#*ap: apterous (T.G. Wilson) location: 2-55.2. references: Metz, 1914, Am. Naturalist 48: 675-92. Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 236 (fig.). Stevens and Bryant, 1985, Genetics 110: 281-97. 1986, Genetics 112: 217-28. phenotype: Wings and halteres reduced to traces. Bristles eliminated from area around wing base (including posterior notopleurals, anterior and posterior supra-alars, and anterior postalars); posterior scutellars erect when present but miss- ing in first counts; dorsocentrals smaller and fewer; hairs on thorax sparse and irregular. Sutural furrow reduced; thorax disproportionately small. Flies small, pale, weak, and very short lived. Viability about 70% that of wild type but erratic. Both sexes sterile. RK2. alleles: Apterous alleles generally fall into three groups based on phenotypic differences. Most of the characterized apterous alleles belong to the first group and have basically the ap or ap4 phenotype. Some alleles (apblt2 and apT60) have a less severe wing phenotype, being straplike. Alleles also vary in their expressivity of the precocious adult death and nonvitellogenic ovary phenotypic characters; some alleles result in a low number of escapers, similar to ap4, while oth- ers have an escaper percentage of as much as 50%. There is little correlation between expressivity of the wing deficiency phenotype and either precocious adult death or nonvitellogenic ovary development, but a good correlation exists between expressivity of the latter phenotypic characters (Wilson, 1980). Generally, heterozygous combinations of these alleles do not show complementation for any phenotypic characters. Another group, represented by apblt, exhibits a less severe, somewhat different phenotype; attributable to localized lyso- somal cell death in the presumptive wing blade. (Sedlock, Mango, and Stevend, 1984, Dev. Biol. 104: 489-96). A third group includes two dominant alleles. The apterous locus appears to be a complex locus, containing several partially complementing groups for the wing deficiency and adult- death/female-sterility phenotypic characteristics. However, by studying the effects of a number of different temperature regimens on phenotypic expression of three different temperature-sensitive alleles, Stevens and Bryant (1986) con- clude that all phenotypes are explicable in terms of changes in quantity rather than quality of gene product. 120.if 264<72 .nr 85 72 allele origin discoverer synonym ref ( phenotype | _________________________________________________________________ *ap1 spont E.M. Wallace, 4, 8, 13h 14 *ap2 spont Bridges, 16j20 ap-c 3, 4, 8 ap4 ap2a EMS Wilson, 1978 20 *ap3 spont Morgan, 23a ap-c, no wings 8, 17 ap4 ap3a EMS Wilson, 1978 20 ap56f ap4 Medvedev, ap-d 8, 13, / 32a15 20 ap4a EMS Wilson, 1978 20 ap5 U.V. Byers, 49f 8, 16 ap4 ap6 spont Faulhaber 6, 8, 10 ap4 ap13 EMS Wilson 20 ap18 EMS Wilson, 1978 20 ap25 EMS Wilson, 1978 20 ap32 EMS Wilson, 1978 20 ap40 EMS Wilson, 1978 20 ap56f ap46 EMS Wilson, 1978 20 ap49 EMS Wilson, 1978 20, 21 ap49j spont Ritterhoff, 8, 11, ap4 49j 20 ap54 EMS Wilson, 1978 8, 20, ap78j 21 ap56f spont Thompson, 5, 8, / 56f 20 ap57 EMS Wilson, 1978 20 ap58 EMS Wilson, 1978 20 ap67e spont Lee 12 ap69c1 EMS Au 7 ap69c2 EMS Gottschalk 7 ap69c3 EMS Nadler 7 ap73n spont Altorfer, 73n 1 ap4 ap77f EMS Wilson, 77f 20, 23 / ap78e EMS Wilson, 78e ap78j EMS Wilson, 78j 20, 21, / 24 apblt spont Groscurth, blt 8 / 31b1 apblt* 20 apblt2 spont Whittinghill, 8, 22 < ap4 44h apblt3 spont Semenza, 49k bltS49k 2, 8 ap4 apc 20 ape spont 18 / apID apid 20 apXa? apT60 X ray Thomas, 60g 8, 15 < ap4 aptrw spont trw 9 / apXa X ray Serebrovsky, Xa 8, 19, / 28a 20 ( 1 = Altorfer, 1977, DIS 52: 2; 2 = Barigozzi, 1950, DIS 24: 54; 3 = Bridges, 1919, J. Exp. Zool. 28: 370. 4 = Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. 278: 236 (fig.); 5 = Burdick, 1956, DIS 30: 69; 6 = Butterworth and King, 1965, Genetics 52: 1153-74; 7 = Butterworth, Nolph, Au, Gottschalk, Nadler, and Tuma, 1970, DIS 45: 36; 8 = CP627; 9 = Crist, Fontaine, and Merrell, 1980, DIS 55: 204; 10 = Faulhaber, 1963, DIS 37: 48; 11 = Glass, 1951, DIS 25: 76-77; 12 = Lee, 1972, DIS 48: 18; 13 = Medvedev and Bridges, 1935, Tr. Inst. Genet. Akad. Nauk. SSR 10: 119-209; 14 = Metz, 1914, Am. Nat. 48: 675- 92 (fig.); 15 = Meyer, 1963, DIS 37: 50; 16 = Meyer, Edmondson, Byers, and Erickson, 1950, DIS 24: 59; 17 = Mor- gan, 1929, Carnegie Inst. Washington Publ. 399: 183; 18 = Roberts and Bownes, 1982, DIS 58: 209; 19 = Serebrovsky and Dubinin, 1930, J. Hered. 21: 259-65; 20 = Stevens and Bryant, 1985, Genetics 110: 281-97; 21 = Stevens and Bryant, 1986, Genetics 112: 217-28; 22 = Whittinghill, 1947, DIS 21: 71; 23 = Wilson, 1980, Dev. Genet. 1: 195- 204; 24 = Wilson, 1981, Dev. Biol. 85: 425-33. | Designation of allele with similar phenotype. / Phenotypes described below in separate entries. cytology: Placed in salivary region 41B-C (Schultz). # ap4 phenotype: Wings less than 10% normal length, lacking all wing blade structures. Halteres reduced to structureless remnants less than 25% normal size. Scutellar and dorsocentral bris- tles sometimes missing (Butterworth and King, 1965, Genetics 52: 1153-74). Wing phenotype disc autonomous in ap4/ap+ mosaic flies, although small patches of ap4 wing structures are found in ap4/ap+ mosaic wings. Haltere phenotype disc autonomous (Wilson, 1981, Dev. Biol. 85: 434-45). Adults become paralyzed about 30 hr following eclosion and die soon thereafter. Around 1% of adults are long-lived "escapers" of this phenotype (Wilson, 1980, Dev. Genet. 