# am: see Dfdr # Ama: see ANTC # Ama: see RpIIC4 # Ama-1: (-amanatin resistant 1 location: 3-19. origin: Recovered from natural populations from India, Malay- sia, and Taiwan. references: Phillips, Willms, and Pitt, 1982, Can. J. Genet. Cytol. 24: 151-62. phenotype: Flies homozygous or heterozygous for Ama-1 and Ama-2 have LD5O to (-amanatin 10-30 times that of wild type. Sensi- tivity of RNA polymerase II activity to (-amanatin same as wild type. Ama-1 alone sufficient to confer resistance, but in three independent isolations both Ama-1 and Ama-2 present. # Ama-2 location: 3-100. origin: Recovered from natural populations in India, Malaysia, and Taiwan. references: Phillips, Willms, and Pitt, 1982, Can. J. Genet. Cytol. 24: 151-62. phenotype: Same as for Ama-1. # Amalgam: see Ama under ANTC Amanatin resistant: see also Amr and RpII # amb: amber location: 1-6.8. origin: Induced by triethylenemelamine. discoverer: Fahmy, 1950. references: 1958, DIS 32: 67. phenotype: amb has pale yellow body color; bristles very thin and short; hairs less affected. Eyes slightly brighter red. Males sterile. Viability 10-50% wild type. RK2. amb2 less extreme, males viable and fertile, females sterile. alleles: *amb1, amb2 (Fahmy, 1958 and CP627). Also one allele each induced by triethylenemelamine, DL-p-N,N-di-(2- chloroethyl)amino-phenylalanine, 2-chloroethyl methanesul- fonate, and nitrogen mustard and two alleles induced by p- N,N-di-(2-chloroethyl)amino-phenylethylamine. cytology: Placed in 4C7-8 on the basis of its inclusion in Df(1)bi-D3 = Df(1)4C5-6;4C7-8 but not Df(1)rb41 = Df(1)4B6- C1;4C7-8 (Banga, Bloomquist, Brodberg, Pye, Larrivee, Mason, Boyd, and Pak, 1985, Chromosoma 93: 341-46). # amd: alpha methyldopa hypersensitive location: 2-53.9 [.002 units (2.1 kb) to the left of Ddc]. synonym: amd; l(2)amdH, l(2)37Bk. references: Sparrow and Wright, 1974, Mol. Gen. Genet. 130: 127-41. Wright, 1977, Am. Zool. 17: 707-21. Wright, Black, Bishop, Marsh, Pentz, Steward, and Wright, 1982, Mol. Gen. Genet. 188: 18-26. Gilbert, Hirsh, and Wright, 1984, Genetics 106: 679-94. Marsh and Wright, 1986, Genetics 112: 249-65. Black, Pentz, and Wright, 1987, Mol. Gen. Genet. 209: 306-12. Wright, 1987, Adv. Genet. 24: 127-222. phenotype: amd/+ flies die when reared on levels of alpha methyl dopa that are not lethal to wild type; resistance pro- portional to the number of amd+ loci present. Adult amd/+ females fed alpha methyldopa become sterile and lay eggs that cannot complete embryogenesis. Dopa decarboxylase levels normal. amd homozygotes lethal; lethal phase at times of lar- val hatching, larval molts, and pupariation; larval anal organ extruded and necrotic; pupal cuticle thin and friable. Appears to play role in cuticle formation. amd1/amd6 complementing adults deficient for one or more unidentified catecholamines involved in the colorless sclerotization of cuticle. alleles: The first seven alleles selected as alpha methyl dopa hypersensitive in the heterozygous condition; the remainder recovered as recessive lethal mutations. Interallelic comple- mentation observed, suggesting dimeric product. allele origin discoverer synonym ref ( comments ______________________________________________________________________ amd1 EMS Sparrow l(2)amdH1 1, 2 amd2 EMS Sparrow l(2)amdH7 2 amd3 EMS Sparrow l(2)amdH14 2 amd4 EMS Sparrow l(2)amdH45 2 amd5 EMS Sparrow l(2)amdH82 2 amd6 EMS Sparrow l(2)amdH89 1, 2 amd7 EMS Sparrow l(2)amdH121 