h: hairy From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 202. # h: hairy location: 3-26.5. synonym: barrel (Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69). references: Mohr, 1922, Z. Indukt. Abstamm. Vererbungsl. 28: 17. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 202 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 214 (fig.). Neel, 1944, Genetics 26: 52-68 (fig.). Nusslein-Volhard and Wieschaus, 1980, Nature (London) 287: 795-801. Holmgren, 1984, EMBO. J. 3: 569-73. Ingham, Howard, and Ish-Horowicz, 1985a, Nature (London) 318: 439-45. Ingham, Pinchin, Howard, and Ish-Horowicz, 1985b, Genetics 111: 463-86. Ish-Horowicz, Howard, and Ingham, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 135-44. Ish-Horowicz, Howard, Pinchin, and Ingham, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 135-44. Ish-Horowicz and Pinchin, 1987, Cell 51: 405-15. Carroll, Laughon, and Thalley, 1988, Genes Dev. 2: 833-90. Howard, Ingham, and Rushlow, 1988, Genes Dev. 2: 1037-46. Carrol and Whyte, 1989, Genes Dev. 3: 905-16; Rushlow, Hogan, Pinchin, Howe, Lardelli, and Ish-Horowicz, 1989, EMBO J. 8: 3095-3103. phenotype: The pair-rule gene hairy regulates the development of alternate segments in the embryo as well as the spatial expression of another pair-rule gene fushi tarazu (Holmgren, 1984; Carroll et al., 1988; Rushlow et al., 1989). A later phenotypic expression of hairy, the adult bristle pattern, is established during larval and pupal stages (Nusslein-Volhard and Wieschaus, 1980; Ingham et al., 1985a, 1985b). In the embryo, h mutations delete the posterior part of each odd- numbered segment, weak alleles deleting less than a whole seg- ment and strong alleles deleting regions greater than one seg- ment. In mutant adults, extra microchaetae are found along wing veins, L2 more so than L4 or 5, and on wing membrane; also on dorsal and ventral scutellum and top of head. Extra sensilla present on longitudinal wing veins in a gradient in which sensilla are concentrated proximally and hairs distally; intermediate structures found in the middle (Spivey and Thomp- son, 1984, Genetics 107: s102). Extra acrostichal row on either side of midline between dorsocentral bristles (Claxton, 1971, DIS 46: 133); also occupy thin arch of cuticle connect- ing ventral scutellum and pleurae. Microchaetae found on mesopleurae (mean of 13 in males and 20 in females versus none in wild type) and pteropleurae (Murphy, 1972, J. Exp. Zool. 179: 51-62). Used by Garcia-Bellido and Ferrus (1975, Wilhelm Roux's Arch. Dev. Biol. 178: 337-40) to provide cuticular markers on pleurae for fate mapping. Additional hair-forming cells present in 19-hr pupa (Lees and Waddington, 1942, DIS 16: 70). Autonomous expression in clones produced prior to the last eight hr of larval life; clones produced during the last eight hr before pupation exhibit normal pheno- type; attributable to perdurance of wild-type gene product (Garcia-Bellido and Merriam, 1971, Proc. Nat. Acad. Sci. USA 68: 2222-26). Reduced ac+ function as in ac3 or ac3/+ suppresses h phenotype; extra doses of ac+ enhance h expres- sion and can render h partially dominant (Sturtevant, 1969, Dev. Biol. 21: 48-61; Botas, Moscoso del Prado, and Garcia- Bellido, EMBO J. 1: 307-10). Three doses of h+ suppress Hw (Botas, et al.). h expression also enhanced by combination with rearrangements that place the ac-sc region in juxtaposi- tion with substantial quantities of heterochromation (Green, 1960, Proc. Nat. Acad. Sci. 46: 524-28). Interactions with sc alleles detailed by Sturtevant (1969). h2 less severe than and partially complements h1 (Sturtevant). As with ci+, expression of h+ may be altered in the direction of h by rear- rangements with breakpoints in the vicinity of the h locus (Dubinin and Sidorov, 1934, Biol. Zh. 3: 307-31; see also Jeffrey, 1979, Genetics 91: 105-25). Unlike the ci case, however, rearranged h chromosomes do not show evidence of altered gene action (Stern, 1944, DIS: 18:56). alleles: alleles origin discoverer synonym ref ( comments cytology _____________________________________________________________________________ h1 | spont Mohr, 18l11 1, 3, viable 10, 12 h2 spont Bridges, 28d23 3 viable *h3 spont Bridges *h26c 2 *h4 spont Bridges *h30a 2 *h5 spont Nichols- *h33k 2 Skoog *h6 spont Bridges *h34e 2 *h7 spont Curry *h38d 2 *h8 spont Neel *h41k 2 *h9 spont Neel *h42a 2 *h10 X ray Alexander *h100.12 14 viable In(3L)61A2-3; 66D *h11 X ray Alexander *h100.239 14 semilethal In(3L)66D11-12; 80C *h12 X ray Alexander *h100.271 14 lethal T(2;3)41; 66D14-E1 h13 / X ray Green hs 4 nearly lethal h14 X ray Braver hR06 9 T(1;3)1B10-C1; 66D14-E1 h15 X ray Braver hR15 9 lethal In(3LR)66D14-E1; 85B5-C12 h16 X ray Jeffrey hR38 8, 9 15% viable In(3L)66D14-E1; 80F h17 X ray Jeffrey hR40 8, 9 lethal Tp(3;2)30B7-C1; 66D14-E1; 73B7-C1 h18 X ray Jeffrey hR44 8, 9 27% viable Tp(3;4)63A3-B1; 66F2-67A1; 101F h19 X ray Jeffrey hR47 8, 9 5% viable T(2;3)23A2-B1; 34C2-4; 66D6-10; 98F12-99A1 h20 / EMS Jurgens, hbrr 12 lethal Nusslein- Volhard h21 EMS Nusslein- h9N53 5 lethal Volhard h22 EMS hC1 5, 7 lethal h23 EMS hC2 12 lethal h24 EMS h1K93 7, 10 lethal h25 EMS in h1 Jurgens h5H07 7, 13 lethal h26 EMS in h1 Jurgens h7H94 7, 13 lethal h27 EMS Jurgens h8K115 7, 13 lethal h28 EMS in h1 Jurgens h9K78 7, 13 lethal h29 EMS in h1 Nusslein- h11D 7, 13 lethal Volhard h30 EMS Nusslein- h12C 7, 13 lethal Volhard h31 EMS Nusslein- h14H 7, 13 lethal In(3LR)66D14-E1; Volhard 85B5-C12 h32 HD Ingham hd1.1 7 lethal h33 HD Ingham hd1.2 7 lethal h34 HD Ingham hd3 7 lethal h35 HD Ingham hd4.1 7 lethal h36 HD Ingham hd6 7 lethal h37 HD Ingham hd7 7 lethal h38 HD Ingham hd8 7 lethal h39 HD Ingham hd9 7 lethal h40 HD Ingham hd11 7 lethal In(3L)66D10-15; 