1: 195-204). Precocious adult-death phenotype fate-maps to proximity of Malpighian tubules, and tubule malfunctioning postulated to result in this phenotype (Wilson, 1981). Foregut of females swollen owing to accumulation of peritrophic membrane (King and Sang, 1958, DIS 32: 133). Female sterile with under- developed ovaries; nurse cell nuclei become pycnotic after stage 7, and stage-8 oocytes are the most advanced (King and Burnett, 1957, Growth 21: 263-80; Wilson, 1980). ap4 ovaries develop nonautonomously when transplanted to a wild-type host (King and Bodenstein, 1965, Z. Naturforsch. 20B: 292-97). Application of juvenile hormone mimic, ZR-515, to newly eclosed ap4 females results in vitellogenic oocytes [Postlethwait and Weiser, 1973, Nature (London) New Biol. 244: 284-85]. Membranes of vitellogenic oocytes lack micro- villi and pinocytoxic vesicles normally present; development of these structures stimulated by administration of ZR-515 (Tedesco, Courtwright, and Kumaran, 1981, J. Insect. Physiol. 27: 895-902). Corpora allata from adult ap4 are juvenile- hormone deficient when bioassayed [Postlethwait, Handler, and Gray, 1975, The Juvenile Hormones (L.I. Gilbert, ed.). pp. 449-69]. Nonvitellogenic oocyte phenotype fate-maps to same or similar location as precocious adult death phenotype (Wilson, 1981). Escaper females develop stage-14 oocytes (King and Sang, 1958) and are fertile (Wilson, 1980). Males show immature sexual behavior and are sterile, but testes appear normal with motile sperm (King and Sang, 1958). Larval fat body histolysis delayed; this phenotype is nonautonomous as determined by transplantation experiments (Butterworth, 1972, Dev. Biol. 28: 311-25). Application of ZR-515 accelerates larval fat body histolysis in ap4 adults (Postlethwait and Jones, 1978, J. Expt. Zool. 203: 207-14). Ovarian acid phosphatase level low in ap4 females and is restored after application of ZR-515 (Postlethwait et al., 1975). ap4 ovaries cultured in vitro are capable of yolk pro- tein synthesis (Redfern and Bownes, 1982, Mol. Gen. Genet. 195: 181-83). ap4/Df(2L)M41A-54 hemizygote has nearly normal complement of bristles but otherwise resembles ap4 homozygote (Butterworth and King, 1965). # ap56f phenotype: Wing and haltere phenotype like ap4. Scutellar and dorsocentral bristles missing (Butterworth and King, 1965, Genetics 52: 1153-74). Rear and middle legs occasionally twisted, more frequently in female than in male. Both sexes fertile and long lived when homozygous and in combination with other ap alleles. ap56f/M(2)S24 have normal complement of dorsocentral and scutellar bristles (Butterworth and King, 1965). # ap77f phenotype: Weakest non-temperature-sensitive allele known. Wing has reasonably good wing blade development, with missing triple-row elements and posterior wing margin. Haltere less well developed but more so than ap4. Adults long lived and fertile. Less dominant in heteroallelic combination with ap4-like alleles than is ap56f. ap77f/Df(2R)M41A4 has more severe phenotype than ap77f homozygotes. # ap78j phenotype: A temperature-sensitive allele of apterous. When raised at 22, wing and haltere phenotype approaches wild type except for missing patches of triple-row bristles and poste- rior wing margin. When raised at higher temperatures, pheno- type becomes more severe and resembles ap4 at 29. Two nono- verlapping temperature-sensitive periods in development, one in late-second to middle-third instar for wing and haltere deficiency phenotype and the other during the first day of pupal development for precocious adult death and nonvitello- genesis phenotype. Wing discs of heat-pulsed larvae failed to exhibit cell death by trypan blue exclusion. # apblt: apterous-blot phenotype: Wings blistered, sometimes inflated and dark due to trapped hemolymph. Mirror-image duplication of posterior wing blade structures occurs [Waddington, 1939, Proc. Nat. Acad. Sci. USA 25: 299-307; Whittle, 1979, J. Embryol. Exp. Mor- phol. 53: 292-303 (fig.)]. Wing venation may be disrupted. Portions of posterior wing compartment may be transformed into anterior compartment structures, an effect like that of engrailed (en; 2-62.0). Despite relatively mild adult pheno- type, extensive cell death observed, localized to wing pouch of imaginal discs; associated with acid phosphatase and lyso- somal activity (Sedlak, Manzo, and Stevens, 1984, Dev. Biol. 104: 489-96). Clonal analysis revealed nonautonomous expres- sion of phenotype. Heterozygotes with ap4 or ap56f and hemizy- gotes show blistering phenotype only (Whittle). apblt/ap73n shows transformation phenotype, and aldehyde oxidase histo- chemical staining of these wing discs is consistent with transformation (Whittle and Sprey, 1982, Wilhelm Roux's Arch. Dev. Biol. 191: 285-88). Much overlapping with wild type, and expressivity variable. Adults long lived and fertile. # ape phenotype: Homozygotes display extreme wing reduction, particu- larly of the posterior wing compartment. Approximately 50% of the flies have duplications of the anterior wing margin, distal costa, and triple row bristles. In wings with large amounts of wing blade, very little venation is present; how- ever, these may often have triplications or even four copies of the anterior wing margin, some located in the posterior part of the wing. Dried hemolymph sometimes trapped between the dorsal and ventral wing surfaces giving the wing a puffy blackened appearance. This mutant therefore has duplications and deficiencies characteristic of cell death followed by regulation in the wing, but also has transformations of the posterior wing compartment to the anterior wing compartment. 