#*ob: oblique location: 1-37.2. origin: Spontaneous. discoverer: Neel, 41f30. references: 1942, Genetics 27: 532. 1942, DIS 16: 51. phenotype: Wings obliquely truncated from inner margin outward. Venation disturbed. Viability about 20% wild type. RK3. # obl: oblique wings location: 1-60.1. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1953. references: 1958, DIS 32: 72. phenotype: Wings slightly upheld and outspread; small blister occasionally present. Body color slightly darker. Male via- bility and fertility good; female viability about 40% wild type and fertility reduced. RK2. other information: One allele induced by CB. 1506. # oblique: see ob # oblique wings: see obl # obt: obtuse location: 3-77.5. discoverer: E. M. Wallace, 35g1. phenotype: Wings shorter and blunter but overlap wild type slightly. Thorax somewhat humpy; body chunky; eyes slightly bulging. RK3. cytology: Not in 94A-E (Jones, 1971, DIS 47: 90). oc: ocelliless "Edith M. Wallace, unpublished." # oc: ocelliless location: 1-23.1. synonym: otd: orthodenticle. references: Wieschaus and Noell, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 63-73. Finkelstein, Smouse, Capaci, Spradling, and Perrimon, 1990, Genes Dev. 4: 1516-27. phenotype: Ocelli completely absent. Bristles in ocellar area and on top of head irregular and more numerous; postverticals usually absent. Eyes somewhat reduced and body size dwarfed. Phototaxis normal (Benzer, 1967, Proc. Nat. Acad. Sci. USA 58: 1112-19). Viability about 90% wild type. oc and defi- ciencies for oc show partial dominance to oc+; ocelli placed somewhat far back on head and slight indentation apparent between postvertical bristles (Craymer and Roy, 1980, DIS 55: 204). Eggs from oc1 homozygotes have defective chorions and abnormal beta yolk spheres (Johnson and King, 1974, Int. J. Insect. Morphol. Embryol. 3: 385-95). Sterility is due to the presence of In(1)oc, one breakpoint of which disrupts oc, and the other of which interferes with amplification of the chorion-protein genes Cp36 and Cp38 (Spradling and Mahowald, 1981, Cell 27: 203-09). oc1 in heterozygous combination with non-complementing lethal alleles survives and is female fer- tile. Ubl/+ enhances dominance of oc; Df(1)RA2/+ exhibit delayed hatch and an oc phenotype; oc2/+ display strong oc phenotype, and oc1/oc1 are lethal in combination with Ubl/+ (Mortin and Lefevre, 1981, Chromosoma 82: 237-47). Lethal alleles (recovered as otd: orthodenticle) die as embryos; all denticles in anterior abdominal segments point posteriorly; defects at ventral midline; head defects. Also cause embryonic neural defects (Finkelstein et al., 1990): In developing ventral cord, commissures within each segment appear fused. At the cellular level, certain ventral unpaired medial (VUM) neurons do not seem to migrate ventrally (as do the normal VUMs at approximately 14 hours of embryogenesis) and are absent from most segments. Other "midline-associated" neurons are missing as well in otd-type embryos. Homozygous germ-line clones survive in females; homozygosity for lethal alleles in germ-line clones without effect on survival of heterozygous offspring or on phenotype of hemizygotes (Wieschaus and Noell). Putative oc transcript abundant in embryos, peaking between 4 and 13 hours, before and coincident with neural-developmental defects observed in central nervous system of embryos hemizygous for lethal alleles; there is also putative maternally derived oc mRNA (which could be alter- nately spliced form of the "major" transcript). Northern sig- nals weaken in L1 and L2, are still detectable in early pupae, but are absent in late pupae and adults. In situ hybridiza- tion reveals earliest embryonic expression at cellular