72C h41 HD Jurgens hIL79K 7 lethal h42 ` X ray Ingham hK1 6, 7 viable In(3L)65B1-2; 66D6-10 h43 X ray Moscoso hM1 viable del Prado h44 X ray Moscoso hM2 viable del Prado h45 X ray Moscoso hM3 viable del Prado *h46 EMS Moscoso *hM4 T(1;3) del Prado h47 X ray Ingham hm1 7 lethal T(2;3)41A; 66D9-11 h48 X ray Ingham hm2 7 lethal In(3L)66D5-11; 80C h49 ` X ray Ingham hm3 6, 7 lethal Tp(3;3)61E; 66C;66D h50 ` X ray Ingham hm7 6 lethal In(3L)66D6; 67D8 h51 ` X ray Ingham hm8 6 lethal ( 1 = Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 202 (fig.); 2 = CP552; 3 = CP627; 4 = Green, 1960, Proc. Nat. Acad. Sci. USA 46: 524-28; 5 = Holmgren, 1984, EMBO J. 3: 569-73; 6 = Howard, Ingham, and Rushlow, 1988, Genes Dev. 2: 1037-46; 7 = Ingham, Pinchin, Howard, and Ish-Horowicz, 1985, Genetics 111: 463-86; 8 = Jeffrey, 1971, DIS 47: 37; 9 = Jeffrey, 1979, Genetics 91: 105-25; 10 = Mohr, 1922, Z. Indukt. Abstamm. Vererbungsl. 28: 17.; 11 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 214 (fig.); 12 = Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801; 13 = Tearle, and Nusslein-Volhard, 1987, DIS 66: 209-69; 14 = Ward and Alexander, 1957, Genet- ics 42: 42-54. | Result of gypsy insertion (Holmgren, 1984). / Phenotype described separately; alleles also described in h20. ` Regulatory mutation causing alterations in hairy expression in cellular blastodern that result in a partial version of the wild-type pattern (Howard et al., 1988). cytology: Placed in 66D15 on the basis of the h phenotypes of many rearrangements with breakpoints between 66D14 and 66E1 (Jeffrey, 1979). Placed in 66D9-11 by Ingham et al. (1985) based on the left breakpoint of T(2;3)hm1 = T(2;3)66D9-11;41A. molecular biology: The hairy region was tagged and cloned with the transposing element gypsy (Holmgren, 1984) and with P ele- ments (Ish-Horowicz et al., 1985). Cloned genes were able to rescue h segmentation mutants when introduced into flies by P-element transposition (Rushlow et al., 1989). The gene hairy encodes a major transcript of 2.1 to 2.3 kb that is expressed at high levels in 2-4 hr embryos but at lower levels later (Ish-Horowicz et al., 1985; Rushlow et al., 1989) and a minor 2.0 kb transcript that is expressed at low levels in 2-4 hr embryos but at higher levels in larvae and adults. Two other transcripts, 1 kb and 3 kb, have been reported during larval life (Ish-Horowicz et al., 1985); the time of expression and chromosomal origin of these RNAs indicate that they are involved in hairy bristle function. All RNAs are transcribed from distal to proximal and must differ at their 5 ends. Genomic and cDNA sequences have been obtained (Rushlow et al., 1989); they show that the hairy transcription unit is inter- rupted by two introns. The gene encodes a 337 amino acid pro- tein, which contains a helix-loop motif (Rushlow et al., 1989), and functions both in segmentation in the embryo and bristle patterning in the adult. The protein is found in cell nuclei and is localized in eight distinct regions of the early embryo (Carroll et al., 1988); the major protein stripes are located in the posterior and adjacent anterior parts of alter- nate segment primordia. There are striking patterns of nuclear protein distribution during larval and pupal imaginal disc development with transient hairy expression in the eye, leg, and wing discs (Carroll and Whyte, 1989). other information: h1 shown to recombine with and lie to the right of h2 (Sturtevant; Rasmussen). # h13 synonym: hs, hairy-subliminal. phenotype: Homozygote nearly lethal but has no h phenotype. Heterozygote with h and h2 also wild type. hs/+ has extra hairs on wings, head, pleurae, halteres, and occasionally on scutellum if also heterozygous for certain X-chromosome inver- sions that variegate for Hw, including In(1)sc8, In(1)scS1, and In(1)y3P. Presence of y+Y also induces extra hairs. RK3. # h20 synonym: hbrr, hairy-barrel. phenotype: Homozygous lethal. Newly hatched larvae lack denti- cle belts of alternate segments; i.e. the prothoracic, metathoracic and even numbered abdominal segments; naked cuti- cle missing from mesothorax and odd numbered abdominal seg- ments (a member of the pair-rule class of Nusslein-Volhard and Wieschaus). Pattern of persisting segments often slightly irregular. alleles: Eight embryonic lethal alleles, including four with weak expression, reported by Jurgens, Wieschaus, Nusslein- Volhard, and Kluding (1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95). H: Hairless From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 161. # H: Hairless location: 3-69.5. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 161 (fig.). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 170 (fig.), 227. Nash, 1965, Genet. Res. 6: 175-89. Bang, Hartenstein, and Posakony, 1990, Development, in press. phenotype: Bristles, especially postverticals and abdominals, missing in heterozygous H flies. Bristle sockets present at some sites, not at others. Expressed most distinctly on head; occipital; post vertical and ocellar bristles affected. Bris- tles of antennae and vibrissae show mutant phenotype much less frequently. Sockets without shafts also found on thorax, scu- tellum, abdominal tergites, external genitalia, wings, and legs. No shaftless sockets appear on the bracted costa of the wing. Some 40% of bristle organs located on distal part of femur differentiate neither shaft nor bract; bracts absent whenever shaft missing but present when shaft present; abnor- mally short shaft may be accompanied by normal-sized bract (from description of H2, by Tobler, Rothenbuhler, and Nothiger, 1973, Experientia 29: 370-71). Veins L4 and L5 do not reach wing margin; occasionally true of L2 also. Eyes larger than wild type; body color somewhat