8% of the flies have defective third legs, more frequently in females than in males. Halteres and scutellar bristles appear to be normal. Homozygotes viable and fertile. # aptrw: apterous-torn wing phenotype: Distal part of wing in homozygotes shows sawtooth pattern as if tip torn away. Expression uniform in males and females. Viability and fertility good. other information: Genetic location and phenotype suggests allelism with apterous, but not tested with viable ap alleles. apXa: apterous-Xasta From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 228. # apXa: apterous-Xasta phenotype: Wings reduced in length to about 70% normal; irregu- lar in outline with a V-shaped incision with apex at L2, uni- formly present giving wing a mitten-like shape with the thumb between marginal vein and L2. Excellent dominant with no overlap. Fertile and fully viable in heterozygote. Usually lethal in homozygous conditions, but occasionally ecloses very late as pale dwarf with wings and balancers like vg. Deep notch visible in tip of wing fold in prepupa (Waddington, 1939, Proc. Nat. Acad. Sci. USA 25: 299-307). In homozygotes and in combination with ap4, ap6, or Df(2R)M41A4, wings are straplike and 30-70% normal length, and haltere length is 25- 50% normal; longevity and fertility like ap4/ap4 except for an occasional long-lived apXa/Df(2R)M41A4 female that may be fer- tile [Butterworth and King, 1965, Genetics 52: 1153-74 (fig.)]. In heterozygous combination with apID, duplications of the notum occur frequently. Wing disc cell death found in both apXa/+ (Fristrom, 1969, Mol. Gen. Genet. 103: 363-79) and apXa/apID [Postlethwait, 1978, Genetics and Biology of Drosophila (Ashburner and Wright, eds.). Academic Press, Lon- don, New York, San Franciso, Vol. 2C, pp. 418-19 (fig.)]. cytology: Shown by Sturtevant (1934, DIS 2: 19) to be associ- ated with T(2;3)apXa = T(2;3)41F;89E8-F1 which is superimposed on In(2R)Cy and In(3R)P (Morgan, Bridges, and Schultz, 1936, Year Book - Carnegie Inst. Washington 35: 294; Lewis, 1951, DIS 25: 109). # ap-c: see ap2 # ap-c: see ap3 # ap-d: see ap4 # apang: see apg # Apart: see Apt #*apb: apterblister location: 2-44.7. origin: Ultraviolet induced. discoverer: Edmondson, 49k. references: Meyer, Edmondson, Byers, and Erickson, 1950, DIS 24: 59-60. phenotype: Wings always notched, nearly always spread, and usu- ally blistered but expression somewhat variable. Homozygous imagos live less than 24 hr, owing to intestinal obstructions. Abdomens characteristically turn dark grey before death because of accumulation of digested food products. Although not at same locus as ap, apb +/+ ap4, flies show slight notch- ing of wings and many die within a day; those that survive are fertile. ap5 gives a similar heterozygous effect. RK2. # Ape: Apurinic endonuclease location: 3-{47}. synonym: AP3. references: Kelly, Venugopal, Harless, and Deutsch, 1989, Mol. Cell Biol. 9: 965-73. phenotype: Encodes an apurinic-apyrimidinic DNA endonuclease, AP3. Biochemical studies by Spiering and Deutsch (1986, J. Biol. Chem. 261: 3222-28). cytology: Placed in 79C-D by in situ hybridization. molecular biology: Isolated from a cDNA expression library using antiserum directed against human enzyme known to cross react with the Drosophila enzyme (Spiering and Deutsch). The conceptual translation product predicts a 317-amino-acid polypeptide of molecular weight 34.2 kd. Region between nucleotides 30 and 173 shows 66% homology with recA of E. coli and 42% amino-acid identity. Two helix-turn-helix domains detected in the carboxy-terminal end of the polypeptide. Northern blots identify a 1.3-kb transcript at all stages of development, but somewhat reduced in pupae and adult males; there is also transiently present, a 3.5-kb transcript in four-to-eight-hour embryos that disappears after second larval instar. # apexless: see apx # aperA: abnormal proboscis extension reflex A (J.C. Hall) location: 1-22.1. origin: Induced by ethyl methanesulfonate. discoverer: Kimura. references: Kimura, Shimozawa and Tanimura, 1986, J. Exp. Zool. 239: 393-99. phenotype: Variable phenotypic defects in the sugar-induced proboscis extension reflex (PER): some aperA flies cannot extend their probosces at all, whereas they are able to open the labellar lobes; some individuals extend their probosces only to the right or the left side of the body; each mutant individual seems to have a fixed phenotype, e.g., a fly which shows one-sided PER always extends its proboscis to the same side; the array of aberrant phenotypes is different under the influence of the two mutant alleles: for aperA1, 47.0% were unable to extend their probosces, 16% only to the left side, and the