-bx: see E(bx) # engrailed-related: see inv # enhancer: see e( ) # Enhancer: see E( ) # Enhancer-of-split mimic: see Esm # Eno: Enolase location: 2-{3}. references: Bishop, and Corces, 1990, Nucleic Acids Res. 18: 191. phenotype: Structural gene for enolase [2-phospho-D-glycerate hydrolase (EC 4.2.1.11)]. cytology: Placed in 22A by in situ hybridization. molecular biology: Isolated from genomic library using cloned rat sequence. Coding sequence lacks introns; specifies a 433-amino-acid, 46,563-dalton polypeptide. # eo: extra organs location: 1-{66}. references: Schalet and Lefevre, l973, Chromosoma 44: 183-202. Schalet and Lefevre, 1976, The Genetics and Biology of Droso- phila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902. Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31. phenotype: Homozygous lethal; in rare surviving genotypes, a leg may be branched or completely duplicated, an antenna or arista duplicated, or triplicated; eyes and wings malformed; usually only eye effect present. Phenotype expressed in pres- ence of y+Ymal126. Homozygous germ-line clones are maternal- effect lethals; eo25 clones produce embryos with head defects and ventral holes; rescuable by eo+ sperm. eo1 and eo28 clones produce embryos that are U-shaped as a result of incom- plete germ-band retraction; have poor cuticle differentiation and ventral holes. eo27 clones also form ovarian tumors after approximately six days. alleles: allele origin discoverer synonym ref ( comments ___________________________________________________________________ eo1 3HT Kaplan l(1)A7 6, 8, 9 larval lethal; maternal-effect lethal eo2 X ray Lifschytz l(1)B3 3, 4 eo3 X ray Lifschytz l(1)B145 4 eo4 l(1)E3 eo5 l(1)E6 eo6 EMS Lifschytz l(1)E54 4, 8, 9 eo7 EMS Lifschytz l(1)M112 5 on y+Ymal+ eo8 Himoe l(1)N30 eo9 l(1)P313 eo10 l(1)P414 eo11 EMS Lifschytz l(1)R-9-4 4 eo12 EMS Lifschytz l(1)R-9-12 4 eo13 EMS Lifschytz l(1)R-9-20 4 eo14 EMS Lifschytz l(1)R-9-22 4 eo15 EMS Lifschytz l(1)R-9-30 4 eo16 EMS Lifschytz l(1)R-10-2 4 eo17 EMS Lifschytz l(1)R-10-12 4 eo18 EMS Lifschytz l(1)R-10-13 4 eo19 X ray Lefevre l(1)C120 1 eo20 X ray Lefevre l(1)GA109 1 eo21 X ray Lefevre l(1)KC18 1 eo22 X ray Lefevre l(1)L63 1 eo23 EMS Lefevre l(1)DA602 2 eo24 EMS Lefevre l(1)DC712 2 eo25 EMS Lefevre l(1)DC726 2, 6 embryonic-to-larval lethal eo26 EMS Lefevre l(1)DC801 2, 6 eo27 EMS Lefevre l(1)EA13 2, 6 larval lethal; maternal-effect lethal eo28 spont Schalet l(1)17-44-2 6, 7 pupal lethal; some escapers l(1)eoS1 maternal-effect lethal eo29 spont Schalet l(1)17-252 7 l(1)eoS2 eo30 P Gergen l(1)4-2 10 eo31 P Gergen l(1)47-1 6, 10 eo32 P Gergen l(1)51-1 10 eo33 l(1)17-36 6 eo34 l(1)17-260 6 ( 1 = Lefevre, l981, Genetics 99: 461-80; 2 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 3 = Lifschytz and Falk, l968, Mut. Res. 6: 235-44; 4 = Lifschytz and Falk, l969, Mut. Res. 8: 147-55; 5 = Lifschytz and Yakobovitz, l978, Mol. Gen. Genet. 161: 275-84; 6 = Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31. 7 = Schalet, 1986, Mutat. Res. 163: 115-44; 8 = Schalet and Lefevre, l973, Chromosoma 44: 183-202; 9 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902; 10 = Zusman, Coulter, and Gergen, 1985, DIS 61: 217-18. cytology: Placed in 20A1-2 based on its inclusion in Df(1)B12 = Df(1)19E1;20A1-2 and Df(1)JC4 = Df(1)20A1;20E-F. # Epa: see Cos1 # Epidermal growth factor receptor homologue: see Egfr # eq: equational producer location: 1- (to the right of car, probably heterochromatic). origin: X ray induced. discoverer: Schultz, 33a2. references: Morgan, Bridges, and Schultz, 1934, Year Book - Carnegie Inst. Washington 33: 280. phenotype: Produces 1-2% equational nondisjunction of X's in male, producing both X/X and nullo-X, nullo-Y sperm. Original eq male when crossed to attached-X female produced 89/289 equational exceptional X/X daughters. Claimed to generate bb-deficient Y chromosomes. More recent experiments (Valentin, 1984, Hereditas 101: 115-17) produce an order of magnitude fewer equational exceptions from males; none from homozygous females. cytology: Both salivary and mitotic chromosomes appear normal. # eql: equatorial-less (J.C. Hall) location: 2-right arm near bw. origin: Induced by ethyl methanesulfonate. discoverer: Ransom. references: Campos-Ortega, 1980, Current Topics in Developmen- tal Biology 15: 347-71. phenotype: Recessive lethal; in homozygous mutant clones in mosaic eyes, ommatidia lack one, two, or three photoreceptor cells from among two specific outer cells in a given facet (R1, R6) and a specific inner cell (R7). alleles: Two mutant alleles, eql1 and eql2 (published as eqllff40 and eqllff225, respectively), the latter of which is more severe in its effects, often removing three photorecep- tors from each facet instead of one or two. cytology: Not uncovered by Df(2R)bw5. # er: erupt location: 3-71 (60.7 to 80.7; not an allele of k). origin: Spontaneous. discoverer: Glass, 1941. references: 1943, DIS 17: 50. 1944, Genetics 29: 436-46. 1957, Science 126: 683-89 (fig.). phenotype: Exhibits eruption of underlying hypodermis in center of one or both eyes. Eruption may be segmented and have hairs. Less extreme expression produces derangement of cen- tral or anterior-central facets. Eruption may occur as encroachment of chitin with bristles and hairs into anterior edge of eye. Extra tissue derived from eye portion of eye- antennal disk (Aubele, 1968, DIS 43: 139). RK2. other information: Alleles of at least five different strengths present in different wild stocks. Present in many wild stocks in suppressed condition. #*Er: Erect location: 3-50. origin: Spontaneous. discoverer: Neel, 41c9. references: 1942, DIS 16: 50. phenotype: Posterior scutellars at greater than normal angle with body, vary from slight effect to conditions in which bristles stand at right angles to scutellum. In latter case, bristles usually appear warped and twisted. Wings incom- pletely expanded and crinkled to varying degrees. RK3. # Erased: see enEs # Erect: see Er # erect wing: see ewg # err: erratic (T. Schupbach) location: 2-40. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal effect lethal; embryos from homozygous mothers have variable cuticular defects and holes. alleles: err1, isolated as errRE. cytology: Placed in 31B-32A based on lethality over Df(2L)J27 = Df(2L)31B-D;31F-32A. # erupt: see er # es: ether sensitive location: 2- (not located). origin: Spontaneous. discoverer: Tinderholt. references: Kidd, 1963, DIS 37: 49. phenotype: Hypersensitive to diethyl ether and chloroform. Homozygotes killed by exposure to doses of these agents harm- less to normal flies. Sensitivity probably affected by modif- iers. A male sterility factor seems to be associated but may be separable. Viability of homozygote about 70% that of es/SM1 and remains low in strains selected for less sensi- tivity. Not sensitive to carbon dioxide. RK3. # Es: see enEs # esc: extra sex combs location: 2-{47}. discoverer: Slifer, 40e2. references: 1942, J. Exp. Zool. 90: 31-40 (fig.). Struhl, 1981, Nature (London) 293: 36-41 (fig.). phenotype: Distal portions of second and third legs weakly transformed into first leg and wing blade into haltere; transformation partial and variable in hypomorphic allele, esc1. Sex combs may be present on all six legs of male; at least one extra sex comb present in majority of males. Expression affected by culture conditions. When expressivity high, extra transverse bristle rows appear between sixth and eighth longitudinal rows of bristles, mainly on distal portion of basitarsus and tibia of second and third legs in both sexes; accompanied by shortening of affected leg segments. Sex comb development autonomous in mosaics produced by somatic crossing over [Tokunaga and Stern, 1965, Dev. Biol. 11: 50-81 (fig.)]. For interactions with Pc and Scx see Hannah-Alava [1958, Genetics 43: 878-905 (fig.)]. Leg effects autonomous in homozygous clones of hypomorphic or amorphic alleles. Stu- dies with amorphic alleles demonstrate that esc offspring of esc/+ mothers express the leg transformation, but esc zygotes produced by esc mothers die as newly hatched larvae that exhi- bit drastic homeotic transformations. All abdominal and thoracic and some head segments are transformed into eighth abdominal segments. The effects of the maternal insufficiency partially overcome by the presence in the zygote of a pater- nally derived esc+ allele, more so by two paternally derived esc+ alleles. Larvae with one paternal esc+ range between normal and transformed phenotype; those with two frequently develop into adults, more than half of which show patchy transformations in abdominal and thoracic segments to more posterior segments. Temperature-shift experiments with the temperature-sensitive allele, esc17 (i.e., on the esc/esc pro- geny of esc17/esc mothers when crossed to esc fathers) indi- cate that esc+ product is required only around the time of gastrulation, as that is the only temperature-sensitive period (Struhl and Brower, 1982, Cell 31: 285-92). In the presence of extreme BXC deficiencies (including abdA-, AbdB-, and abdA- AbdB-) which transform the eighth abdominal segment to more anterior segments, esc+ product insufficiency in the zygote causes all segments to develop as the eighth abdominal segment would develop under the influence of the BXC genotype in the presence of esc+ product (Struhl, 1981; Struhl and White, 1985, Cell 43: 507-19). In the esc- embryo produced by esc2/esc10 parents, Ubx transcription is normal early in development, but following gastrulation transcripts appear in ectodermal and mesodermal derivatives of all fourteen paraseg- ments rather than being restricted to parasegments 6-12 as in wild-type (Struhl and Akam, 1985, EMBO J. 4: 3259-64). esc- embryos display reduced levels of Antp protein to levels below those of wild-type in all segments of the nervous system (Car- roll, Laymon, McCutcheon, Riley, and Scott, 1986, Cell 47: 113-22). alleles: alleles origin discoverer synonym ref ( comments _________________________________________________________________ esc1 spont Slifer, 40e2 1, 3 hypomorph *esc2 | spont Stromnaes, 53f escD 1, 2 In(2L)t esc2 spont Struhl 4 amorph in CyO esc3 Struhl 4 amorph esc4 Struhl 4 amorph esc5 Struhl 4 amorph esc6 Struhl 4 amorph esc7 Struhl 4 amorph esc8 Struhl 4 amorph esc9 Struhl 4 amorph esc10 Struhl 4 380 kb deletion esc11 EMS Struhl 5 esc12 EMS Struhl 5 esc13 EMS Struhl 5 esc14 EMS Struhl 5 esc15 EMS Struhl 5 esc16 EMS Struhl 5 esc17 EMS Struhl escts 5 temperature-sensitive esc18 EMS Struhl 5 esc19 EMS Struhl 5 esc20 EMS Struhl 5 esc21 EMS Struhl 5 ( 1 = CP627; 2 = Hannah and Stromnaes, 1955, DIS 29: 121-23; 3 = Slifer, 1942, J. Exp. Zool. 90: 31-40; 4 = Struhl, 1981, Nature (London) 293: 36-41; 5 = Struhl and Brower, 1982, Cell 31: 285-92. | Erroneously designated a dominant allele in CP627. cytology: Placed in 33B1-2 based on Df(2L)esc10, a 380-bp dele- tion (coordinates -315 to +65) deficient for those two bands (G. Richards). molecular biology: Region cloned by walking from sequences cloned from microdissected chromosomes (Frei, Baumgartner, Edstrom and Noll, 1985, EMBO J. 4: 979-87). Transformation experiments restrict locus to a 12-kb fragment from around coordinate -70 kb (0 = left end of a 44-kb EcoRI fragment from the walk; negative values to the left); the 12-kb fragment detects a single transcript of 1.8-kb, which is most abundant in follicles and 0-4 hr embryos, but is drastically reduced in later stages. Genomic sequences homologous to the transcript lie entirely within the segment from -67.8 to -64.6 kb. cDNA's identify the 3 end and a 364-base-pair intron, but not the 5 end of the transcript; transcription from right to left (Frei, Bopp, Burri, Baumgartner, Edstrom and Noll, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 127-34). # Esm: Enhancer-of-split mimic location: 3-{81}. references: Knust, Dietrich, Weigel, Tepass, Vassin, Bremer, and Campos-Ortega, 1987, J. Neurogenet. 