paler. Lees and Waddington [1942, Proc. Roy. Soc. (London), Ser. B. 131: 87- 110 (fig.)] show that trichogen cell forms a socket instead of a bristle shaft at some sites. Phenotypic expression of H responds linearly to dosage of Su(H)+ in region 35B6-10 on the left arm of chromosome 2. The number of microchaetae in H/+ flies varies from approximately 35 in the presence of a single dose of 35B6-10 to fewer than 10 in the presence of four doses (Ashburner, 1982, Genetics 64: 471-79). Interactions with other mutants studied by House (1953, Genetics 38: 199-215, 309-27; 1959, Genetics 44: 516; 1955, Anat. Record 122: 471; 1959, Anat. Record 134: 581-82). H suppresses wing notching of N, fa, fano, and nd, enhances Ax; also H enhances eye effect of spl, and removes more bristles in combination with spl (House, Von Halle). Reduction in the number of copies of the wild-type allele of H decreases the mutant phenotype of heterozygous N and Dl flies, but increase in the number of copies of the wild-type allele of H enhances the mutant pheno- type of heterozygous N, Dl, and E(spl) flies (Vassin, Viel- metter, and Campos-Ortega, 1985, J. Neurogenet. 2: 291-308). H shows some superadditive interaction with en, ci, ciW, and ciD relative to degree of L4 interruption. L2 interruption augmented in combinations with ve and ri; L3 interruption aug- mented in combinations with ve and tt. Triploid, H/+/+, intermediate between wild type and H/+. H/H/+ most extreme type with bristles absent from head, thorax, and abdomen [Gowen, 1933, Am. Nat. 67: 178-80 (fig.)]. Homozygous lethal. H null homozygotes die during larval and pupal stages (Bang et al.). Animals surviving to pharate adult are com- pletely devoid of macrochaetes and microchaetes on the head and notum, with occasional "double sockets" remaining on the abdominal tergites. Bristles on the legs significantly resis- tant to loss of H+ function; many "double sockets" and some normal bristles remain on the legs of H null homozygotes. In regions of the notum exhibiting bristle "loss" in adult H mutants, macrochaete and microchaete primary precursor cells undetectable (Bang et al.). RK1. alleles origin discoverer synonym ref ( comments ________________________________________________________________ H1 spont Bridges, 16c4 H1 5, 7, 10, 11, 13 H2 spont Sturtevant H2 5, 13 H3 Sturtevant H3 *H4 spont Bridges, 30b20 *H4 H5 X ray Dobzansky, 1930 HD1 6, 7 H6 X ray Oliver, 28k4 H28k 6, 12 H7 X ray Oliver, 32l28 H32y 6, 12 H8 X ray Oliver, 32l28 H32z 6, 12 H9 X ray Oliver, 33a2 H33a 6, 12 H10 X ray Oliver, 35a5 H35a 6, 12 H11 32P Bateman,1939 HP2 4 *H12 / ray Ives, 58b25 *H58b 9 T(Y;3) H13 | Gloor H57c 2, 14 H14 / ray Harrington H80 2 H15 ` spont Gallego Hst 8 H16 / spont Albornoz Hr 1 recessive H17 HC19 3 H18 HC20 3 H19 HC25 3 H20 HC28 3 H21 HC 3 like H22 H22 Bang HC 3 recessive H23 EMS Weigle HA4.1 H24 X ray Schrons HKX1 T(2;3)41;92F1-2 H25 X ray Jimenez Hw11 15 H26 Campos-Ortega HXIM ( 1 = Albornoz, 1984, DIS 60: 44-45; 2 = Ashburner, 1982, Genetics 101: 447-59; 3 = Bang, Hartenstein, and Posakony, 1990, Development, in press; 4 = Bateman, 1950, DIS 24: 55; 5 = Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 161; 6 = CP552; 7 = CP627; 8 = Gallego, Garc'a-Dorado, and Lopez-Fanjul, 1982, DIS 58: 64; 9 = Ives, 1959, DIS 33: 95; 10 = Morgan, Bridges, and Stur- tevant, 1925, Bibliogr. Genet. 2: 170, 227; 11 = Nash, 1965, Genet. Res. 6: 175-89; 12 = Oliver, 1939, DIS 12: 48; 13 = Plunkett, 1926, J. Exp. Zool. 46: 181-244; 14 = Van Breugel, Ray, and Gloor, 1968, Genetica 39: 165- 92; 15 = Vassin, Vielmetter, and Campos-Ortega, 1985, J. Neurogenet. 2: 291-308. | Occurred simultaneously with, but independently of Tp(3;3)H57c=Tp(3;3)86F7-11;95C1-2;97D1-2;98C5. / Fuller phenotypic description follows. ` Affects number of sternopleural bristles (Gallego et al., 1982). cytology: Located in 92E12 to 92F1-2 on the basis of the right breakpoint of Df(3R)H-KX2 (Campos-Ortega) and the third chro- mosome breakpoint of T(2;3)HKX1 (Bang, Hartenstein, and Posakony, 1990, Development, in press). # H16 phenotype: Recessive allele of Hairy (formerly called Hairless-recessive). Homozygotes have nearly all bristles and hairs substituted by double and triple abnormal sockets; veins L4 and L5 fail to reach margin. H16/H lethal, probably in pupal stage; few escapers short lived with extreme Hairless phenotype; all bristles and hairs suppressed or substituted by abnormal sockets; wings reduced; veins L2, L4 and L5 abnormal. # H22 phenotype: Less severe than H16. Almost completely recessive. Heterozygotes most frequently wildtype in phenotype, but occa- sionally a "double socket" appears on the head in the position of a postvertical macrochaete or on the abdominal tergites. Homozygotes display a much stronger and more extensive mutant phenotype than H null heterozygotes. Many head and notum macrochaetes and approximately 50% of notum microchaetes miss- ing; remaining 50% exhibit a spectrum of "double socket" phenotypes. Homozygotes also exhibit loss of wing vein tissue from L4 and L5. Approximately 50% of flies carrying H22r in trans to a H null allele die as pharate adults. The remainder survive to eclosion, but are short-lived and exhibit extensive loss of both macrochaetes and microchaetes on the head, notum, and abdominal tergites; only 20% of the notum microchaetes remain, all with a completely transformed "double socket" phenotype. # H: see Lvp # H2.0: Homeobox 2.0 location: 2-. references: Barad, Jack, Chadwick, and McGinnis, 1988, EMBO J. 7: 2151 61. phenotype: Encodes a novel, tissue-specific homeobox. A large deletion including H2.0 is homozygous lethal, but the lethal- ity may not be due to the homeobox gene. Although the struc- ture of most organs as