blasto- derm; later, signals seen in a longitudinal strip along ven- tral midline, then in "head region" and in developing ventral cord. alleles: Except for oc1, alleles are lethal; alleles oc2 through oc5 non complementing; oc6 and oc7 complement oc1 but not one another. allele origin discoverer synonym ref ( comments ___________________________________________________________________ oc1 X ray Bedichek, 30c15 1 In(1)7F1-2;8A1-2 oc2 X ray Lefevre l(1)JA101 2 oc3 X ray Lefevre l(1)KA17 2 oc4 X ray Lefevre l(1)RC42 2 oc5 EMS Lefevre l(1)EF504 3 oc6 EMS Lefevre l(1)VA111 3 complements oc1 oc7 EMS Lefevre l(1)VA126 3 complements oc1 oc8 EMS otdC8 4, 5 embryonic lethal oc9 EMS otdH1 4, 5 embryonic lethal oc10 EMS 5 embryonic lethal ocdb spont Mohler | ( 1 = Bedichek, 1934, DIS 2: 9; 2 = Lefevre, l981, Genetics 99: 461-80; 3 = Lefevre; 4 = Wieschaus and Noell, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 63-73; 5 = Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. | More detailed description follows. cytology: Placed in 8A1-2 on the basis of its assignment to the proximal breakpoint of In(1)oc = In(1)7F1-2;8A1-2. molecular biology: DNA in region 8A1-2 amplifies in oc1 under the influence of In(1)oc (Spradling and Mahowald). Identified by Finkelstein et al., (1990), within approximately 80 kb of cloned material from the region of the distal breakpoint of In(1)oc. A 4 kb EcoRI fragment detects a 4.7 kb transcript; this was designated as oc mRNA because of its embryonic expression pattern. Sequence of a cDNA clone predicts a 670- amino-acid protein with various repeats of single amino acids (e.g. Gly, Ser, Gln), pairs of amino acids (e.g. alternating Gly-Val), and a tandemly-duplicated 19-mer. There is also a "paired-group"-like homeodomain relatively near the N- terminus. other information: Relationship of oc to otd indicated by co- mapping (cf. Spradling and Mahowald, 1981; Wieschaus et al., 1984) and the failure of otd-type alleles to complement oc (Finkelstein et al., 1990). Moreover, otd/+ females have altered adult bristle pattern in ocellar region, similar to that exhibited by homozygotes for the weak allele ocdb (Fink- elstein et al., 1990). # ocdb: ocelliless-disturbed bristles phenotype: Ocelliless; ocellar, interocellar, and postvertical bristles variably extra, missing, or misplaced with about 80% penetrance; acts as a non complementing oc allele. # o.c.c: see BRC # Ocd: Out cold (J.C. Hall) location: 1-55. origin: Induced by ethyl methanesulfonate. references: S|ndergaard, 1975, Hereditas 81: 199-210. 1979, Hereditas 90: 93-101. 1986, Hereditas 104: 313-16. phenotype: Dominant cold-sensitive, reversible paralytic; heterozygous mutant females begin uncoordinated behavior (pro- gressively: abnormal leg movements, leg stretching, wing fluttering) on shift from 25 to 18-20; paralysis eventually occurs, and recovery is gradual on shift back to higher tem- peratures; critical temperature to include the debilitations is ca. 2 lower from Ocd7 than for other alleles; also males hemizygous for Ocd7 have better viability than those express- ing the other alleles, with Ocd4 being the most severely affected i.e., nearly lethal (Ocd4 also causes near lethality when heterozygous with any of the other alleles); at 25, mutant males walk in reeling manner and fall over frequently; none can fly, and attempts to coax jumps (to initiate flight) cause the males merely to fall over when touched; these pheno- types also seen in homozygotes and heteroallelic combinations; certain of the homozygous mutant females (e.g. Ocd2 and Ocd3) hold their wings in drooped position; also seen in Ocd1 males; this phenotype also observed in Ocd2/+ and Ocd3/+ females, which also walk in unsteady