4: 145-46). cytology: Tentatively placed in 95F. molecular biology: May carry EGF-like repeats. # Est-6: Esterase 6 location: 3-35.9 [based on 334 recombinants between h and th (Franklin, 1971, DIS 47: 113)]. discoverer: Wright, 61h. synonym: Est-D. references: 1963, DIS 37: 53. 1963, Genetics 48: 787-801 (fig.). phenotype: The structural gene for the nonspecific carboxy- lesterase, [EST-6 (EC 3.1.1.1)]. One of the ten positively migrating esterases demonstrable with (-naphthyl acetate and Fast Blue BB after starch gel electrophoresis of homogenates. Molecular weight determinations on purified enzyme indicate that the active enzyme is a 62,000 to 65,000 dalton glycopro- tein monomer (Mane, Tepper, and Richmond, 1983, Biochem. Genet. 21: 1019-40). Substrate specificities to different esters explored by Danford and Beardmore (1979). Specific EST-6 activity during development shows a prominant transient peak during second larval instar and shows a male-specific rise in activity beginning 36-48 hr after eclosion; males reach level double that of females (Sheehan, Richmond, and Cochrane, 1979, Insect Biochem. 9: 443-50); similar high lev- els found in male-like triploid intersexes (Aronshtam and Kuzin, 1974, Zh. Obsch. 35: 926-33) and X/X;tra/tra (Johnson, 1964, Genetics 50: 259). High concentrations of EST-6 found in ejaculatory duct; at mating, male level depleted and female level enhanced; transfer of activity from male to Est-60 female detected early during copulation, prior to the transfer of sperm, indicating that EST-6 is a component of seminal fluid (Richmond, Gilbert, Sheehan, Gromko, and Butterworth, 1980, Science 207: 1483-85). Enzyme levels in flies carrying different X chromosomes from natural populations in combina- tion with constant autosomal complement vary suggesting X- linked modifiers (Tepper, Richmond, and Terry, 1981, Genetics 97: s103). In D. melanogaster X D. simulans hybrid males that carry a D. melanogaster X chromosome, the level of the D. melanogaster enzyme is reduced compared to that of the D. simulans enzyme; hybrid females have equivalent activities of the two enzymes (Korchkin, Aronshtam, and Matveeva, 1974, Biochem. Genet. 12: 9-24). Electrophoretic mobility reduced modestly from 1.10 to 1.08 for Est-6F and from 1.0 to 0.98 for Est-6S by m(Est-6) on the third chromosome (Cochrane and Rich- mond, 1979, Biochem. Genet. 17: 167-83). alleles: Allelic variation in Est-6 is expressed in electrophoretic mobility (complicated by heterogeneity for m(Est-6) on chromosome 3), thermal stability, and level of activity. The same alleles have been designated differently by different authors. The accompanying table attempts to define the equivalences. Some use electrophoretic mobility relative to that of Est-6S = 1.00 in designating alleles. Relative mobility estimates vary within and among gels; also relations between mobilities on starch and acrylamide are non- linear; consequently, similar but not identical estimates may not represent real differences. thermal possible relative denaturation allele equivalence mobility constant ref ( ______________________________________________________________ Est-60 | 3 Est-60.73 0.73 5 Est-60.79 0.79 5 Est-60.95 Est-6S m(Est-6) 0.95 2 Est-60.97 Est-6S m(Est-6) 0.97 4 Est-61.07 Est-6F m(Est-6) 1.07 4 Est-61.11 Est-6F 1.11 4 Est-61.15 1.15 1 Est-61.25 1.25 2 Est-6F1 1.10 -.0458 1 Est-6F2 1.10 -.0811 1 Est-6F3a 1.10 -.0959 1 Est-6F36 1.10 -.123 1 Est-6F4 1.10 -.158 1 Est-6S1 1.0 -.0245 1 Est-6S2 1.0 -.0615 1 Est-6S3 1.0 -.0727 1 Est-6Slo / 1.0? 6 Est-6VF 1.21 4 Est-6VS 0.85 4 ( 1 = Cochrane and Richmond, 1979, Genetics 93: 461-78; 2 = Franklin, 1971, DIS 47: 113; 3 = Johnson, 1964, J. Hered. 55: 76-8; 4 = Rodin' and Danieli, 1972, DIS 48: 77; 5 = Triantaphillidis and Christodoulou, 1973, Biochem. Genet. 8: 383-90; 6 = Trippa, Scozzari, Costa, and Danieli, 1979, Egypt. J. Genet. 8: 295-302. | Contains insert of 412. / Requires 3-4 times normal incubation time to detect activity. cytology: Placed in 69A1-5 based on its inclusion within Df(3L)vin-5 = Df(3L)68A3;69A1-2, but not Df(3L)vin-6 = Df(3L)68C8-11;69A4-5 (Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215-25). Further localized to 69A by in situ hybridization (Oakeshott, Collet, Phillis, Nielsen, Russell, Chambers, Ross, and Richmond, 1987, Proc. Nat. Acad. Sci. USA 84: 3359-63). molecular biology: Gene isolated by screening a cDNA library with oligonucleotide probes based on tryptic-peptide amino- acid sequences (Oakeshott et al.). The 1.85-kb cDNA clone sequence is contained within a 2.3-kb EcoRI-BamHI genomic fragment. One strand of the cDNA clone hybridizes to mRNA's of 1.68 and 1.83 kb. Developmental profiles of transcripts concordant with that of EST-6; transcripts absent in Est-60 adults. Conceptual amino acid sequence of larger transcript suggests a signal peptide of 21 amino acids followed by 527 residues of the mature protein (59,380 daltons); potential glycosylation sites at residues -2, 21, 399, 435, and 485. Contains an eight-residue sequence with strong similarity to the consensus of active sites of nine other eukaryotic esterases. # Est-9 location: 2- (probably right arm based on apparent homology to and position of Est-9 in Drosophila pseudoobscura). references: Loukas, 1981, DIS 56: 85. phenotype: The apparent structural gene of an esterase whose detection depends on the presence of 1-leucyl-|-naphthylamide in addition to (-naphthyl acetate as substrate. alleles: Est-9F and Est-9S detected. # Est-A: Esterase A location: Not located. references: Mizianty and Case, 1972, J. Heredity 62: 345-47. phenotype: The most anodally migrating esterase band; migrates considerably in advance of EST-C. Activity weak in standard gel system. alleles: Est-A inferred from absence of band from Swedish-C wild stock; EST-A band present in Oregon-R. Presence and absence segregate as a single genetic character. # Est-C location: 3-47.7 [to the left of p (Ohnishi and Voelker, 1979, Jpn. J. Genet. 