well as the epidermis appears to be normal in these lethal embryos, the midgut forms a balloon like yolk-filled sac. cytology: Located in 26B1-3 by in situ hybridization to the salivaries. molecular biology: Gene cloned from a library of Oregon-R genomic DNA using a Scr probe. The nucleotide sequence of the cDNA and the presumed amino acid sequence were determined. A single major transcript of 1.85 kb is present throughout development, beginning at 6 hr of embryogenesis and becoming abundant between 6 and 24 hours. The cDNA includes a single methionine codon and an open reading frame of 1257 nucleotides with a highly divergent homeobox. There is a M or opa repeat near the center of the ORF with 21 CAX triplets coding for histidine and glutamine. The predicted protein is made up of 410 amino acids. This homeobox shows less than 40% identity to the eve and z2 homeoboxes. Tissue-specific expression of H2.0 was first detected at embryonic stage 10 at the flexure point between the posterior midgut invagination and the extended germ band. In stage 11, the homeobox is expressed in the visceral mesoderm in con- tinual bands on either side of the midline from the posterior midgut invagination to the anterior midgut invagination. It is later detected in all cells destined to form the visceral mus- culature and especially in all cells of the splanchnopleura. Ectodermal expression occurs in a restricted lateral part of the posterior compartment of each segment. A line of H2.0 expressing cells connects each patch of ectodermal expression with the expression in the splanchnopleura. No expression was observed in the gut ectoderm or the somatic mesoderm. #*ha: hair bristles location: 1-22.7. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1954. references: 1958, DIS 32: 70. phenotype: Small fly with extremely fine, short bristles. Males viable and fertile. Females less viable and highly infertile. RK3. # H37: see elf # Hab: see BXC # Had: |-Hydroxy-acid-dehydrogenase location: 1-54.4 (between sl and r). references: Borack, Water, and Sofer, 1971, DIS 46: 43. Borack and Sofer, 1971, J. Biol. Chem. 246: 5345. Borack, 1974, Experientia 30: 31. Tobler and Grell, 1978, Biochem. Genet. 16: 333-42. phenotype: Thought to be the structural gene for | Hydroxy acid dehydrogenase (L-|-hydroxyacid: NAD oxidoreductase, E.C 1.1.1.45). The enzyme is a dimer, based on the formation of hybrid enzyme in D.simulans X D. melanogaster hybrids, of molecular weight 6.3 X 104 daltons. Purification and biochem- istry by Borak and Sofer. Activity high in Malpighian tubules, less in muscles, intestine, and fat body; absent from brain, salivary gland, and imaginal disks. (Borak, 1972, DIS 48: 73). Activity peaks at 72 hr after hatching, then declines through larval and pupal stages, and increases to stable maximum level at 6 days of adult life (Tobler and Grell). Enzyme expendible; hemizygotes and homozygotes for null allele survive normally (Tobler and Grell). alleles: Three electrophoretic variants HadF, HadI and HadS, with fast intermediate, and slow mobility described by Borack et al.; an ethyl-methanesulfonate-induced inactive allele, Hadm1, described by Tobler and Grell. # hair bristles: see ha # Hairless: see H # hairy: see h # Hairy wing: see Hw under ASC # half out: see hat # halfway: see hfw # Haltere mimic: see CbxHm under BXC # Hang-glider: see Hg # hap: hapless location: 1-50.2. origin: Induced by ethyl methanesulfonate. references: Eberle and Hilliker, 1988, Genetics 88: 109-120. phenotype: The embryonic lethal phenotype is characterized by an undispersed central yolk plug, no visible Malpighian tubules, unsclerotized mouthparts, and poorly visible cuticle. cytology: Located in 12B9-13F. # Haplo-diplo lethal: see Hdl # haplo-female sterile: see Fs(1)10A # hat: half out location: 3-{47}. references: Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23. phenotype: Pharate adults appear morphologically normal, but only partially eclose. Heads and thoraxes may emerge, but fail to complete emergence. Not complemented by T(2;3)Ta1. alleles: alleles origin discoverer synonym _______________________________________ hat1 EMS Denell l(3)d1 hat2 EMS Kaufman l(3)k1 hat3 EMS Kaufman l(3)k13 hat4 EMS R. Lewis l(3)r8 cytology: Located in 84C1-2 since not complemented by T(2;3)Ta1 = T(2;3)51E1-2;84C1-2. Unlike stk, hat is not included in Df(3R)Scx2 = Df(3R)84A4-5;84C1-2. # hau: haunted location: 3-48.4. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). phenotype: Homozygous lethal; only head skeleton visible in homozygous embryo; no differentiation of cuticle. alleles: Four. # hay: haywire location: 3-34.4. origin: Induced by ethyl methanesulfonate synonym: ms(3)nc2. references: Fuller, 1986, Proc. Soc. Dev. Biol. 74: 19-41. Regan and Fuller, 1988, Genes and Development 2: 82-92. phenotype: The original allele, haync2, is homozygous male sterile; some derivative alleles are recessive lethal. Homoz- ygous haync2 males display defects in meiosis, flagellar elon- gation, and nuclear shaping. haync2 also male sterile in trans heterozygotes with recessive male-sterile alleles of | Tub85D or with wrlnc4 suggesting a role for the haywire pro- duct in microtubule function. Deficiencies of hay are fertile in heterozygous combination with the above interacting muta- tions, indicating that the extragenic failure haync2 to com- plement is based on a poison product mechanism. This feature was used to select alleles (haync2rv1-8) that revert the failure of haync2 to complement |2tn (= |Tub85Dn). alleles: allele origin ref ( phenotype | ________________________________________ haync2 EMS 1 a haync2rv1 EMS 2 b haync2rv2 EMS 2 b haync2rv3 EMS 2 b haync2rv4 EMS 2 b haync2rv5 EMS 2 c haync2rv6 EMS 2 b haync2rv7 EMS 2 