1, 2 amd8 EMS Wright l(2)amdH8 3, 4 amd9 EMS Wright l(2)amdH60 3, 4 amd10 EMS Wright l(2)amdH122 3, 4 amd11 EMS Wright l(2)amdH149 3, 4 amd12 X ray Hodgetts l(2)amdHX1 3, 4 amd21 EMS Wright l(2)203 4 amd22 EMS Wright l(2)245 4 amd23 EMS Wright l(2)258 4 amd24 EMS Wright l(2)283 4 amd25 EMS + HCOH Wright l(2)305 4 amd26 EMS + HCOH Wright l(2)329 4 amd27 EMS + HCOH Wright l(2)337 4 amd28 EMS + HCOH Wright l(2)341 4 amd29 EMS + HCOH Wright l(2)346 4 amd30 EMS Wright l(2)602 4 amd31 EMS Wright l(2)616 4 amd32 EMS Wright l(2)638 4 amd33 EMS Wright l(2)640 4 amd34 EMS Wright l(2)674 4 amd35 EMS Steward l(2)RS1 4 amd36 EMS + / ray Wright l(2)7301 4 amd37 EMS + / ray Wright l(2)7401 1, 4 750-bp insert, destroys EcoRI site at -5.6-kb amd38 EMS + / ray Wright l(2)7413 4 amd39 EMS + / ray Wright l(2)7433 4 amd40 EMS + / ray Wright l(2)7439 1, 4 BglII site at -4.8-kb altered; at intron splice acceptor amd41 EMS + / ray Wright l(2)7445 4 amd42 EMS Schupbach l(2)WK26 amd43 EMS + / ray Cecil l(2)C7 amd44 EMS + / ray Cecil l(2)AA3 amd45 EMS + / ray Cecil l(2)BB2 amd46 EMS + / ray Cecil l(2)BB3 amd47 EMS + / ray Cecil l(2)B1 ( 1 = Black, Pentz, and Wright, 1987, Mol. Gen. Genet. 209: 306-12; 2 = Sparrow and Wright, 1974, Mol. Gen. Genet. 130: 127-41; 3 = Wright, Bewley, and Sherald, 1976, Genet- ics 84: 287-310; 4 = Wright, Black, Bishop, Marsh, Pentz, Steward, and Wright, 1982, Mol. Gen. Genet. 188: 18-26. cytology: Placed in 37B9-C1 based on its inclusion in Df(2L)NST but not Df(2L)VA17. molecular biology: Located between coordinates -4.7 and -2.42, where 0 is the axis of symmetry of the HpaI site near the ter- minus of the Ddc coding sequence and positive values extend to the right. Genomic sequence contains a 483-bp intron near the 5 end; the usual upstream regulatory sequences identified as well (Marsh, Erfle, and Leeds, 1986, Genetics 114: 453-67). A 2.0-kb amd transcript first detectable early in embryo- genesis; reaching maximum level at 12-16 hours; low levels observed in adults; concentrated in the nurse cells of stage 8-9 oocytes; smaller transcripts with sequence homology to the 2.0-kb transcript observed in third-instar larvae. amd and Ddc transcribed from opposite strands; two regions of exten- sive homology between amd and Ddc detected; intron sequences and positions not conserved, although homology across intron junctions is high (Eveleth and Marsh, l986, Genetics 114: 469-83). Sequence predicts a 50,481 dalton polypeptide with a slight negative charge; 38% amino acid homology with dopa decarboxylase. # Amdr: Alpha methyl dopa resistant location: 3- (between h and tn). origin: Induced by ethyl methanesulfonate. references: Bishop and Sherald, 1981, DIS 56: 21. phenotype: Based on two of 16 chromosomes selected for confer- ring resistance to ( methyl dopa when heterozygous. LD50 to L-(-methyl dopa for the two chromosomes is 0.325 mM for Amdr1/+ and 0.35 mM for Amdr2/+, compared to 0.10 mM for wild type. Both chromosomes are homozygous lethal, and Amdr1/Amdr2 is nearly lethal, allowing the inference of a single locus. # amethyst: see amy # amiel location: Autosomal. origin: Spontaneous. synonym: Amiel. references: Rushton and Metcalfe, 1971, DIS 46: 61. phenotype: Homozygous males court abnormally; wing vibrations and copulation attempts more vigorous than in wild type, but mutant males take longer to achieve copulation and have higher incidence of unsuccessful courtships. Homozygous females behave