manner; other alleles, when heterozygous, allow for seemingly normal behavior at 25, except that their legs shake under etherization (with Ocd4 causing the strongest aberrant shaking). Abrupt, anomalous changes in Arrhenius activation energy of the mitochondrial enzyme, succinate cytochrome c reductase, are seen at tempera- tures close to those which induce paralysis (S|ndergaard, FEBS Lett. 51: 126). Two-dimension gels of mitochondria isolated from Ocd1 contain an additional polypeptide not seen in extracts of wild-type (S|ndergaard, 1986). cytology: Placed in 13F10-16A2 because the severe effects of any mutant allele are ameliorated in males hyperploid for Dp(1;4)r+ (13F10-16A2 appended to chromosome 4). alleles: Seven mutants; concluded, not from problematical com- plementation tests, but by failure of wild-type recombinants to be recovered from heteroallelic Ocd combinations. Ocd1 (S|ndergaard, Nelson, and Smillic, 1975, FEBS Lett. 51: 126- 29) through Ocd7 (S|ndergaard, 1979). # Oce: Ocellarless location: 1-5.7. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1953. references: 1958, DIS 32: 72. phenotype: One or both ocellar bristles, frequently postverti- cals, missing; other bristles, especially the scutellars, sometimes absent. Oce/Oce females lack 90% of postvertical and ocellar macrochaetae and 10-40% of anterior dorsocentrals; Oce/+ females lack 60-80% of ocellars and 90-95% of postverti- cals but show minimal loss of dorsocentral bristles; in Hw49c/Oce females Oce appears to be epistatic to Hw49c in the thoracic region (10% missing dorsocentrals) and additive in the head with 95% missing postverticals and 100% missing ocel- lars (Stoddard, 1972, DIS 48: 137-38). Wings frequently positioned abnormally, have incised margins; effect more marked in homozygous females. Bristle effect dominant. Good viability and fertility in both sexes. RK1. other information: One allele induced by each of the following: CB. 3025, CB. 1592, CB. 1540, and CB. 1528. # ocelliless: see oc #*ocr: ochracea location: 2-0. discoverer: Serebrovsky, 40g25. references: 1941, DIS 15: 19. phenotype: Eye color lighter at eclosion, darkening with age. RK1. # Octanol dehydrogenase: see Odh # Ocr: Octopamine receptor (J.C. Hall) location: 3-{100}. origin: Molecular cloning (using a putatively homologous clone from human and by synthesis of appropriate oligonucleotide probes). synonym: Tyr-dro. references: Arakawa, Gocayne, McCombie, Urquhart, Hall, Fraser, and Venter, 1990, Neuron 4: 343-54. Saudou, Amlaiky, Plassat, Borrelli, and Hen, 1990, EMBO J. 9: 3611-17. phenotype: Independent cDNAs were cloned into expression vec- tors and transfected into CHO-1 (Arakawa et al., 1990) or Cos-7 (Saudou et al., 1990) cells. Membranes from such cells had high-affinity binding activity to the adrenergic receptor agonist yohimbine; other agonists or antagonists used to com- pete with this substance showed the octopamine analog, synephrine, to have the highest agonist affinity, higher than octopamine itself; these results along with others which showed greater affinity of the cloned/transduced protein for yohimbine and chlorpromazine than for metoclopramide, sug- gested that this Drosophila receptor is an "octopamine-1" sub- type (Arakawa et al., 1990). Membranes preparations from the Cos-cell transfectants also had high affinity for yohimbine, and tyramine (e.g. greater than octopamine), suggesting to Saudou et al. (1990) that this Drosophila gene encodes a tyramine receptor. Stably transfected mouse cell lines were also made (Saudou et al., 1990); additions of monoamines to them (e.g. tyramine, octopamine) do not by themselves lead to changes in cAMP levels, but forskolin-elicited cAMP increases were