remainder extended their probosces normally; for aperA2: 32% could not extend their probosces, 23% could extend them only to the right side, and 22% only to the left side (the remainder behaved normally). alleles: Two alleles; aperA1 (=TT1), aperA2 (=TT360), with the overall penetrance for the former ca. 79%; 77% for the latter. # aperB (J.C. Hall) location: 1-0.6. origin: Induced by ethyl methanesulfonate. discoverer: Kimura. references: Kimura, Shimozawa and Tanimura, 1986, J. Exp. Zool. 239: 393-99. phenotype: Given sugar stimuli aperB flies extended their pro- bosces, not straight forward (as does wild-type), but back- ward; when these mutants show a partial extension of their probosces, the direction of the extensions is normal; the expression of the aperB gene is sensitive to culture tempera- ture: when the aperB1 mutants were reared at low temperature (18 or 20C), over 90% of the flies were normal, whereas the high culture temperature (over 25C) caused an abnormal PER; the temperature at which the proboscis extension reflex was tested did not affect the phenotype. cytology: Maps to 2D3-F3; based on its inclusion in Df(1)Pgd = Df(1)2D3;2F5 but not Df(1)JC19 = Df(1)2F3;3C5; w+Y = Dp(1;Y)2D2;3D2-3 covers aperB1. alleles: Two alleles: aperB1 (=TT665) and aperB2 (=TF48), which lead to indistinguishable phenotypic defects. other information: aperB mutations are completely recessive, and complement the closely linked aperC mutation. # aperC (J.C. Hall) location: 1-0.4. origin: Induced by ethyl methanesulfonate. discoverer: Kimura. references: Kimura, Shimozawa and Tanimura, 1986, J. Exp. Zool. 239: 393-99. 1986, Devel. Biol. 117: 194-203. 1987, J. Neurogenet. 4: 21-28. phenotype: Sugar-induced proboscis extension nearly absent (i.e. no extension at all of rostrum and haustellum), but not until adults are three to six days old; this defect, which is completely recessive, wanes such that at least half of the adults behave normally again by approximately day 10-11; correlated with these behavioral changes is time-dependent degeneration and regeneration of a pair of muscles, the ros- tral protractors; behavioral and histological phenotypes are temperature-sensitive: 18 causes defects later in adult life, and yet there is no recovery; 29 causes lower than usual (i.e. 25) proportion of adults developing the defects, and high tem- perature is compatible with recovery; temperature-sensitive period is from two to four days post-eclosion. cytology: Maps to 1F5-2A, based on its inclusion in Df(1)A94 = Df(1)1F5;2B15 and Df(1)S39 = Df(1)1E4;2B11-20 plus the fact that the X-chromosome duplication from the distal tip to 2A, from T(1;Y)G20, covers aperC. other information: aperC completely recessive and complements the closely linked aperB mutations. # apg: apang location: 2-7.7. origin: Induced by ethyl methanesulfonate. references: Shakaron and Sharma, 1983, DIS 59: 110 (fig.). phenotype: Homozygotes when raised at 19 show occasional absence of one or both claws; veins L4 and L5 interrupted; fertile at 19 but become sterile when shifted to 28; produce embryos with range of germ band abnormalities. Homozygous pupal lethal when raised at 28; pharate adults show defective tarsal development of all six legs; condensed, poorly developed and curved metatarsus and tarsi; duplications in tibial and tarsal segments; claws absent. Temperature sensi- tive period first instar to early pupa. # Aph-1: Alkaline phosphatase-1 location: 3-47.3 (between W and p) (Wallis and Fox). references: Beckman and Johnson, 1964, Nature 201: 321 (fig.). 1964, Genetics 49: 829-35 (fig.). Wallis and Fox, 1969, Biochem. Genet. 2: 141-58. phenotype: Locus responsible for one of several different alka- line phosphatase species [APH1 (EC 3.1.3.1)] formed during the life cycle. Specifies the enzyme that becomes active in the larval cuticle and muscle during the third instar. Electro- phoretic mobility of a pupal form of the enzyme, which differs from that found in the larva, also appears to be controlled by this locus (Wallis and Fox). Dimeric nature of enzyme inferred from the presence of enzymes of hybrid mobility in larvae heterozygous for electrophoretic variants. Biochemical characterization of larval enzyme by Harper and Armstrong (1972, Biochem. Genet. 6: 75-82; 1973, Biochem. Genet. 10: 29-38; 1974, Biochem. Genet. 11: 177-80). alleles: Naturally occurring alleles superscripted F and S reported by Beckman. Wallis and Fox describe AphA which specifies larval enzyme migrating faster than AphF, but a pupal enzyme with same characteristics as that produced by AphF. Aph0 reported by Johnson (1966, Science 152: 361-62) produces no detectable enzyme activity but causes the appear- ance in extracts of AphS/Aph0 larvae of a band migrating slightly faster than the hybrid band produced by AphF/AphS larvae. Naturally occurring alleles superscripted 2, 4, 6, and 10 characterized by Harper and Armstrong (1972, 1973, 1974); 4 is synonymous with F as is 6 with S; 2 migrates more slowly than S and 10 more rapidly than F; not clear that 10 and A are different. That the larval and pupal enzymes are differently modified products of the same locus is indicated by genetic inseparability and by concordance in the orders of mobilities of electrophoretic alleles (Wallis and Fox). # Aph-2 location: 2- not mapped. references: Schneiderman, Young, and Childs, 1966, Science 151: 461-63. phenotype: The alkaline phosphatase found in adult hindgut. alleles: Two different alleles recorded superscripted A and B. Enzyme produced by Aph-2A homozygotes migrates more rapidly than that produced by Aph-2B homozygotes; enzyme produced by Aph-2A/Aph-2B has same mobility as that produced by Aph-2A homozygotes. # apo: altered pattern orientation (J.C. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. synonym: apoS129. references: Heisenberg, 1979, Handbook of Sensory Physiology (H. Autrum, ed.). Springer-Verlag, Berlin, Vol. VII/6A, pp. 665-79. Bulthoff, 1982, DIS 58: 31. 1982, Biol. Cybernet. 45: 63-70. phenotype: Poor orientation to objects, including spots in Y- maze test; electroretinogram normal. # app: approximated location: 3-37.5. discoverer: Curry, 34a25. references: 1935, DIS 3: 6. phenotype: Crossveins close together; veins diverge at greater angle than wild type; effect visible in prepupal wing [Wad- dington, 1940, J. Genet. 41: 75-139 (fig.)]. Legs short with four-jointed tarsi; the penultimate joint characteristically swollen [Waddington, 1939, Growth Suppl. 37-44 (fig.)]. Joint between second and third tarsal segments often incomplete; invaginations or internalization of cuticle seen in tarsi 1, 3, and 4 (Held, Duarte, and Derakhshanian, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 145-57). Thickset body. Poste- rior scutellars farther apart than normal. Eyes smaller and flatter than normal, also bumpy. Spread wings; thickened veins. RK1. alleles: app61e (CP627). cytology: Placed in 69A2-4 on the basis of its inclusion in Df(3L)vin6 = Df(3L)68C8-11;69A4-5 but not Df(3L)vin5 = Df(3L)68A3;69A1-2 (Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215-26). # Appl: |-Amyloid protein precursor like (K. White; J.C. Hall) Location: 1-{0}. origin: Isolated as cDNA clones derived from cloned genomic DNA in the 1B division. references: Rosen, Martin-Morris, Luo, and White, 1989, Proc. Nat. Acad. Sci. USA 86: 2478-82. Martin-Morris, and White, 1990, Dev. (In press). molecular biology: A 6.5 kb transcript corresponding to the cDNA clones encodes a polypeptide that is conceptually an 886 amino acid transmembrane protein; this predicted amino-acid sequence shows strong homology in certain of its regions to the |-amyloid protein precursor protein of humans (Rosen et al., 1989). Two forms of the actual protein, which is N- glycosylated, are detectable (in studies involving extracts, primary cultures, and transfected cells); an 145 kd membrane- associated precursor and a 130 kd secreted form lacking the cytoplasmic domain inferred from sequencing (Luo, Martin- Morris, and White, 1990, J. Neurosci., in press). The source of the Appl transcript spans ca. 38 kb of genomic DNA; this RNA localizes to post-mitotic neurons (and apparently not to non-neuronal tissues) in all developmental stages and in adults (Martin-Morris and White, 1990). Consistent with these in situ hybridization data are those showing APPL protein immunoreactivity in developing neurons, concomitant with axo- nogenesis; this staining remains associated with differen- tiated neuronal cell bodies and axonal tracts (including neu- ropil regions) in embryos, APPL immunoreactivity is observed exclusively in post-mitotic CNS and PNS neurons (Luo et al., 1990). other information: The APPL-encoding gene initially suggested (Rosen et al., 1989) to correspond to vnd (which was defined originally by embryonic neural-lethal mutations). This has been disproved, in that a terminal deletion Df(1)78 which retains vnd+ function removes most of the Appl coding sequences (Martin-Morris and White). # apr: see wa # Aprt: Adenine phosphoribosyltransferase location: 3-1.49 (0.13 cM to the right of R; estimated by John- son and Friedman to be 3.03 units from the tip of 3L). synonym: aprt. references: Johnson and Friedman, 1981, Science 212: 1035-36. 1983, Proc. Nat. Acad. Sci. USA 80: 2990-94. phenotype: Is the structural gene for adenine phosphoribosyl- transferase [APRT, AMP: pyrophosphate phosphoribosyl- transferase (EC 2.4.2.7)], a homodimer with 23,000 dalton subunits. It is a purine salvage enzyme which catalyzes the synthesis of AMP from 5-phosphoribosyl-1-pyrophosphate. Flies homozygous for a null allele Aprt1 survive on 15 times the concentration of purine that wild type tolerates and show about 2% wild-type enzyme activity; Aprt1/+ exhibit about half wild-type activity. Aprt2 has 9% normal enzyme activity. The dosage response suggests that the mutant affects the struc- tural gene for APRT. alleles: Electrophoretic variants AprtA (more acidic) and AprtB (more basic) in wild-type stocks Oregon R and Canton S, respectively. Aprt1 (Duck), Aprt2 and Aprt3 (Gelbart and Chov- nick) induced by ethyl methanesulfonate; Aprt4 and Aprt5 selected on purine food by Johnson and Friedman (1983). cytology: Placed in 62B8-12 based on its inclusion in the region of overlap of Df(3L)R-G7 = Df(3L)62B8-9;62F2-5 and Df(3L)R-G2 = Df(3L)62B2-4;62B11-12 (Sliter, Henrich, Tucker, and Gilbert, 1989, Genetics 123: 327-36). in situ hybridiza- tion identifies 62B9 as the site of Aprt (Johnson et al.). molecular biology: Genomic clone isolated by chromosomally walking from sequences isolated and cloned