normally. # Amiel: see amiel # Aminoimidazole ribotide synthetase: see ade2 # amn: amnesiac (J.C. Hall) location: 1-63. discoverer: Sziber. origin: Induced by ethyl methanesulfonate. references: Quinn, Sziber, and Booker, 1979, Nature (London) 277: 212-14. phenotype: Homozygous or hemizygous mutant flies can be condi- tioned to avoid odors associated with electric shocks, but effects of conditioning decay with a half life of 15 min com- pared to 60 min for normal. Memory decay biphasic; rapid for first hour and slow thereafter (Tully). Substitution of reward (1.0 M sucrose) for punishment (electric shock) lengthens memory span from one hour to six hours (Tempel, Bonini, Dawson, and Quinn, 1983, Proc. Nat. Acad. Sci. USA 80: 1482-86). Groups of amn flies exhibit apparently abnor- mal acquisition of learning in tests using visual cues (Folk- ers, 1982, J. Insect. Physiol. 28: 535-39); it appears that short-term memory is defective in the mutant (in shock-odor tests), with long-term memory being normal (Tully and Quinn, 1985, J. Comp. Physiol. 157: 263-77); in experiments involv- ing "operant" conditioning, with heat as the aversive uncondi- tioned stimulus, amn exhibits a small decrement in learning per se and subsequently has no detectable memory (Mariath, 1985, J. Insect Physiol. 31: 779-81). In tests of "simple learning," amnesiac individuals habituate to or are sensitized by sugar stimuli subnormally; the sensitization defect maps to the same proximal locus as that affecting associative condi- tioning (Duerr and Quinn, 1982, Proc. Nat. Acad. Sci. USA 79: 3646-50). The effects on courtship behavior or pre- exposure to fertilized females decay more rapidly in amnesiac than in normal males (Siegel and Hall, 1979, Proc. Nat. Acad. Sci. USA 76: 3430-34; Ackerman and Siegel, 1986, J. Neuro- genet. 3: 111-23), but amnesiac males are defective in expressing after-effects of exposure to immature wild-type males when tested immediately after such exposure (Gailey, Jackson, and Siegel, 1982, Genetics 102: 771-82). Females defective in ability to be primed by courtship song (Kyriacou and Hall, 1984, Nature (London) 308: 62-65). cytology: Placed in 19A1 based on its inclusion in Df(1)mal12 = Df(1)19A1;20F but not Df(1)mal11 = Df(1)19A2-3;19E1 or Df(1)mal3 = Df(1)19A2-3;20E-F (Tully and Gergen, 1986, J. Neu- rogenet. 3: 33-47). # Amplification Control Element: see ACE # Amr: Amanatin resistant location: 3- (not mapped). origin: Induced by ethyl methanesulfonate. references: Nishiura, 1981, Biochem. Genet. 19: 31-46. phenotype: Heterozygotes survive 5 ug/ml ( amanatin. RNA polymerase II activity in Amr-bearing flies resistant to ( amanatin. alleles: Three lines possibly containing different alleles designated Amr010, Amr018, and Amr106. other information: Genetic analysis lacking. If it is demon- strated that this locus codes for an RNA polymerase II subunit, it will be renamed RpII plus a subunit designation. # amx: almondex location: 1-27.7 [to the left of lz (Green and Green, 1956, Z. Indukt. Abstamm. Vererbungsl. 