d ( 1 = Regan and Fuller, 1988, Genes and Development 2: 82-92; 2 = Regan and Fuller, 1990. | a = Recessive male sterile with defects in meiosis, flagel- lar elongation and nuclear shaping during spermatogenesis. Reduced female fertility. Homozygous viable at 25 but semi-lethal at 28. Dominant enhancer of tubulin mutations; b = Recessive larval lethal; c = Recessive zygotic lethal, and dominant maternal effect embryonic semi-lethal; d = Recessive male sterile. cytology: Located in 67E-F by Regan and Fuller (1988) on basis of its being uncovered by Df(3L)lxd6 = Df(3L)67E1-2;68C1-2 and Df(3L)lxd15 = Df(3L)67E;68C10-15 but not by Df(3L)vin2 = Df(3L)67F2-3;68D6. Also uncovered by Df(3L)E(z)1R1 and Df(3L)E(z)1R4 (Mounkes, Jones, and Fuller). molecular biology: hay is the next transcription unit distal to E(z), and encodes a 2.6 kb message present in embryos, larvae, pupae and adults (Mounkes, Jones, and Fuller). # hb: hunchback location: 3-48 (distal to p). synonym: Rg-pbx. references: Lewis, 1968, Proc. Int. Congr. Genet. 12th 2: 96- 7. Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801. Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. Bender, Turner, and Kaufman, 1987, Dev. Biol. 119: 418-32. Lehmann and Nusslein-Volhard, 1987, Dev. Biol. 119: 402-17. Tautz, Lehmann, Schurich, Schuh, Seifert, Kienlin, Jones, and Jackle, 1987, Nature 327: 383-89. Bender, Horikami, Cribbs, and Kaufman, 1988, Dev. Genet. 9: 715-32. Hulskamp Schroder Pfeifle Jackle and Tautz 1989 Nature 338: 629-32. Irish, Lehmann, and Akam, 1989, Nature 338: 646-48. Struhl, 1989, Nature 338: 741-44. Stanojevic, Hoey, and Levine, 1989 Nature 41: 331-35. Treisman and Desplan, 1989, Nature 41: 335-37. phenotype: Homozygotes for null alleles of hb (class I alleles of Lehmann and Nusslein-Volhard) are embryonic lethals of the gap type. Gastrulation abnormal; no cephalic fold; cell death evident at 6 hr later becoming extensive, predominantly in the neuroectoderm; germ band extension curtailed at 50% of embryonic length. After germ band shortening embryos lack thoracic and labial segments; cephalopharyngeal skeleton present but poorly formed; head involution fails. Seventh and eighth abdominal segments fused by the deletion of parasegment 13; A1 segment 1.5 times normal width, with eight to ten deranged denticle rows compared to the normal number of four, and a widened region of naked cuticle. Filzkorper material reduced; posterior spiracles fail to evert. Three ventral gan- glia absent; gap appears between suboesophogeal region of ven- tral nerve cord and more posterior trunk ganglia. Extreme mutants display a reduced number of stripes of ftz expression at cellular blastoderm; the first stripe is widened and fol- lowed by a narrowed gap of nonexpression preceding the second stripe; the last pair of stripes are fused (Carroll and Scott, 1986, Cell 45: 113-26). Hypomorphic alleles display variably less severe disruption depending on allele (hbDrv6 = hbb2 = hbe21 > hbb7 > hbDrv9), the least severe, hbDrv9 lacking only T2. Class II alleles (Lehmann and Nusslein-Volhard) resemble the null alleles except that some or all of the prothorax and A7 are retained. The class III allele retains the labial seg- ment as well. Class IV alleles lack only the mesothoracic segment. Class V mutants exhibit segment transformations as well as gaps and are described separately below. Temperature sensitive period of hbts1 during first four hr of development. hb/+ offspring produced from homozygous oogenic clones develop normally; homozygous embryos resulting from such clones display enhanced zygotic phenotype; gnathal, thoracic, and the first three abdominal segments replaced by two or three seg- ments of abdominal identity in mirror image relation to the more posterior abdominal segments; weak alleles without mater- nal effect; extra doses of hb+ in female without effect on phenotype of hb offspring. The anterior zone of hb expression extended posteriorly by six additional cells in the absence of Kr+; conversely the zone of Kr expression expanded anteriorly by six to eight cells in hb mutants; posterior zone appears insensitive to Kr constitution (Jackle, Tautz, Schuh, Seifert, and Lehmann, 1986, Nature 324: 668-70). hb+ appears to set the boundaries of Ubx expression (White and Lehmann, 1986, Cell 47: 311-21); zone of Ubx expression expanded in both anterior and posterior directions in hb mutant embryos at the stage of full germ band elongation; segmental disposition of expression characteristically deranged prior to the advent of cell death. Although Ubx expression in the ventral nerve chord at the stage of fully shortened germ band extends from parasegments 5-13, Ubx protein detected in parasegments 1, 7- 12 and 14 in hb12, 3 and 7-14 in hb1, and head to parasegment 1 plus parasegments 7-12 and 14 in hb7 (White and Lehmann). Phenotypic effects of ftz and hb in double mutants additive in thorax and anterior abdomen, but more severe than expected in head and posterior regions. alleles: hbDrv alleles derived from hbD1. allele origin discoverer synonym ref ( comments _____________________________________________________ hb1 EMS hbIIU 3, 5 class III hb2 EMS hb6N 2, 3 class I hb3 EMS hb7L 2, 3 class II hb4 EMS hb7M 2, 3 class I hb5 EMS hb7O 2, 3 class II hb6 EMS hb9K49 2, 3 class V | hb7 EMS hb9K57 2, 3 class V | hb8 EMS hb9Q 2, 3 class I hb9 EMS hb9R 2, 3 class IV hb10 EMS hb11C 2, 3 class II hb11 EMS hb14C 2, 3 class V | hb12 EMS hb14F 2, 3 class I hb13 EMS hb349 2, 3 class II hb14 X ray hbFFE 2, 3 class I hb15 X ray Lehmann hbFB92 3 class I hbb1 Bender Rg-pbxb1 1 amorph hbb2 Bender Rg-pbxb2 1 hypomorph hbb7 Bender Rg-pbxb7 1 hypomorph hbb16 Bender Rg-pbxb16 1 amorph hbb50 Bender Rg-pbxb50 1 amorph hbbs23 Bender Rg-pbxbs23 1 amorph hbD1 EMS Bacher Rg-pbx 4 viable | hbD2 / ray Groger lethal | hbDrv1 / ray Lewis Rg-pbx+RG1 1, 3 class II hbDrv2 / ray Lewis Rg-pbx+RG2 1, 3 class II hbDrv3 / ray Lewis Rg-pbx+RG3 1 hbDrv4 EMS Bender Rg-pbx+RE1 1 hbDrv5 EMS Bender Rg-pbx+RE2 1 hbDrv6 EMS Bender Rg-pbx+RE3 1 hbDrv7 EMS Bender Rg-pbx+RE4 1 hbDrv8 EMS Bender Rg-pbx+RE5 1 hbDrv9 EMS Bender Rg-pbx+RE6 1 hypomorph hbDrv10 EMS Bender Rg-pbx+RE7 1 hbDrv11 EMS Bender Rg-pbx+RE9 1 hypomorph hbe21 Rg-pbxe21 1 hypomorph hbts1 Rg-pbxts1 1 ( 1 = Bender, Turner, and Kaufman, 1987, Dev. Biol. 119: 418-32 (fig.); 2 = Jurgens, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.); 3 = Lehmann and Nusslein-Volhard, 1987, Dev. Biol. 119: 402-17 (fig.); 4 = Lewis, 1968, Int. Congr. Genet. 