54: 203-209); 0.006 from Odh (Mukai and Voelker, 1977, Genetics 86: 175-85)]. references: Beckman and Johnson, 1964, Hereditas 51: 212-20 (fig.). phenotype: Specifies EST-C (EC 3.1.1.1), the next-to-most rapidly migrating of six anodally migrating esterases detect- able with (-napthyl acetate and Fast Blue BB following starch gel electrophoresis. Enzyme a monomer. Putative null alleles homozygous viable, consistent with failure to find lethal com- plementation group within the interval. alleles: Selected from natural populations. Since they were isolated from the same population, either Est-CnNC1 and Est-CnNC4, or Est-CnNC2 and Est-CnNC3, or Est-CnGB1 and Est-CnGB2 could represent reisolates of the same allele. cytology: Placed in 84D3-5 on the basis of its position between Df(3R)Scx4 = Df(3R)84B1-2;84D3-4 and Df(3R)D7 = Df(3R)84D3- 5;84F1-2 (Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23). relative relative allele synonym ref ( mobility activity _________________________________________________ Est-CF Est-C6 1, 2 1.00 Est-CnNC1 3 null Est-CNC2 3 0.91? low Est-CNC3 3 0.91? low Est-CnNC4 3 null Est-CnGB1 3 null Est-CnGB2 3 null Est-CS Est-C4 1, 2 0.91 Est-CVF Est-C8 2, 4 1.07 Est-CVS Est-C2 2 ( 1 = Beckman and Johnson, 1964, Hereditas 51: 212-20 (fig.); 2 = Johnson and Schaeffer, 1973, Biochem. Genet. 10: 149- 63; 3 = Langley, Voelker, Leigh Brown, Ohnishi, Dickson, and Montgomery, 1982, Genetics 99: 151-56; 4 = Triantaphillidis and Christadoulou, 1973, Biochem. Genet. 8: 383-90. # Est-D: see Est-6 # Etd: Eye tissue determiner location: 1-23 (approximate). origin: Spontaneous. references: Gethman, 1971, Mol. Gen. Genet. 114: 144-55. phenotype: Removes lower half of eye. # Eth: Ether resistant (J.C. Hall) location: 3-61. origin: Strain produced by 29 generations of selection. references: Ogaki, Nakashima-Tananka, and Murakami, 1967, Jpn. J. Genet. 42: 387-94. Gamo, Ogaki, and Nakashima-Tanaka, 1979, Jpn. J. Genet. 54: 229-34. Gamo, Nakashima-Tanaka, and Ogaki, 1980, Jpn. J. Genet. 55: 133-40. phenotype: The major determinant in a selected strain that is more resistant than usual to killing effects of ether vapors administered to adults; resistance dominant to sensitivity; minor factors on chromsomes 1 and 4; Eth-bearing strain also relatively resistant to killing effects of chloroform or halothane; these phenotypes are dominant and semidominant, respectively; chloroform resistance due to major factor on chromosome 1 and a minor one on chromosome 2; halothane resis- tance caused by major factor on third chromosome (not known if same locus as that responsible for most of the ether resis- tance), and minor components on chromosomes 1 and 2; halothane resistance also seen with respect to anesthesia, and genetic difference for this maps to chromosome 1. # ether-a-go-go: see eag # ether sensitive: see es # Etre: see Fs(2)Sz4 # Ets2: Ets-2 proto-oncogene homologue location: 2-{100}. references: Pribyl, Watson, McWilliams, Ascione, and Papas, 1988, Dev. Biol. 127: 45-53. phenotype: Encodes a Drosophila homologue to the ets gene from the avian erythroblastosis retrovirus E26. mRNA constitu- tively present in all developmental stages, with elevated lev- els of expression in 0-9-hr embryos and pupae. cytology: Placed in 58A-B by in situ hybridization. molecular biology: Genomic clone isolated using restriction fragment from a Drosophila Ets clone previously derived from Schneider cells. The sequence shows homology to the last two exons of chicken ets or mammalian ets-2 (as does v-ets from E26) with an intron of 63 base pairs separating the two exons; the intron is smaller in size, but identical in position to that of ets genes in other species. Ets sequences detect a single 4.7-kb mRNA on Northern blots. Between Drosophila Ets and v-ets, there is 71% homology at the nucleotide level and 91% at the predicted amino-acid level; these figures with respect to human ets-2 are 76% and 94%. # eve: even skipped location: 2-58. references: Nusslein-Volhard and Wieschaus, 1980, Nature (Lon- don) 287: 795-801 (fig.). Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.). Nusslein-Volhard, Kluding, and Jurgens, 1985, Cold Spring Har- bor Symp. Quant. Biol. 50: 145-54 (fig.). phenotype: Homozygous lethal; embryos homozygous for a null allele or a deficiency fail to undergo segmentation and their ventral surfaces are covered by a lawn of short denticles pointed toward the midline; denticles in the anterior region show thoracic characteristics suggesting that segmental iden- tities persist in the absence of segmentation. All deriva- tives of gnathal segments are missing, such as maxillary sense organs, cirri, mouth hooks, labial sense organs and the mandi- bular parts of the cephalopharyngeal skeleton; the labrum, antennal sense organs, and a rudimentary skeleton are the only remains of the larval head. Posteriorally, anal plates and some sensory organs persist as do remnants of spiracles, filzkorper, and tufts. Homozygotes and hemizygotes for hypo- morphic alleles display pair-rule segmentation defects. Den- ticle bands and adjacent naked cuticle of the prothoracic, metathoracic and even-numbered abdominal segments removed; some naked cuticle of the adjacent segment removed as well (i.e., the odd numbered parasegments are removed). Combina- tions of alleles with Df(2R)eve raised at different tempera- tures can achieve an array of phenotypes between these extremes. Expression of eve is first detected at the eleventh nuclear division following fertilization; at this stage, eve protein is uniformly distributed among the nuclei, both at the periphery and deep within the egg; by the thirteenth nuclear division, the anterior one-third of the embryo is devoid of detectable protein; over the next 20 minutes, the antibody staining in the posterior two-thirds of the embryo becomes concentrated in seven transverse stripes four or five cells wide separated by stripes three to four cells wide with lower levels of