87: 708-21)]. origin: X ray induced. discoverer: Ball, 32k20. phenotype: Eyes slightly reduced, narrower below. Trident pat- tern stronger than in lz. Maternal effect lethal. Studies by Shannon [1972, Genetica (The Hague) 43: 244-56] show that amx progeny and many amx/+ progeny of amx mothers are embryonic lethals. Ovaries and egg production of amx females normal. General disorganization of early embryo with amx/+ progeny of amx mothers less extreme than amx progeny (Shannon, 1973, J. Exp. Zool. 183: 383-400); amx/+ daughters show 0.2% survival; amx/Dp(1;1)lz-2 show considerably higher survival (Campos- Ortega); Lethal embryos exhibit hypertrophy of central nervous system at the expense of epidermal tissue (Lehmann, Dietrich, Jimenez, and Campos-Ortega, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 226-29; Lehmann, Jimenez, Dietrich, and Campos- Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 62-74). Similarly peripheral nervous elements, the sensilla, exhibit increased numbers and abnormal morphology; cells diverted from epidermal to neurological pathway (Hartenstein and Campos- Ortega, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 210-21). Embryonic phenotype locally rescuable by injections of ooplasm from wild-type or pcx ova during preblastoderm stages (Campos-Ortega, La Bonne and Mahowald, 1985, Dev. Biol. 110: 264-67). lz/amx is wild type. Mosaics in amx/+ daughters of _/_ or amx/+ females show that ventral tissues are sensitive to reduced amx+ activity; no clones of amx tis- sue found in cuticle of amx/+ daughters of amx mothers (Ger- meraad and Disano, 1984, Genetics 107: s36). RK2. cytology: Located in 8D (region 8D4 through 8E2) by Green and Green (1956). # amx55: see lzK #*amy: amethyst location: 2- (not located). discoverer: Bridges. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 218. phenotype: Transparent, light-purplish eye color. RK3. # Amy: Amylase location: 2-77.9 (based on 5039 c-wt recombinants). origin: Polymorphic locus. discoverer: Kikkawa, 1957. references: Kikkawa and Abe, 1960, Annotationes Zool. Jpn. 33: 14-23. Kikkawa, 1960, Jpn. J. Genet. 35: 382-87. Kikkawa and Ogita, 1962, Jpn. J. Genet. 37: 394-95. Kikkawa, 1963, DIS 37: 94. Bahn, 1967, Hereditas 58: 1-12. 1964, Jpn. J. Genet. 39: 401-11. Doane, 1969, J. Exp. Zool. 171: 321-42. 1969, Problems in Biology: RNA in development (Hanly, ed.). U. of Utah Press, Salt Lake City, pp. 73-109 (fig.). Hickey and Benkel, 1986, CRC Crit. Rev. Biotech. (fig.). phenotype: The structural gene for (-amylase [AMY (EC 3.2.1.1)]. A monomeric protein based on failure to form hybrid enzyme molecules of intermediate mobility in heterozy- gotes for alleles coding for electrophoretic variants. Activity mainly in midgut and hemolymph with smaller amounts in other tissues; activity found in anterior or posterior, or both, but not middle, region of midgut; three spatial patterns of adult posterior midgut activity encountered on standard medium; controlled by the trans-regulatory effect of map (2- 80) (Abraham and Doane, 1978, Proc. Nat. Acad. Sci. USA 75: 4446-50); adult anterior midgut activity under regulation of another separable regulatory locus (Doane, 1980, DIS 55: 36-39). Larval midgut activity affected by closely linked cis-acting regulatory elements (Klarenberg, Kisser, Willemse, and Scharloo, 1986, Genetics 114: 1131-45). Amylase activity is glucose repressible (Hickey and Benkel, 1982, Biochem. Genet. 