12th 2: 265-70; 5 = Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801; 6 = Jurgens, Wieschaus, Nusslein- Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). | Described more fully below. cytology: Placed by cytological mapping in 85A3-B1 (Tautz et al., 1987) or in 85A5-7;85B2-3 (Bender et al., 1987; Lehmann, and Nusslein-Volhard, 1987). molecular biology: Genomic sequences that include the gene hb cloned by chromosome walking (Tautz et al., 1987; Bender et al., 1988); gene also sequenced. Two embryonic mRNAs were identified (Tautz et al., 1987), one of 2.9 kb and another of 3.2 kb; the larger is present in the maternal RNA and persists during the first eight hours of embryonic development, whereas the smaller is detected only between the second and sixth hours. The two primary transcripts are transcribed from the same strand and have identical exons; the 3.2 kb mRNA has a 5 exon of 500 nucleotides separated from exon 2 by a 3.2 kb intron, and is separated from the 3 exon by a short intron; the same splice acceptor site is utilized in both messages. The experiments of Bender et al. (1988) identified five embryonic transcripts in two discrete classes; one class includes transcripts of 2.6 and 2.8 kb that are expressed only during embryogenesis with their highest level at 2-4 hr; and the other class includes transcripts of 3.0, 3.2, and 3.5 kb that accumulate to their highest levels over the first eight hours of embryogenesis, but are also present in adult females and males. The 5 to 3 direction of transciption of all five transcripts was found to be from distal to proximal along the chromosome. Primer extension and S1 protection experiments indicate the presence of two distinct promoters and three polyadenylation sites; transcripts from the upstream promoter are found in adults (males and females) as well as in 0-12 hr embryos (Bender et al., 1988). Maternal message is uniformly distributed at the time of egg deposition, but in stage 8 embryos, a gradient decreasing posterior is visible (Foe and Alberts, 1983, J. Cell Sci. 61: 31-70). Zygotic message first seen in stage 11 in the anterior 45% and the posterior 25% of the embryo; message subsequently disappears from the two poles of the embryo and becomes distributed in three and then two stripes in the anterior region; in general, the regions of hb message do not overlap those of Kr message. An overlap in protein distribution is shown by hb and Kr (Gaul and Jackle, 1989, Development 107: 651-62). The proteins encoded by hb (and Kr) show sequence-specific DNA binding to sites upstream of the two hb promoters (Stanojevic et al., 1989; Treisman and Desplan, 1989). The posterior-group gene nos suppresses the activity of hb in the posterior half of the body; if both nos and hb are absent, the embryo is normal (Hulskamp et al., 1989; Struhl, 1989). # hb6 phenotype: hb6/hb6 embryos lack meso- and metathorax, but nine abdominal segments are formed, the most anterior being T2 transformed into A1 and the next the normal A1. # hb7 phenotype: Homozygous embryos lack labium and all thoracic seg- ments; head and gnathal segments transformed into posterior abdominal segments as is A1. Expressed only in homozygotes, not in hemizygotes; hb7/Df(3R)hb displays class III phenotype. Lethality of hb7 homozygotes not rescued by Dp(3;Y)P92 which is able to cover the other alleles; attempts to implicate a linked lethal mutation negative. # hb11 phenotype: As in the case of hb7, resembles a class I mutant, but with transformation of gnathal and first abdominal seg- ments into posterior abdominal segments. Expression in homozy- gotes more extreme than in hemizygotes. # hbD1: hunchback-Dominant phenotype: A gain-of-function mutation; viable both in hetero- zygous and homozygous condition. Phenotype resembles that of pbx; insensitive to additional doses of hb+ but suppressed by extra doses [e. g., five copies of BXC+ (Lewis)]; enhanced in heterozygous combination with null alleles of ftz. cytology: Associated with In(3R)hbD1 = In(3R)85B;88C. The inversion is lethal homozygous, but lethality covered by duplication for 88C breakpoint; hbD1 associated with proximal breakpoint. # hbD2 phenotype: Homozygous lethal; lethal when heterozygous to hb null alleles (e.g. hb12). Has two dominant phenotypes: 1) homeotic transformation of parasegment six to parasegment five, resembling that produced by bxd pbx; 2) a pair-rule segmentation defect, consisting of partial deletion of even- numbered abdominal segments, principally A2 and A4. Homozygote shows more extreme expression of both phenotypes; penetrance and expressivity of first effect enhanced in double heterozy- gous combination with null alleles of ftz (e.g. hbD2/ftzr14); second phenotype enhanced by Df(2R)eve, such that only a few adult escapers of the doubly heterozygous genotype are observed. Also has a recessive phenotype, revealed either when homozygous or heterozygous to an hb null allele; deletion of parasegment 13 and reduction of filzkorper; labial