reduced by added tyramine (which was more effective than octopamine). Rough anatomical localization revealed a head- enriched mRNA (3.6 kb: Arakawa et al., 1990; 3.5 kb: Saudou et al., 1990). cytology: Mapped to 99A10-B1 by in situ hybridization (Arakawa et al., 1990). molecular biology: A cDNA encoding human brain |2-adrenergic receptor used in low stringency hybridizations to clone a Dro- sophila genomic fragment, partial sequence analysis of which revealed homology to adrenergic receptors (Arakawa et al., 1990). A similar approach, starting with degenerate oligonu- cleotides corresponding to sequences found in vertebrate receptors, led to an independent genomic clone (Saudou et al., 1990). Complete sequencing of head cDNAs, hybridizing to these genomic clones (Arakawa et al., 1990; Saudou et al., 1990), reveals a 601-amino-acid "G-protein-coupled" type of receptor protein, with highest homology to (2-adrenergic receptor subtypes, containing seven putative membrane-spanning regions and a N-terminal signal sequence. other information: Saudou et al. (1990) call their form of the gene Tyr-dro (based on their different results from, and interpretation of, pharmacological experiments; see above). # od: see oso # odd: odd skipped location: 2-8. references: Nusslein-Volhard and Wieschaus, 1980, Nature 287: 795-801 (fig.). Nusslein-Volhard, Kluding, and Jurgens, 1985, Cold Spring Har- bor Symp. Quant. Biol. 50: 145-54. phenotype: Embryonic lethal; posterior part of the denticle band and adjacent naked cuticle replaced by mirror-image duplication of the anterior part of the denticle band and adjacent naked cuticle in T2, A1, A3, A5, and A7. Pole-cell- transplantation experiments indicate that odd+ not maternally required. Positional expression of ftz unaffected (Carrol and Scott, 1986, Cell 54: 113-26). However, stripes of en expression are broader than normal in even-numbered, but of normal width in odd-numbered parasegments; Ubx expression is consequently low in broader-than-normal stripes in even- numbered parasegments (Martinez-Arias and White, 1988, Development 102: 325-38). alleles: allele origin synonym ref ( comments _________________________________________ odd1 EMS odd7L 2, 3 amorph odd2 EMS odd9P 2, 3 hypomorph odd3 X ray odd1.36 1, 3 odd4 EMS oddIIIC 3 odd5 EMS oddIIID 3 ( 1 = Nusslein-Volhard, Kluding, and Jurgens, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 145-54; 2 = Nusslein- Volhard and Wieschaus, 1980, Nature 287: 795-801 (fig.); 3 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. cytology: Located in 23E-24B; to the left of the breakpoint of T(1;2)1.10 = T(1;2)4A3-4;24B and within the transposed segment of Tp(2;?)5.1 = Tp(2;?)23E;24E (Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267- 82). # odd paired: see opa # odd skipped: see odd # Odh: Octanol dehydrogenase location: 3-49.2. discoverer: Ursprung. references: Ursprung and Leone, 1965, J. Exp. Zool. 160: 147- 54. Courtright, 1966, DIS 41: 59. Courtright, Imberski, and Ursprung, 1966, Genetics 54: 1251- 60. phenotype: The structural gene for octanol dehydrogenase [ODH (EC. 1.1.1.73)], a multimer of 109,000 molecular weight (Sieber, Fox, and Ursprung, 1972, FEBS Lett: 26, 274-76); evidence for tetrameric structure in other Drosophila species (Pipkin, 1969, Genetics 63: 405-18); immunologically unre- lated to ADH (Courtright, 1968, DIS 43: 144). Preferred sub- strates are long-chain primary alcohols, with lesser activity on short-chain and branched-chain primary alcohols; inactive on secondary alcohols (Bremner, Douglas, and Ogonji, 1971, DIS 47: 93-94). Enzyme activity higher in adults than in larvae or pupae (Debec, 1974, Wilhelm Roux's Arch. Dev. Biol. 174: 1-9); mobility also increases