20: 1117-29); the degree of repression can be greater than one hundred fold in larvae and occurs at a pretranslational, probably transcriptional, level of regula- tion (Benkel and Hickey, 1985, Genetics 110: S25; 1986, Genetics 114: 137-44, 943-54; 1987, Proc. Nat. Acad. Sci. USA 84: 1337-39). alleles: Eight electrophoretic variants of a-amylase have been recorded; they are numbered, in order of decreasing rates of migration toward the anode, from -1 through +7 (Doane, Treat- Clemons, Gemmill. Levy, Hawley, Buchenberg, and Paigen, 1983, Isozymes: Curr. Top. Biol. Med. Res. 9: 63-70). Enzymes with mobilities 2 and 3 exist in forms with different heat sensi- tivities: Amy1 the most frequent allele, may be expressed at three different activity levels in different strains, 1a, 1b, and 1c in which 1a has twice the activity of 1b and 1b has twice the activity of 1c; purified (-amylases from 1a and 1c strains have identical specific activities (Treat-Clemmons and Doane, 1982, Isozyme Bull. 15: 90-91); enzyme levels here are apparently under the control of closely linked transacting regulatory elements (Hickey, 1981, Biochem. Genet. 19: 783- 96). A chromosome may express none, one, or two of these forms. Bahn recovered one Amy1,3 and two Amy2 recombinants from Amy1/Amy2,3 heterozygotes and one Amy4,3 and two Amy2,6 recombinants from Amy4,6/Amy2,3 heterozygotes. From these observations it was concluded that the Amy locus is duplicated and the two copies are separated by 0.008 cm; furthermore, flanking marker segregations indicated that determinants of forms 1,2 (thermostable), and 4 are to the left of those for 3 (thermostable) and 6. Conservation of restriction endocuclease sites in DNA from Bahn's Amy2,3 in comparison with Amy1,3 (from Canton-S) and Amy1,6 (from Suyama, Japan) indicates that the determinant of form 1 is to the left of those of forms 3 and 6 in the latter two chromosomes (Gemmill, Schwartz, and Doane, 1986, Nucl. Acids Res. 14: 5337-52). Amy1 monomorphic allele in Oregon-R has been shown to be Amy1,1 (Hawley, 1989, Ph.D thesis, Arizona State University). cytology: Placed in 54A based on in situ hybridization (Gem- mill, Levy, and Doane, 1985, Genetics 110: 299-312). # Amy-d: Amylase distal The distal member of the Amy repeat. Electrophoretic alleles include Amy-d3 (thermostable). Amy-d6 and likely Amy-d2 (thermolabile); some chromosomes apparently lack Amy-d activity. # Amy-p: Amylase proximal The proximal member of the Amy repeat. Electrophoretic alleles include Amy-p1, Amy-p2 (thermostable), Amy-p4, prob- ably Amy-p3 (thermolabile), and Amy-p5; a null allele also exists. Allelic compositions of various strains are tabulated in the accompanying table. strain source Amy-p Amy-d ref ( _______________________________________________________ Amy1a Amy-p1a inactive? Amy1b Amy-p1b inactive? Amy1c Amy-p1c inactive? Amy1.2 | adpfs, Amy-p1 Amy-d2 2, 3, Kaduna thermo- 4, 5 labile Amy1.3 Canton-S Amy-p1 Amy-d3 3, 4, 5, 6 Amy1.4 Amy-p1 Amy-d4 Amy1.6 Suyama Amy-p1 Amy-d6 3, 4, 5 thermo- labile Amy2 Amy-p2 inactive? Amy2.3 Copenhagen Amy-p2 Amy-d3 1, 3, 5 Amy2.6 Amy-p2 Amy-d6 Amy3.6 | Kyoto Amy-p3 Amy-d6 3, 4 thermo- thermo- labile labile Amy4.5 Amy-p4 Amy-d5 Amy4.6 adp60, Amy-p4 Amy-d6 1, 3, 4 Kaduna thermo- thermo- labile labile Amy5 Africa Adp-p5 inactive ? 8 Amy5.6 Africa Adp-p5 Adp-d6 8 Amyn Texas inactive inactive 7 ( 1 = Bahn, 1967, Hereditas 58: 1-12; 2 = Doane, 1967, J. Exp. Zool. 164: 363-78; 3 = Doane, 1969, Problems in Biol- ogy. RNA in Development (W. E. Hanley, ed.). Univ. Utah Press, Salt Lake City, pp. 73-109; 4 = Doane, 1969, J. Exp. Zool. 171: 321-42; 5 = Gemmill, Schwartz, and Doane, 1986, Nucl. Acids Res. 14: 5337-52; 6 = Levy, Gemmill, and Doane, 1985, Genetics 110: 313-24; 7 = Haj-Ahmed and Hickey, 1982, Nature 299: 350-52; 8 = Puijk and DeJong, 1972, DIS 49: 61. | Tentative assignments. molecular biology: Clones homologous to mouse (-amylase gene isolated from Maniatis library (Doane, Treat-Clemons, Gemmill, Levy, Hawley, Buchberg, and Paigen, 1983, Curr. Top. Biol. Med. Res. 9: 63-90). \Dm32 hybridizes to polytene region 53CD; no homologous mRNA detected; postulated to be pseu- dogene. \Dm65 hybridizes to 54A1-B1 and is homologous to a 1450-1500 nucleotide transcript (Gemmill, Levy, and Doane, 1985, Genetics 110: 299-312). 