staining. By the time of germ-band elongation, the seven stripes have become narrowed and sharply defined and seven new weakly expressing stripes, one to two cells wide, appear between the major stripes; during germ-band elongation all stripes gradually disappear. As eve stripes become more sharply defined so too do ftz stripes, no longer overlapping eve stripes, but forming a complementary pattern. At the same time, a group of expressing cells appears at the posterior end of the germ band; these cells form a ring around the anal plate during germ-band shortening. Also during germ-band shortening, a specific subset of sixteen neurons in each hem- isegment of the CNS expresses eve product as does a row of cell clusters on either side of the dorsal midline; lateral to these clusters are curious rings of weakly staining cells; the dorsal cells do not appear to be neuronal (Frasch, Hoey, Rush- low, Doyle, and Levine, 1987, EMBO J. 6: 749-59; Frasch and Levine, 1987, Genes Dev. 1: 981-95). In homozygous eve1 embryos switched to restrictive temperature during neuro- genesis, four specifically studied eve-expressing neurons in each hemisegment are found to persist; two of them develop normally, but two send axonal processes to abnormal destina- tions [Doe, Smouse, and Goodman, 1988, Nature (London) 333: 376-78]. Frasch and Levine observe that segmentation- gene-mutations generally have reciprocal effects on the expression of eve and ftz, leading them to postulate that their promoters respond reciprocally to the same positional cues. eve concluded to be an early pair-rule gene, since its expression is modified by gap-gene mutations, but not by most other pair-rule gene mutations nor by segment-polarity gene mutations. Three pair-rule genes do influence eve expression: in either eve or h genotypes, eve expression is reduced and in run embryos eve is overexpressed (Frasch and Levine, 1987). In eve embryos, en stripes do not appear (Macdonald, Ingham, and Struhl, 1986, Cell 47: 721-34). Ubx protein is detected at high level in odd-numbered parasegments from 7 through 13 rather than in every parasegment from 6 through 12 (Martinez- Arias, and White, 1988, Development 102: 325-38). ftz stripes are disrupted in regularity of position, size, and timing (Carroll and Scott, 1986, Cell 45: 113-26). alleles: allele origin synonym ref ( comments ________________________________________________________________________ eve1 EMS ID19 1, 2, 3, 5 temperature-sensitive allele; 121arg -> his eve2 EMS IIR59 1, 2, 3, 5 weak allele; 75thr -> ile eve3 EMS R13 1, 4, 5 strong allele; -> no eve protein eve4 X ray 3.77.17 1, 5 intermediate allele; molecular deletion -> frame shift -> 134 C-terminal residues replaced by 79 extraneous ones ( 1 = Frasch, Warrior, Tugwood, and Levine, 1988, Genes Dev. 2: 1824-38; 2 = Nusslein-Volhard and Wieschaus, 1980, Nature (London) 287: 795-801 (fig.); 3 = Nusslein- Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.); 4 = Nusslein-Volhard, Kluding, and Jurgens, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 145-54 (fig.); 5 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. cytology: Placed in 46C3-11 based on Df(2R)eve = Df(2R)46C3- 4;46C9-11. molecular biology: Gene isolated based on homology to known homeobox sequences (Macdonald et al., 1986; Frasch et al., 1987). Probing Northern blots with the genomic sequence iden- tifies a single RNA species of 1.4 kb whose expression is strong during early embryogenesis, persisting at declining levels until first instar. Sequence data reveals the presence of a 71-bp intron between the initiating AUG and the homeobox; the conceptual amino-acid sequence defines a basic 40-kd polypeptide of 376 amino acids with a 60-amino acid homeobox domain extending from residue 70 to 130; the homeobox sequence shows only about 50% identity with those of previously sequenced homeoboxes. Repeats of the trinucleotide GCX are found in positions 564-608 producing a polyalanine sequence, as is also seen in en, N, and cad. Promoter fusion experi- ments utilizing a LacZ reporter gene identify promoter ele- ments for stripe 1 (tentative), stripe 3, and stripes 2 and 7 within 8 kb of upstream sequence; in addition a target for an autoregulatory function of eve protein identified in this region (Goto, Macdonald, and Maniatis, 1989, Cell 57: 413-22; Harding, Hoey, Warrior, and Levine, 1989, EMBO J. 8: 1205- 12). eve protein shown to repress Ubx transcription in vitro (Biggin and Tjian, 1988, Cell 58: 433-40); in DNA footprint studies eve protein can be shown to bind to specific sequences 5 to both en and eve, but the sequences in the two genes do not appear to have features in common [Hoey and Levine, 1988, Nature (London) 332: 858-61]. # ewg: erect wing (J.C. Hall) location: 1-0.0. references: Deak, 1978, Dev. Biol. 66: 422-41. Fleming, Zusman, and White, 1983, Dev. Genet. 3: 347-63. Fleming, DeSimone, and White, 1989, Mol. Cell Biol. 9: 719- 25. phenotype: Viable allele causes wings to be held upright; wing posture phenotype shows incomplete penetrance. Dorso-ventral flight muscles often absent, especially when the mutation is heterozygous with a deficiency. Ultrastructure of tergal depressor of trochanter jump muscle normal. Flies hemizygous for lethal alleles die either just prior to hatching of the larva from the egg or immediately thereafter; mosaic analysis of certain lethal alleles suggests primary defect in develop- ing muscles; however, in situ studies of transcription reveal that expression is confined to the nervous system and not the muscles (Fleming et al., 1989). alleles: Survival of lethal alleles in combination with ewg1 variable and temperature-sensitive ewg11 complements at least partially ewg4, ewg5, ewg10, and ewg12. allele origin discoverer synonym ref ( comments _______________________________________________________________________ ewg1 EMS Hanratty viable allele ewg2 EMS White ewgl1 1, 2 late embryonic lethal ewg3 EMS White ewgl2 1, 2 first-instar lethal ewg4 EMS White ewgl3 1, 2 late embryonic lethal ewg5 X ray Lim l(1)EC3, ewgl4 1, 2, 3 ewg6 EMS Lim l(1)EC363 ewg7 EMS Lim l(1)EC392 ewg8 EMS Lim l(1)EC3112 ewg9 EMS Lim l(1)EC3118 ewg10 EMS White ewgl5 1, 2 late embryonic lethal ewg11 EMS White ewgl6 1, 2 ewg12 EMS White ewgl7 1, 2 late embyro, early larval lethal ewg13 X ray Lefevre l(1)A58 3 ewg14 EMS Lefevre l(1)DA659 4 ewg15 EMS Lefevre l(1)DA678 4 ewg16 EMS Lefevre l(1)DA687 4 y mutant *ewg17 EMS Lefevre l(1)DC729 4 *ewg18 EMS Lefevre l(1)VA270 4 ewg19 EMS Fleming ewgl18 2 viable hypoactive, flightless hypomorph; indirect flight muscles intact ( 1 = Fleming, Zusman, and White, l983, Dev. Genet. 