by microdissection of region 62B from polytene chromosomes. Gene recognized by hybrid selection of an 1-kb mRNA that translated an APRT pro- duct. cDNA's have a common 5 initiation site but two dif- ferent 3 polyadenylation sites. The primary transcript con- tains two introns, the first of which has alternative 5 sites, which are spliced to the same 3 site; one product encodes the functional enzyme and the other a prematurely ter- minated and presumably nonfunctional polypeptide (Johnson and Henikoff, 1989, Mol. Cell Biol. 9: 2220-23). Conceptual amino-acid sequence predicts a polypeptide of 194 amino acids and about 20 kd in molecular weight. Drosophila APRT amino- acid sequence displays approximately 40% identity and nearly 80% homology with all known APRT proteins (Johnson, Edstrom, Burnett, and Friedman, 1987, Gene 59: 77-86). #*Apt: Apart location: 3- (between h and p). origin: X ray induced. discoverer: Belgovsky, 34e23. references: 1935, DIS 3: 27. phenotype: Wings spread widely. Viability, fertility, and separability good. Homozygous lethal. RK2A. cytology: Associated with In(3L)Apt - no salivary analysis. other information: Apt/D survive; therefore not an allele of D. # apterblister: see apb # apterous: see ap # Apurinic endonuclease: see Ape #*apx: apexless location: 1-11.3. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine. discoverer: Fahmy, 1954. references: 1959, DIS 33: 83. phenotype: Slightly larger fly with large eyes containing vari- ous numbers of deranged ommatidia. Wings broad and blunt; in many flies, margin removed to various degrees, from a small incision of inner margin to removal of entire inner margin, costal vein, and parts of the membrane as far as L3. Region from L3 to costal cell unaffected. Rarely L4 and 5 are inter- rupted. Males viable and fertile; female fertility reduced. RK3. # Apx: Antennapedex (R.E. Denell) location: 1-70 (said to map 12 units to the right of B). origin: Neutron induced. references: Ginter, 1969, DIS 44: 50. phenotype: Males and heterozygous females show variable expres- sion from small additional segment on the third antennal seg- ment to a nearly complete leg including femur, tibia, and tarsus. Arista usually present. Homozygous females lethal but X0 males survive. Crosses involving either Apx males or females produce many inviable embryos. cytology: Polytene X appears normal, but genetic results sug- gest a T(1;3) with breakpoints in the proximal part of Xh and at Antp. # Apx-2: see Antp # ar: abdomen rotatum location: 4- (proximal to bt; Fung and Stern, 1951, Proc. Nat. Acad. Sci. USA 37: 403-4. origin: Spontaneous. discoverer: Beliajeff, 1926. references: 1931, Biol. Zentralbl. 51: 701-8 (fig.). Bridges, 1935, Biol. Zh. 4: 401-20. Marengo and Howland, 1942, Genetics 27: 604-11 (fig.). phenotype: Abdomen twisted clockwise through 45 to 60. No over- lapping with wild type. Male external genitalia often miss- ing. Males usually sterile; females partially fertile. Puparia not so smooth as normal; larval segmentation remains. Puparia have deep constriction near posterior end just ante- rior to spiracles. Existing chromosomes marked ar also carry l(4) and, in combination with Df(4)M, show counterclockwise rotation of male abdomen when viewed from behind (Hochman). RK2. alleles: ar2, *ar57d, and *ar57g X ray induced (CP627). Ethyl methanesulfonate induced alleles superscripted 65f, 65h, 68i, and 69g described by Hochman (1971, Genetics 67: 235-52; 1972, DIS 48: 17). ar68i shows best viability and fertility. cytology: Placed in salivary chromosome region 101E through 102B16 on basis of its inclusion in Df(4)M = Df(4)101E- F;102B6-17. # Ar: see AntpLC # arc: see a # arch: arch location: 2-60.5. origin: Spontaneous. discoverer: Curry, 36g3. references: 1937, DIS 7: 5. phenotype: Wings curved evenly downward, both longitudinally and transversely; sometimes shorter and blunter; rarely diver- gent. RK2. # arclike wing: see alw # arcoid: see ad # arctops: see at # arctus oculus: see at # ard: see Acr64B # aret: arrest (T. Schupbach and E. Wieschaus) location: 2-48. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female sterile; homozygous females often have under- developed ovaries which seem to lack germ cells altogether. In some females a small number of developing egg chambers is found. These never develop beyond the first few stages of oogenesis. alleles: Eight, aretWQ = aret1, aretWH, aretPA, aretPC, aretPD, aretPE, aretQB, aretRM. Females homozygous for aretPC and aretQB usually have a number of egg chambers in their ovaries in which the nurse cells and oocyte never seem to develop beyond stage 2 or 3 of oogenesis, but the follicle cells nevertheless synthesize a tiny round chorion around the cysts. Females homozygous for aretPA, aretPD and aretRM usually have almost normal numbers of early stages of egg chambers in their ovaries which degenerated before yolk uptake occurs. cytology: Placed in 33B3-F2, since uncovered by Df(2L)Prl = Df(2L)32F1-2;33F1-2 and Df(2L)prd1.7 = Df(2L)33B2-3;34A1-2. # Argentine Curly: see CuA # Argk: Arginine kinase location: 3-25.2. references: Fu and Collier, 1981, Genetics 97: 537-38. 