15kb insert in \Dm65 contains reverse repeat by restriction mapping; subclones, each con- taining one of the repeated sequences, injected into Xenopus oocytes; one subclone capable of producing isozyme 1 of (- amylase; the other capable of producing isozyme 3; confirms duplicated nature of locus (Levy, Gemmill, and Doane, 1984, Isozyme Bull. 17; 1985, Genetics 110: 313-24). Directions of transcription of the two genes divergent. (Levy, 1985, Genet- ics 110: 137); separated by 4 kb. Seven strains exhibiting no, one, or two electrophoretic forms of (-amylase all carry the duplication as ascertained from restriction analysis. Amy1c contains an approximately 10 kilobase insert some 10 kb proximal to Amy-p. 12% of chromosomes isolated from diverse natural populations contain large inserts in the vicinity of the Amy loci (Langley, Shrimpton, Yamazaki, Miyashita, Matsuo, and Aguadro, 1988, Genetics 119: 619-29). Two molecular inversions that could have arisen through interlocus exchange recorded; one had normal levels of amylase activity (Langley et al.) and the other was a null allele that produced reduced levels of mRNA and was insensitive to glucose repression (Hickey, Benkel, Abukashawa, and Haus, 1988, Biochem. Genet. 26: 757-68; Schwartz and Doane, 1989, Biochem. Genet. 27: 31-46). An amylase cDNA has been cloned and sequenced (Boer, and Hickey, 1986, Nucleic Acid Res. 14: 8399-8411). This sequence shows 57% identity to mouse amylase; the predicted amino-acid sequence indicates a 54.5-kd polypeptide of 493 residues, the 18 N-terminal ones of which are signal sequence; there is 55.4% amino-acid identity with mouse amylase. Upstream sequence contains a repeated motif also found in a negatively regulated mammalian gene (Hickey, Genest, and Benkel, 1987, Nucleic Acid Res. 15: 7184). Northern blots probed with this cDNA show that the glucose repression effect is at the level of amylase mRNA abundance. # Amy4: see Amy1,4 # Amy+: see Amy1 # Amyad: see Amy4,6 # Amys: see Amy2,6 # Amywh: see Amy1,4 # Amyloid protein precursor-like: see Appl # an: ancon location: 2-44 (34-54). discoverer: Bridges, 30e3. phenotype: Wings and legs somewhat short in an1; an2 (CP627) more extreme with gnarled legs, scraggly abdominal bristles, etched sclerites; eyes small and roughish. an1/an2 like an2. alleles: an1 and an2. # anarista: see aa # ancon: see an # And: Andante (J.C. Hall) location: 1-36.2 origin: Induced by ethyl methanesulfonate. discoverer: Konopka, R. Smith and Orr, 1976. references: Jackson, Gailey, and Siegel, 1983, J. Comp. Phy- siol. 151: 545-52. phenotype: The normal free-running 24 hr periods of the cir- cadian rhythms of eclosion and adult locomotor activity (in constant conditions) are lengthened by 1.5-2 hr/cycle; And/+ heterozygotes have a period phenotype intermediate between wild-type and mutant homozygotes (Konopka, R. Smith and Orr). The phase-response curves (PRCs) for eclosion and activity rhythms, indicating light-induced phase shifts, show