and thora- cic segments normal. Thus, affects posterior, but not ante- rior, domain of hb+ function. Viable in trans to some hypo- morphic alleles that do not affect parasegment 13 (e.g. hb6). cytology: Associated with In(3R)hbD2 = In(3R)84B;85A. Break- point of associated inversion approximately 1 kb upstream of transcription start for 3.2 kb transcript. # Hdl: Haplo-diplo lethal location: 1-{43}. references: Merriam, Yamamoto, Stewart, Rahman, and Nicolau, 1986, unpublished. phenotype: Females with one dose of the normal allele and males with two are almost completely lethal; escapers normal in phenotype. alleles: No mutant alleles known. cytology: Localized to 12A by segmental aneuploidy. # hdp: heldup At least three different genetic entities appear to have been designated hdp on the basis of similarity of phenotype and map position to the now-lost hdp of Fahmy (1958, DIS 32: 70). Deak (1977, J. Embryol. Exp. Morphol. 40: 35-63) so designated wup-A of Hotta and Benzer [1972, Nature (London 240: 527-35)]. Lifschytz and Green (1979, Mol. Gen. Genet. 171: 153-59) selected reversions and suppressors of Bx, both of which had a held-up phenotype and were so designated. Engels and Preston (1981, Cell 26: 421-28) selected P-factor induced sex-linked mutants with held-up wings; 93% are associ- ated with chromosome rearrangements with one breakpoint in 17C2-3; the other 7% are not associated with rearrangements and act as suppressors of Bx; the latter group of mutants com- plement both the other 93% of mutants recovered by Engels and Preston and those described by Deak. We resurrect the name wupA: wingsupA for the mutants studied by Deak; we designate the Bx suppressors hdp-a and the mutants associated with 17C2-3 breakpoints hdp-b. In addition Fahmy (1956, DIS 32: 74) describes rwg: reduced wings, a mutant with the same map position and a slightly different phenotype from other held-up-like mutants; we arbitrarily designate it an hdp-a allele. # hdp-a location: 1-59.4 (0.0045 unit to the left of Bx based on separation of Bx3 and hdp-a). synonym: hld: heldwing (Deak, Bellany, Bienz, Dubuis, Fenner, Gollin, Rahmi, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81); fliH (Homyk, 1977, Genet- ics 87: 105-28; Homyk and Sheppard, 1977, Genetics 87: 95- 104). phenotype: Wings held up to various degrees; may overlap wild type. hdp-a alleles act as dominant suppressors of Bx in either cis or trans (Lifschytz and Green, 1979, Mol. Gen. Genet. 171: 153-59). Lifschytz and Green consider hdp-a mutants to be hypomorphic or amorphic alleles of a gene that is under cis control of Bx+; Bx mutants cause overproduction hdp-a+ product. alleles: selected male allele synonym origin ( as | ref / fertility _______________________________________________________________ *hdp-a1 hdp CB3007 2 + hdp-a2 RB6 X ray Bxr 4 - hdp-a3 RB7 X ray Bxr 4 - hdp-a4 RB13 X ray Bxr 4 + hdp-a5 RBE1 EMS Bxr 4 - hdp-a6 SBMI X ray Su(Bx3) 4 - hdp-a102 ` fliH EMS 3 hdp-ap1 - hdp P factor 1 + *hdp-arwg rwg CB1506 2 - ( CB1506 = 2-chloroethyl methanesulfonate; CB3007 = DL-p-N,N- di-(2-chloroethyl) aminophenylalanine | Bxr = revertant of Bx3; Su(Bx3) recovered as a trans suppressor of Bx3. / 1 = Engels and Preston, 1981, Cell 26: 421-28; 2 = Fahmy, 1958, DIS 32: 67-77; 3 = Homyk and Emerson, 1988, Genetics 119: 105-21; 4 = Lifschytz and Green, 1979, Mol. Gen. Genet. 171: 153-59. ` Shows partial complementation over hdp-a2. - Representative of 7% of the hdp-like mutants spontaneously generated by hybrid dysgenesis in an X chromosome that car- ries a P factor inserted at 17C2-3. These alleles associ- ated with P-factor excision. cytology: Placed in 17C2-3 on the basis of perfect correlation between hdp-a mutation in a dysgenic cross and the loss of a P element from 17C2-3 (Engels and Preston, 1981, Cell 26: 421- 28). other information: Relation between hdp-a and hdp-b unclear, they are in the same polytene bands but complement each other completely. They are separated by Bx (Mattox). # hdp-b location: 1-59.4 (inferred from polytene position). origin: Induced by hybrid-dysgenesis in an X chromosome with a P-factor in 17C2-3. references: Engels and Preston, 1981, Cell 26: 421-28. phenotype: Same as hdp-a, except that there is no interaction with Bx. alleles: 93% of the hybrid-dysgenesis-induced hdp-like mutants in an X chromosome in which a P factor resides at 17C2-3 are hdp-b alleles. cytology: All dysgenesis induced hdp-b alleles, are associated with rearrangements with one breakpoint in 17C2-3. # hdp: see wupA # Heat-shock cognate: see Hsc # Heat-shock protein: see Hsp # Heat-shock RNA at 93D: see Hsr93D # Heat-shock RNA ( |: see Hsr ( | # heavy-vein: see hv # hedgehog: see hh # heldout: see dppho # heldup: see hdp # heldwing: see hpd-a # Henna: see Hn # her: hermaphrodite (G.S. Carson) location: 2-52.9 (between b and pr). origin: Induced by ethyl methanesulfonate. references: Baker and Belote, 1983, Ann. Rev. Genet. 