3: 347- 63; 2 = Fleming, DeSimone, and White, 1989, Mol. Cell Biol. 9: 719-25; 3 = Lefevre, l981, Genetics 99: 461-80; 4 = Lefevre and Watkins, 1986, Genetics 113: 869-95. cytology: Placed in 1A7-8 based on inclusion in Df(1)SJ1a = Df(1)1A1-3;1A8-B1 but not Df(1)SJ1d = Df(1)1A1-3;1A6-B1. To the right of cin, which is in the same interval and separated from ewg by the breakpoint of T(1;4)cin. molecular biology: Region cloned by an extension of the chromo- some walk of Campuzano et al. (Cell 40: 327-38). Gene local- ized to a 9.5-kb segment at approximately 140 to 150 kb on the molecular map by means of germ-line-transformant rescue of lethal alleles of ewg. Probing developmental Northern blots with this sequence reveals a collection of at least five tran- scripts ranging in size from 3.7 to 6 kb; transcription is most pronounced in six-to-twelve hour embryos with subsets of these transcripts appearing in 0-6 hr embryos and in adults (Fleming, DeSimone, and White, 1989, Mol. Cell Biol. 9: 719- 25). ex: expanded From Stern and Bridges, 1926, Genetics 11: 503-30. # ex: expanded location: 2-0.1. origin: Spontaneous. discoverer: Bridges, 17k21. references: Stern and Bridges, 1926, Genetics 11: 514 (fig.). phenotype: Wings extremely wide and large, sometimes curved and divergent. Effect produced in prepupal wing, probably by influence on cell division (Waddington, 1940, J. Genet. 41: 75-139). Eyes slightly reduced in size and roughish. Body large. RK2. alleles: *ex2 (Mickey, 1950, DIS 24: 60). cytology: Salivary chromosome location in or near 21C3 (Lewis, 1945, Genetics 30: 137-66). Between 21C2 and 8 by deficiency analysis [Golubovsky, 1979, Genetika 14: 294-305 (fig.)]. # Exaggeration of Bar: see E(B) # exb: extreme bar location: 3-47.4. origin: Occurred with TE#68. discoverer: Ising. Phenotype: Very narrow eyes (smaller than B/B); no ocelli. # exd: extradenticle location: 1-54. origin: Induced by ethyl methanesulfonate. references: Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Homozygous lethal; meso- and metathoracic segments resemble prothorax; first abdominal like posterior abdominal segments. In combination with Pc-like mutants shows abdominal transformations. alleles: Two. exd1 and exd2, isolated as XP and YO. cytology: Placed in 14A1-B1 based on inclusion in the region of overlap of Df(1)sd72b = Df(1)13F1;14B1 and Dp(1;4)r+ = Dp(1;4)14A1-2; 16A1-2; 102F2-3. #*exi: exiguous location: 1-51.5. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1958, DIS 32: 70. phenotype: Small fly with rather dusky body color. Not easily classified. Viability and fertility good in male, slightly reduced in female. RK3. # exo: exocephalon location: 1-58. origin: Induced by ethyl methanesulfonate. references: Eberl and Hilliker, 1988, Genetics 118: 109-20. phenotype: Sex-linked recessive lethal; variably differentiated cuticle; complete failure of head involution with well developed head structures on exterior of the embryo. Many embryos slightly twisted with defective ventral denticle pat- terns. alleles: exo1 and exo2 isolated as l(1)EH354 and l(1)EH406. cytology: Placed in 16C2-18B11 between breakpoints of Dp(1;3)f+71b = Dp(1;3)15A4;16C2-3;80-81 and T(1;Y)B50 = T(1;Y)18B4-11. # expanded: see ex #*exr: extra venation location: 1- (associated with In(1)exr). origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1952. references: 1958, DIS 32: 70. phenotype: Eyes slightly rough and smaller than normal. Wings have irregularly distributed extra vein tissue. Males viable and fertile; females viable but sterile. RK3A. cytology: Associated with In(1)exr = In(1)12E8-10;15D1-3. #*ext: extended location: 2- (not located). origin: Spontaneous. discoverer: Stroher, 1958. references: Mainx, 1958, DIS 32: 82. phenotype: Wings held out at about a 75 angle from body axis, are wavy, and gradually curve downward. Distal parts of wings often crumpled and folded. Halteres normal. Function of wings reduced. Viability and fertility good. RK3. # Ext: Extras location: 1-15.2. discoverer: Schultz, 33l8. phenotype: Heterozygous female has thickened, branched, and extra veins. Overlaps wild type. Lethal in male. RK3. cytology: Tentatively placed in 7C-E on the basis of Ext pheno- type of segmental deficiency (Merriam and colleagues). # ext-b: see bat # Ext-sct-3: see Su(sc) # extended: see ext # extended-b: see bat # extra bristles: see eb # Extra combs: see Eco # extra eye: see ee # extra lamina fiber: see elf # extra macrochaetae: see emc # extra organs: see eo # Extra sex comb: see Scx # extra sex combs: see esc # extra wing hairs: see xwh # extra venation: see exr # extradenticle: see exd # Extras: see Ext # extreme bar: see exb # exu: exuperantia (T. Schupbach) location: 2-93. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 302-17. Mlodzik, DeMontrion, Hiromi, Kraus, and Gehring, 1987, Genes Dev. 1: 603-14. Fronhofer and Nusslein-Volhard, 1987, Genes Dev. 1: 880-90. Schupbach and Wieschaus, 1989, Genetics 121: 101-17. phenotype: Maternal-effect lethal mutant; embryos from homozy- gous mothers lack anterior-most head structures. Instead they form an inverted posterior midgut and proctodeal region at their anterior end. Cephalic furrow at gastrulation is shifted towards anterior. Analysis of germline clones indicates that the mutation is germline autonomous (Schupbach and Wieschaus, l986, Dev. Biol. 113: 443-48). Causes shift in blastoderm fate map as indicated by ftz expression; thoracic stripes broadened and shifted anteriorly; abdominal stripes narrowed and compressed posteriorly (Mlodzik et al.). Eggs produced by exu mothers appear to have a more uniform distribution of bcd+ product, i.e., less concentration anteriorly (Fronhofer and Nusslein-Volhard). cytology: Placed in 56F-57B by segmental aneuploidy (Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26). alleles: exu1 - exu4 isolated as PJ, QR, SB, and SC, respec- tively. # ey: eyeless location: 4-2.0 (located by recombination in diplo-4 triploids by Sturtevant, 1951, Proc. Nat. Acad. Sci. USA 37: 405-7). origin: Spontaneous. discoverer: Hoge, 14e. references: 1915, Am. Naturalst 49: 47-49. Bridges, 1935, Biol. Zh. 4: 401-20 (fig.). phenotype: Eye size variably reduced depending on allele (see table); expressivity more variable for some alleles than for others. Tetragonal packing of facets and face-centered tetragonal bristle lattice (eyR) in place of hexagonal array of wild type [Hartman and Hayes, 1971, J. Hered. 62: 41-43 (fig.)]; associated with a failure of the horizontal secondary pigment cell to expand to give rise to the horizontal boun- daries between ommatidia [Ready, Hanson, and Benzer, 1976, Dev. Biol. 53: 217-40 (fig.)]. Some ey2 flies show duplica- tions of antennae or antennal segments with or without dupli- cation of aristae; extra maxillary structures also observed (Shatouri, 1963, Caryologia 16: 431-37). Optical disks reduced in size [(ey1) Richards and Farrow, 1922, Proc. Oklahoma Acad. Sci. 2: 41-45; (ey2) Medvedev, 1935, Z. Indukt. Abstamm. Vererbungsl. 70: 55-72 (fig.); 1935, Tr. Inst. Genet. Akad. Nauk SSSR 10: 119-51; Steinberg, 1944, Proc. Nat. Acad. Sci. USA 30: 5-13; (ey4) Chen, 1929, J. Mor- phol. 47: 135-99]. Degenerating cells abundantly observed in the optic disks of third-instar larvae of ey2 [Fristrom, 1969, Mol. Gen. Genet. 103: 363-79 (fig.); Ransom, 1979, J. Embryol. Exp. Morphol. 53: 225-35]. Expressivity sensitive to genetic background [(ey4) Spofford, 1956, Genetics 41: 938-59; (ey1, ey2, ey4, eyK) Hunt and Burnet, 1969, Genet. Res. 13: 251-65]. Phenotype also responds to develop- mental temperature, larval density, and composition of medium. Eye size reported to increase with increased temperature in e1 (Baron, 1935, J. Exp. Zool. 70: 461-90) and eyK (Sang and Burnet, 1963, Genetics 48: 1683-99) but to decrease in eyW (Meyer, 1959, DIS 33: 97). Phenotype less extreme in flies raised under crowded conditions at 18 but not 25 (Sang and Burnet, 1963; see also Chester, 1971, DIS 46: 62-63). Eye size of four alleles increased by cholesterol deprivation and decreased by dietary deficiencies in thiamine or RNA (Hunt and Burnet, 1969). Larval feeding of lactamide to ey2 causes decreased eye size, which is of opposite sign from its effect on B (Grant and Rapport, 1980, DIS 55: 53); no such effect of lactamide on eyK observed by Sang and Burnet (1963). ey2 flies exhibit normal visual orientation in Y maze (Bulthoff, 1982, DIS 58: 31). ey2, ey4, and eyK in combination with eyg (3-35.5) results in almost complete curtailment of eye development and synthetic lethality, with the major lethal crisis at the end of the pupal stage and a minor lethal phase at pupation; rare surviving adults have brain in anterior thorax [Hunt, 1970, Genet. Res. 15: 29-34 (fig.)]. alleles: ey2 is the most frequently used allele. Four lethal alleles, formerly l(4)10 = l(4)33, assigned to the ey locus by Hochman (1971, Genetics 62: 235-52); they produce a low incidence of escapers with reduced eyes and but partially com- plement eyR. allele discoverer origin ref ( phenotype | _______________________________________________________________ ey1 Hoge, 14e spontaneous 4, 8 .50-.75 ey2 Nonidez, 1919 spontaneous 2, 4 .25-.50 ey4 Li, 25f10 spontaneous 2, 4 .50_ *ey34 Gottchewski, 34g2b cold treatment 4, 5 .25-.50 *ey36 Spencer, 36e25 spontaneous 4, 15 .50-.75 ey46 King, 46l X ray 4, 9 .25_ ey67 Biggen, 67b spontaneous 1 eyAD Das, 63a7 spontaneous 4, 13 0-1.0 eyD / Muller, 27k X ray 3, 4, 11 see entry *eyD39 Sutton, 39k X ray 4, 6 ?-1.0 eyK spontaneous 4, 12 .50-1.0 eyl1 Hochman EMS 7 eyl2 Hochman EMS 7 eyl3 Hochman EMS 7 eyl4 Hochman spontaneous 7 eyopt ` eyR Sacharov, 23h13 spontaneous 4, 14 .25-.50 *eyta Datta, 63c26 spontaneous 4, 13 *eyW White, 59f spontaneous 4, 10 .25_? ( 1 = Biggen, 1967, DIS 43: 61; 2 = Bridges, 1935, Biol. Zh. 4: 401-20 (fig.); 3 = Bridges, 1935, Tr. Dinam. Razvit. 10: 463-73; 4 = CP627; 5 = Gottchewski, 1935, DIS 4: 15; 6 = Hinton, 1940, DIS 13: 49; 7 = Hochman, 1971, Genetics 67: 235-52; 8 = Hoge, 1915, Am. Nat. 49: 47-49; 9 = King and Poulson, 1948, DIS 22: 54; 10 = Meyer, 1959, DIS 33: 97; 11 = Patterson and Muller, 1930, Genetics 15: 495-577 (fig.); 12 = Sang and McDonald, 1954, J. Genet. 52: 392-412 (fig.); 13 = Sarkar, 1963, DIS 38: 28; 14 = Serebrovsky and Sacharov, 1925, Z. Eksperim. Biol. 1: 75-91; 15 = Spencer, 1937, DIS 7: 8. | Eye size relative to wild type. / See eyD entry. ` See OptG. ey4: eyeless-4 Edith M. Wallace, unpublished. eyD: eyeless-Dominant Left: head. Right: first pair of legs. From Patterson and Muller, 1930, Genetics 15: 495-577. # eyD: eyeless-Dominant origin: X ray induced. discoverer: Muller, 27k. references: Patterson and Muller, 1930, Genetics 15: 495-577 (fig.). Bridges, 1935, Biol. Zh. 4: 401-20. 1935, Tr. Dinam. Razvit 10: 463-73. phenotype: Eyes of heterozygotes small, outline irregular, dis- placed toward top and rear. Head large, often with duplicated antennae or ocelli. Basitarsus broadened distally and incom- pletely separated from second tarsal segment owing to interr- uptions of the intersegmental membrane. Polarity of bract- bristle arrangement locally reversed in regions of membrane gaps [Poodry and Schneiderman, 1976, Wilhelm Roux's Arch. Dev. Biol. 180: 175-88 (fig.)]. 