a similar degree of lengthening as seen in free-running periodicities. And rhythms are highly temperature-compensated, as are those of wild-type (Konopka et al.). And males are defective in after effects on courtship behavior that are usually induced by prior exposure to mated females or very young males (Jack- son et al., 1983). cytology: Placed in 10E1-2;10F1. The And homozygote-like activity rhythm phenotype is uncovered by Df(1)KA6 = Df(1)10E1;11A7-8 and Df(1)KA7 = Df(1)10A9;10F6-7, but hetero- zygotes involving And and Df(1)N105 = Df(1)10F7;11D1, Df(1)RA47 = Df(1)10F1;19F9-10, or Df(1)m259-4 = Df(1)10C2- 3;10E1-2 are like And/+ (Konopka et al.). The two And- uncovering Df's just noted over wild type give normal periods. An anomaly then, is that Df(1)HA85 = Df(1)10C1-2;11A1-2, which uncovers And as it should (see above), leads to significantly longer-than-normal periods when over wild type (Konopka et al.). other information: And lengthens in an additive manner, the periodicities associated with certain other rhythm mutants, i.e., those which by themselves cause shorter- or longer- than-normal locomotor activity periods (viz, perS, perL1, perL2, Clk). And, on its isolation, was associated with a dy wing phenotype, and the rhythm abnormality maps to the dy-m locus (see "cytology"); but dy and mD have normal activity rhythm periods, and And over either of these two visibles gives the same periods as seen in And/+ (Konopka et al.); how- ever, of four gamma-ray induced dy's - dyn1, dyn2, dyn3, and dyn4, all but dyn2 are And-like in their locomotor activity rhythms (Jackson, Newby, and DiBartolomeis, 1989, Neurosci. Abstr. 15: 461). # ang: angle wing location: 2-10.5. origin: Spontaneous. discoverer: Mittler and Goldberg, 48i16. references: Mittler, 1950, DIS 24: 61. phenotype: Wings held up from dorsal surfaces and extended out- ward 15-90 from the mid-dorsal line. Longitudinal dorsal median muscles 5 and 6 fused (Goldberg, 1954, Ph.D. Thesis, Ill. Inst. Technol.). No increase in expressivity with tem- perature. Does not overlap wild type. RK2. # ang: see ano # angle wing: see ang # angle wing: see agl # angle winglike: see agl #*ano: anomogenitals location: 1-35.7. origin: Induced by triethylenemelamine. discoverer: Fahmy, 1952. synonym: Originally symbolized ang, but this symbol preoccu- pied. references: 1958, DIS 32: 67. phenotype: Many bristles on head and thorax either reduced in size or absent. Thoracic and abdominal hairs appreciably fewer. External male genitalia invariably abnormal, sometimes completely absent. Melanized exudate frequently present in furrow between mesonotum and scutellum near anterior scutellar bristles. Males sterile; viability less than 10% wild type. RK3. # ant: antennaless location: 2- (not located). origin: Spontaneous. discoverer: Gordon, 1936. references: 1941, DIS 14: 39. 1941, Proc. Intern. Congr. Genet., 7th. p. 131. Gordon and Sang, 1941, Proc. Roy. Soc. (London), Ser. B 130: 151-84 (fig.). Vogt, 1947, Biol. Zentralbl. 66: 388-95 (fig.). phenotype: Antennae missing on one or both sides. Expression affected by residual genotype, nutritional environment, and temperature. Time of action about 70 hours after hatching [Begg and Sang, 1945, J. Exp. Biol. 21: 1-4 (fig.)]. Used in experiments to locate chemoreceptors [Begg and Hogben, 1946, Proc. Roy. Soc. (London), Ser. B 133: 1-19] and in studies of mating behavior (Begg and Packman, 1951, Nature 168: 953). RK3.