1983, Bull. Inst. Zoo. Acad. Sinica 22: 25. James and Collier, 1988, J. Exp. Zool. 248: 185-91. phenotype: Structural gene for arginine kinase [ARGK (EC 2.7.3.3)] based on gene dosage studies. Cellular and mitochondrial forms behave as if both are products of the gene. (Munneke and Collier, 1985, Genetics 110: s85). In 108-hour third-instar larvae, activity is high in body-wall and digestive-tract musculature; lower in brain, imaginal discs, and salivary glands; present in head, thorax, and abdo- men of adults, being highest in indirect flight muscle of thorax. Activity levels increase during development reaching a peak at the pupal stage; then an abrupt decrease during the pupal stage is followed by a second increase beginning around the time of eclosion and climbing to high adult levels (James and Collier). cytology: Located to 66B by segmental aneuploidy. # Arista: see Ata # aristaless: see al # aristaless-b: see aa # Aristapedia: see AntpLC # Aristapedioid: see Arp # arm: armadillo location: 1-1.2. origin: Induced by ethyl methanesulfonate. references: Nusslein-Voelhard, Wieschaus, and Jurgens, 1982, Verh. Dtsch. Zool. Ges. 1982: 91-104. Gergen and Wieschaus, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 49-62. Klingsmith, Noll, and Perrimon, 1989, Dev. Biol. 134: 130-45. phenotype: Homozygous lethal; embryonic segmentation defective by time of germ-band shortening; naked cuticle ordinarily comprising the posterior two thirds of each segment replaced by mirror-image duplication of the anteriorly situated denti- cle belt; strong alleles delete first denticle row in abdomi- nal segments. May have dorsal hole in cuticle. Embryonic CNS development quasi normal (Patel, Schafer, Goodman, and Holmgren, 1989, Genes Dev. 3: 890-904). Autonomous at the level of single cells as shown by denticulate clones of homoz- ygous cells in the naked cuticle of abdominal segments in arm/+ embryos (Wieschaus and Riggleman, 1987, Cell 49: 177- 84). Clones of homozygous female germ cells arrested at stage 10 of oogenesis (Wieschaus and Noell, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 63-73). An exception is arm8 for which progeny from homozygous germ-line clones have been recovered (Klingsmith et al.). Cell lethal in imaginal discs; although clones of homozygous cells not observed in adults, their formation seems to engender mirror-image duplications, which are not seen in response to homozygosing other cuticular cell lethals (Wieschaus). Transcript found with minor fluctuations in amount, in all cell types at all stages in development (Riggleman, Wieschaus, and Schedl, 1989, Genes Dev. 3: 96- 113). alleles: allele origin synonym ref ( comments ___________________________________________________________________ arm1 EMS armXK22 3 strong allele arm2 EMS armXM19 3 hypomorphic allele arm3 EMS armXP33 3 strong allele arm4 EMS armYD35 3 strong allele arm5 P armTD5 2 1.2-kb P insert arm6 P arm18.3 2 1.3-kb P insert arm7 P armTD5 2 complex molecular rearrangement arm8 EMS armH8.6 1 temperature-sensitive allele ( 1 = Klingsmith, Noll, and Perrimon, 1989, Dev. Biol. 134: 130-45; 2 = Riggleman, Wieschaus, and Schedl, 1989, Genes Dev. 3: 96-113; 3 = Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296- 307. cytology: Located in region 2B15 by in situ hybridization. Complementation with other lethals in 2B apparently not tested. molecular biology: Gene isolated by transposon tagging and identified by germ-line transformation (Klingsmith, Noll, and Perrimon, 1989, Dev. Biol. 134: 130-45). Genomic sequences identify a single 3.2-kb transcript; two classes of cDNA's isolated which have different first exons spliced to six com- mon exons; the first exons are 500 base pairs apart, so that exon 1 of one transcript is within the first intron of the other; they also show slightly different 3 polyadenylation sites. The mature transcript contains an open reading frame of 2529 nucleotides, which encodes a predicted 843-amino-acid, 91.1-kd acidic protein with an isoelectric point of 5.86. The conceptual amino-acid sequence contains no indication of either a signal or a transmembrane sequence; it does contain a 23-amino-acid glycine-rich sequence, which lacks charged amino acids, near the C terminus. In addition, internally there are 12.5 tandem repeats of a 42-amino-acid sequence with a con- sensus sequence to which the various repeats show 28 to 80% identity. # arp-1: see ssaSp # Arp: Aristapedioid (P. Adler) location: 2-67 (inseparable from vg) origin: Hybrid dysgenesis. references: Adler, 1984, Genetics 107: s1. Adler, Charlton, and Brunk, 1989, Dev. Genet. 10: 249-60. Brunk and Adler, 1990, Genetics 124: 145-56. phenotype: Homozygous lethal. Two dramatic dominant phenotypes: One is a partial transformation of arista to tarsus, the other is the loss or reduction in size of medially located macrochaetae on the dorsal thorax. Both phenotypes show high penetrance but variable expressivity. alleles: Arp1 and Arp2. cytology: Both alleles associated with In(2R)49A12-B3;49E5-F1 with P-derived sequences at either end. Deficiency analysis shows that lethality common to the two alleles associated with the 49A12-B3 breakpoint and thus localizes Arp. Both alleles revert by reinversion in dysgenic (1/200) and control (1/2000) crosses. other information: Concluded to be homeotic gain-of-function alleles of Su(z)2 (Brunk and Adler). # arr: arrow location: 2-66. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.). Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Embryonic lethal. Additional denticle bands anterior and posterior to normal denticle bands, especially in ventral midline. Strongest at 18. alleles: Nine ethyl-methanesulfonate-induced alleles; arr1 and arr2 (recovered as IB and IIW) retained. # Arr1: Arrestin 1 location: 2-{53}. references: Smith, Shieh, and Zuker, 1990, Proc. Nat. Acad. Sci. USA 87: 1103-07. Hyde, Mecklenburg, Pollock, Vihtelic, and Benzer, 1990, Proc. Nat. Acad. Sci. USA 87: 1108-12. LeVine, Smith, Whitney, Malicki, Dolph, Smith, Burkhart, and Zuker, 1990. phenotype: Encodes a Drosophila homologue of mammalian arres- tin, a protein that interacts stoichiometrically with activated rhodopsin, inhibiting its ability to interact with the G protein, transducin, thus terminating the visual response. ARR1 presumed to be the 41-kd protein that is phosphorylated by exposure to light in the presence but not the absence (i.e., ninaE flies) of rhodopsin. Expression first detected in late pupae, when other genes involved in phototransduction are also first expressed. Transcript local- ized to photoreceptor cells of the compound eye, the ocelli, and the larval light sensitive organ. cytology: Placed in 36D1-2 by in situ hybridization. molecular biology: Sequence isolated from an eye specific genomic library produced by subtractive hybridization with cDNA from body and eya flies. The genomic clone identifies an 1.4-1.5-kb transcript in late pupae. Sequencing of genomic and cDNA clones indicates a primary transcript with four exons separated by introns of 421, 233, and 60 nucleotides; the con- ceptual amino-acid sequence indicates a protein of 364 resi- dues that displays 42-45% amino-acid identity with bovine and human arrestins. Drosophila arrestin, however, lacks the 30 C-terminal amino acids, which share homology with (-transducin in human and bovine arrestins. # Arr2 location: 3-{26}. references: Yamada, Takeuchi, Komori, Kobayashi, Sakai, Hotta, and Matsumoto, 1990, Science 248: 483-86. Levine, Smith, Whitney, Malicki, Dolph, Smith, Burkhart, and Zuker, 1990. phenotype: Encodes a second Drosophila homologue of mammalian arrestin, a 49-kd (or 46-kd) protein that is phosphorylated by exposure to light in wild type but not in ninaE flies which lack rhodopsin in photoreceptor cells 1-6, nor norpA flies which are deficient in phospholipase C activity. Phosphoryla- tion dependent on the presence of Ca++, whose intracellular levels are regulated by phospholipase C. Expression first detected in late pupae, when other genes involved in photo- transduction are also first expressed. Arr2 expression is approximately seven times that of Arr1. In the adult, tran- script localized to photoreceptor cells of the compound eye and the ocelli. cytology: Placed in 66D10-11 by in situ hybridization (Levine et al.). molecular biology: Sequence isolated by screening an expression library with a monoclonal antibody raised to the Drosophila 49-kd protein (Yamada et al.). or with a synthetic oligonu- cleotide based on partial amino-acid sequence (LeVine et al.). Also apparently isolated as autonomous head-specific clones by Levy, Ganguly, Ganguly, and Manning (1982, Dev. Biol. 94: 451-64). The sequence identifies a single transcript of 1.8 kb (or 1.65 kb) on Northern blots; the conceptual amino- acid sequence indicates a protein of 401 amino acids, a calcu- lated molecular mass of 44,972 daltons, and an isoelectric point of 8.9. ARR2 shares 206 residues with ARR1, and 181 with bovine arrestin; 146 residues are conserved in all three polypeptides. ARR2 shares with bovine arrestin virtually identical hydropathy plots and potential glycosylation sites but differs in being basic (pI = 8.9) rather than an acidic (pI = 6.0). The carboxy terminus of ARR2 displays only par- tial homology to the sequence of the proposed rhodopsin bind- ing site of (-transducin; also, the arrestin sequences that resemble the adenosine diphosphate- ribosylation sites of transducin are not found in ARR2. # Ars: Arylsulfatase references: MacIntyre, 1974, Isozyme Bul. 7: 23-24. phenotype: Inferred as structural gene for arylsulfatase [ARS (EC 3.1.6.1)] on basis of response of enzyme level to gene dosage. cytology: Placed in 74A-79D by segmental aneuploidy. # art: aristatarsia location: 3- (not mapped; modifying factors on chromosome 2). origin: Spontaneous. discoverer: Ouweneel, 69e. references: 1970, DIS 45: 35. phenotype: In homozygotes, arista replaced by tarsus-like structure. Penetrance more than 70%. Complements ssa but enhances AntpB in heterozygous condition; penetrance of AntpB/+ less than 1%, of AntpB/art more than 60%; Antp49 also enhanced. # arth: arthritic location: 1-0.0 [between ewg and y (Fleming). references: Schalet and Roberts, 1973, DIS 50: 23. phenotype: Legs weak with pigmented joints; tarsal segments frequently askew with claws fused; movements somewhat uncoor- dinated. Brownish-black pigment present at joints of over 90% of males, most frequently in meso- and metathoracic legs between femur and tibia but sometimes between coxa and tro- chanter or proximal to coxa. cytology: Placed in 1A5-8 based on arthritic phenotype of males carrying Df(1)y15 = Df(1)1A4-5;1A8-B1 in combination with l(1)1Ar+Y. Included in Df(1)sc19, whereas ewg is not (Schalet).