27-48 sex-comb teeth disposed in more-or-less parallel longitudinal rows in males; number of transverse-bristle rows increased in females (Stern and Toku- naga, 1967, Proc. Nat. Acad. Sci. USA 57: 658-64). Extra leg joints tend to form as mirror-image duplications proximal to the normal joint between the first and second tarsal joints (Held, Duarte, and Derakhshanian, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 145-57). Clones of ey+ tissue in eyD/+ back- ground exhibit eyD/+ phenotype (Stern and Tokunaga, 1967), but both ey+ leg disks transplanted into eyD hosts and the reciprocal transplant develop autonomously (Tokunaga, 1970, Dev. Biol. 18: 401-13). fj eyD flies have but three tarsal joints (Postlethwaite and Schneiderman, 1975, Annu. Rev. Genet. 7: 381-433). Fully dominant in triplo-4 flies (Stur- tevant, 1936, Genetics 21: 448). Eye size of B; eyD/+ males larger than of B alone. Produces extreme phenotype in combina- tion with D. D/+; eyD/+ almost completely lethal (Sobels, Kruijt, and Spronk, 1951, DIS 25: 128). Homozygous lethal; two lethal crises, one during first or second larval instar and the other just prior to or during pupal stage. Cell degeneration observed in optic disks of homozygous second- instar larval (Ransom, 1979, J. Embryol. Exp. Morphol. 53: 225-35). Larvae which are unable to pupate rescuable by injection of (-ecdysone (Arking, 1969, J. Exp. Zool. 171: 285-96). Homozygotes reaching pupal stage lack adult derivatives of eye-antennal disks; adult derivatives are formed by eyD/eyD eye-antennal disks transplanted into wild- type hosts; brain present but number of cortical cells severely reduced (Arking, Putnam, and Schubiger, 1975, J. Expt. Zool. 193: 301-12). RK2. cytology: Salivary chromosomes show duplication of about a dozen bands inserted into middle of fourth chromosome as a reversed repeat. Source of duplication unknown (Bridges, 1935) but suggested to be 4L (Hochman, 1971, Genetics 67: 235-52). other information: May not be an allele of ey. # eyopt: see Opt # eya: eyes absent location: 2-. origin: Viable allele eya1 spontaneous; other alleles X-ray induced or induced by ethyl methansulfonate. references: Sved, 1986, DIS 63: 169 (fig.). Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29. phenotype: Eye facets completely absent in strong alleles; other aspects of head development appear normal; antennae and ocelli, which also arise from eye-antenna disc, present. Eye portion of disc markedly reduced; no morphogenetic furrow or putative photoreceptor-cell clusters seen; little or no stain- ing with monoclonal antibodies that normally stain presumptive photoreceptor cells. alleles: More than 40 alleles obtained (Leiserson, 1990); most of them are homozygous lethal. Some alleles are temperature- sensitive. cytology: Located in 26E. Associated with In(2L)eya = In(2L)22D;34B. molecular biology: Gene cloned, the region involved spanning seven breakpoint alleles. other information: Used by several groups in subtractive hybridization protocols for the isolation of eye-specific cDNA's. #*Eye: Eyeless dominant in chromosome 2 location: 2-62.7. origin: Probably ultraviolet induced. discoverer: Edmondson, 51g. synonym: ey-IID. references: 1952, DIS 26: 60. phenotype: Eyes may be greatly reduced in size with frequent doubling of antennae. Overlaps wild type, especially in old vials. Recessive in triploids. Eye/+; eyD/+ has smaller eyes than either alone. Homozygous lethal. RK3. # eye gone: see eyg # eye missing: see eym # Eye tissue determiner: see Etd # eyeless: see ey # Eyeless dominant in chromosome 2: see Eye # eyelisch: see eyh # Eyeluf: see Eyl # eyes absent: see eya # eyes reduced: see ldeyr # eyg: eye gone location: 3-37.5 [between 37 and 38, to the right of Est-6 (Roberts and Malpica, 1972, DIS 49: 40)]. origin: Spontaneous. discoverer: Ives, 40g20. references: 1942, DIS 16: 48. phenotype: Eyes and head much smaller than normal. Consider- able pupal mortality, probably from inability to push open pupa cases. Adults normal in viability and productivity. Character subject to genetic modifiers and possibly environ- mental influences. Expression varies from complete absence of facets to formation of about 100 facets. Homozygotes show reduced larval and pupal survival (Inoue, 1980, DIS 55: 206). Lethal in combination with ey; phenotype described under ey [Hunt, 1970, Genet. Res. 15: 29-34 (fig.)]. RK2. alleles: eyg64e, X ray induced, slightly dominant (Mittler, 1967, DIS 42: 38). cytology: Placed in 69C on the basis of its exclusion from Df(3L)vin7 = Df(3L)68C8-11;69B3-C1 and its mutant phenotype in combination with In(3LR)gsU = In(3LR)69B5-C4;81 (Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215-25). # eyh: eyelisch location: 3-58 (0.47 units from Sb but order unspecified). origin: Spontaneous. references: Kalisch, 1980, DIS 55: 206-07. phenotype: Eyes variably reduced. 7.5% of flies have no eyes; 0.3% of females and 5.6% of males overlap wild type. The pro- portion of completely eyeless flies increases dramatically and there is no overlap with wild type when eyh is combined with eyg or ey. RK3. #*Eyl: Eyeluf location: 1-18. origin: Spontaneous. discoverer: Marzluf. phenotype: One or both eyes reduced in size. Expression varies from slight reduction to absence of eye. Sometimes extraneous materials protrude through eye; frequently, one or more dupli- cated antennae present. Penetrance incomplete; viability good. In aged and crowded cultures, both penetrance and expressivity increased. Third chromosome carries important modifiers affecting penetrance, and different wild-type and mutant stocks carry different modifiers. Penetrance lower at 18 than at 25. RK3. # eym: eye missing location: 3-67.9. origin: Spontaneous. references: Inoue, 1980, DIS 55: 206. phenotype: Eyes almost completely absent in homozygotes. Heterozygotes with a wild-type chromosome but with eyg (3- 37.5) show variable reduction in eye size. Homozygotes have normal larval but reduced pupal survival. Fertile. RK1. # eyr: see ldeyr