17: 345- 93. phenotype: Original allele was recovered as a recessive temperature-sensitive lethal with low homozygous viability (3-7% of the viability her/+) at 29 C and near-normal viabil- ity at 18 C in both sexes. Surviving 29 C homozygotes have small bodies, rough eyes, incised wings, and etched abdominal tergites. XX homozygotes surviving at 29 C are intersexual, with partially formed sexcombs, male-colored abdominal patches, and rudimentary male and female external genitalia. XY escapers have female-like sixth abdominal sternite bris- tles, but otherwise appear sexually normal. her/her flies of both sexes raised at 18 C are morphologically normal and fer- tile; however, XX homozygotes exhibit reversible temperature- dependent sterility when mated at 29 C. Homozygous females exert a mild maternal effect upon the sexual phenotype of her/+ offspring which develop at 29 C; females show abnormal basitarsal bristle arrangement and patches of male abdominal pigmentation; males show female basitarsal bristles among sex- comb teeth and the presence of sixth sternite bristles. alleles: her2, spontaneous on In(2LR)SM1,Cy. cytology: Placed between 36B4 and 36C2-4 as a result of its complementation by Dp(2;Y)B106 and Dp(2;Y)B108 = Dp(2;Y)35F;- 36DE, Dp(2;Y)H1 = Dp(2;Y)36B4;40F + Df(2L)37F4;39C2 and Dp(2;Y)H3 = Dp(2;Y)36B4;40F + Dp(2L)38B2;39E2 and its exclu- sion from Df(2L)TW137 = Df(2;Y)36C2-4;37B9-C1 and Dp(2L)TW50 = Df(2;Y)36E4-F1;38A6-7. molecular biology: Tritiated uridine incorporation in third instar salivary gland chromosomes suggests X chromosome tran- scriptional activity is reduced in her/her larvae compared with heterozygous siblings. # Hermaphrodite: see dsxD # heterochromatic-recombination-inducer: see hir # Hex-3: see Hex-C # Hex-A: Hexokinase A location: 1-29.2. synonym: Hex-A,B. references: Voelker, Langley, Leigh Brown, and Ohnishi, 1978, DIS 53: 200. Moser, Johnson, and Lee, 1980, J. Biol. Chem. 255: 4673-79. phenotype: The structural gene for hexokinases A, B1, and B2 (EC 2.7.1.1). The enzyme is monomeric and of molecular weight 47,000 _ 3000 for HEX-A and 48,000 _ 3000 for HEX-B1 and HEX- B2. The three forms of the enzyme are immunologically identi- cal but exhibit pI values of 5.1, 5.3, and 5.5 respectively upon isoelectric focusing, and these values covary in allelic variants. All three forms are found in the adult, but HEX-A is absent from larval preparations; HEX-A mainly localized in adult flight muscle. Three forms modified products of same structural gene. For purification and biochemical charactera- tion see Moser et al. alleles: Electrophoretic variants Hex-A2 which migrates more slowly than Hex-A4. cytology: Localized to 8D4-E1 (Voelker). # Hex-C location: 2-74.5 (Mukai and Voelker, 1977, Genetics 86: 175- 85). synonym: Fk: Fructokinase; Hex-3. references: Jelnes, 1971, Hereditas 67: 291-93. Fox and Madhavan, 1971, DIS 46: 42. Madhavan, Fox, and Ursprung, 1972, J. Insect. Physiol. 18: 1523-30. Moser, Johnson, and Lee, 1980, J. Biol. Chem. 255: 4673-79. phenotype: The structural gene for hexokinase-C [HEX-C (EC 2.7.1.1)]. The enzyme is a monomer of estimated molecular weight 42,000 _ 3,000 (Moser et al.) or 35,000 (Leigh Brown in Racine, Langley, and Voelker, 1980, Environ. Mutagen. 2: 167-77). Activity present in all developmental stages except freshly laid eggs; restricted to fat body in larvae, but present in many organs in adult. Weakly active or inac- tive in cell line (Deber, 1974, Wilhelm Roux's Arch. Entwick- lungsmech. Org. 174: 1-9). HEX-C activity not necessary for survival; null mutants viable (Burkhart, Montgomery, Langley and Voelker, 1984, Genetics 107: 295-306). Purification and biochemical characterization of enzyme described by Moser et al.. alleles: allele origin synonym ref ( comments _____________________________________________________________ Hex-C2 Hex-CS 1, 3 natural polymorphism Hex-C2.5 spont Hex-CAW399 4 Hex-C4 derivative on SM1 Hex-C4 Hex-CI 1, 3 natural polymorphism Hex-C6 Hex-CF 1, 3 natural polymorphism Hex-CnGB1 spont 2 natural population Hex-CnMC1 spont Hwx-CnJH302 | 4 Hex-C4 derivative on SM1 Hex-CnNC1 spont 6 natural population Hex-CnNC2 spont 7 Hex-C4 derivative on SM1 Hex-CnR1 / ray Hex-Cn /50036 5 Hex-C4 derivative on SM1 ( 1 = Fox and Madhavan, 1971, DIS 46: 42; 2 = Langley, Voelker, Leigh Brown, Ohnishi, Dickson and Montgomery, 1981, Genetics 99: 151-56; 3 = Madhavan, Fox, and Ursprung, 1972, J. Insect. Physiol. 18: 1523-30; 4 = Mukai and Cockerham, 1977, Proc. Nat. Acad. Sci. USA 74: 2514-17; 5 = Racine, Langley, and Voelker, 1980, Environ. Mutagen. 2: 167-77; 6 = Voelker, Langley, Leigh Brown, Ohnishi, Dickson, Montgomery, and Smith, 1980, Proc. Nat. Acad. Sci. USA 77: 1091-95; 7 = Voelker, Schaffer, and Mukai, 1980, Genet- ics 94: 961-68. | Hex-CJH301, Hex-CJH302, Hex-CJH303, and Hex-CJH309 probably independent recoveries of descendents of a single mutation. cytology: Placed in 51B-52E (Burkhart, Montgomery, Langley, and Voelker, 1984, Genetics 107: 295-306). # hfs: see Fs(1)10A # hfw: halfway location: 1-0.4 [0.008 map units to right of dor (Aizenzon and Belyaeva, 1982, DIS 58: 3-7)]. phenotype: Recessive lethal; for some alleles, development arrested in third instar, the anterior half initiating puparium formation while the posterior half remains larval. Extent of development influenced by administration of ecdysone and by temperature; pupariation occasionally completed at 18. Some alleles yield a few survivors with characteristic wing abnormalities and occasionally swollen abdomens. alleles: Seven alleles, superscripted 1-7. allele origin synonym ref ( comments ____________________________________________________________ hfw1 3 lethal hfw2 EMS swit32 1 lethal hfw3 EMS swit63 1 lethal hfw4 EMS swit200 1 lethal hfw5 EMS swit219 1 rare survivors hfw6 EMS swit251 1 rare survivors hfw7 | EMS swit467 1, 2 lethal as late prepupae ( 1 = Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelova, and Zhimulev, 1980, Chromosome 81: 281-306; 2 = Belyaeva and Zhimulev, 1986, Chromosome 86: 151-63; 3 = Rayle, 1967, Genetics 56: 583. | No late larval or pupal puffs in polytene chromosomes of homozygotes (Belyaeva and Zhimulev, 1986). cytology: Inseparable from dor, which has been placed in 2B11- 12 by Lefevre [1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 31-66]. # Hg: Hang glider (M. Ashburner) location: 2-57.5 (no recombinants with on among 1532 flies). origin: Induced by ethyl methanesulfonate. discoverer: Detwiler. phenotype: Wings upheld and spread from body; wing blade not flat but arced.