from larvae to pupae to adults (Hewitt, 1974, Genetics 77: s30-31). Odh+ not a vital gene; homozygotes for null allele, OdhnNC1, viable and fertile (Voelker, Langley, Leigh-Brown, Ohnishi, Dickson, Montgomery, and Smith, 1980, Proc. Nat. Acad. Sci. USA 77: 1091-95). alleles: Existing alleles recovered from natural populations; designated according to their migration rate toward the cathode in agar gel electrophoresis. OdhF the predominant allele; the incidence of OdhS in populations decreases with distance from the equator (Oakeshott, Gibson, Wilcocks, and Chambers, 1983, Theoret. Appl. Genet. 65: 191-96). allele synonym ( ref | comments ______________________________________ OdhF OdhM 1, 2 fast allele OdhnNC1 3 null allele OdhR 1 rare allele OdhS OdhL 1, 2 slow allele ( Because Costa et al. used a different gel system in which migration was anodal, the designations F and S were not descriptive; accordingly they use M = most common allele, L = less common allele, and R = rare allele, which encodes a polypeptide whose anodal migration is slower than that pro- duced by OdhF. | 1 = Costa, Danieli, and Rodino, 1977, DIS 52: 92; 2 = Cour- tright, Imberski, and Ursprung, 1966, Genetics 54: 1251-60; 3 = Voelker, Langley, Leigh-Brown, Ohnishi, Dickson, Montgomery, and Smith, 1980, Proc. Nat. Acad. Sci. USA 77: 1091-95. cytology: Localized to 86D1-4 based on its inclusion in Df(3R)M86D = Df(3R)86D1;86D4 (Clark, 1983, Biochem. Genet. 21: 375-90). # odsy: see os # Of: see DlOf #*Off: Off location: 2-82. origin: Spontaneous. discoverer: Bridges, 23e14. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 232. phenotype: Some bristles missing in heterozygotes, especially from side of abdomen; basal rings remain as in H. Homozygote lacks more bristles. Eyes large, creased, and roughened. RK2. other information: Agrees with abr in locus and description; may have been an allele. # ogre: optic ganglia-reduced (J.C. Hall) location: 1-18.8. references: Niklas and Cline, 1983, Genetics 103: 617-631. Lipshitz and Kankel, 1985, Dev. Biol. 108: 50-77. Watanabe and Kankel, 1990, Genetics 126: 1033-44. phenotype: Original allele (ogre1) recovered on the basis of simple lethality (Niklas and Cline, 1983); viable mutant (ogre2) isolated with respect to inability of adults to orient to vertical line of black-white contrast (Lipshitz and Kankel, 1985); optic lobes generally disorganized, as seen in adults expressing the viable allele, or in late pupae/pharate adults expressing a lethal allele; such lethals (all except ogre2) cause the behavioral and anatomical abnormalities just noted when heterozygous with viable allele; viability associated with one of these heteroallelic types, i.e., ogre1/ogre2 is poor, especially when reared at 18C (vs 29C); temperature shift experiments using this combination implies gene action in late larval stage; hemizygosity for lethal alleles causes development to cease in late larval-pupal stages, when parts of CNS appear abnormal (e.g., holes in sections of brain and thoracic ganglia, with severe defects appearing in the optic lobe formation centers); holes in CNS are also seen in "escapers", e.g., rare adults hemizygous for alleles other than ogre2, or heterozygous for ogre1 and ogre2; mosaic analysis suggests that CNS defects are due to action of this gene in those developing tissues (Lipshsitz and Kankel, 1985). alleles: Five mutant alleles, four of which are embryonic lethal. allele origin discoverer synonym ref ( comments __________________________________________________________________ ogre1 EMS Niklas l(1)jnL3 3 ogre2 EMS Kankel ogrevcb8 | 1, 2 viable allele ogre3 ENU Lipshitz l(1)ogreij555 2 ogre4 ENU Lipshitz l(1)ogrell523 2 ogre5 spont Schalet l(1)18-183 4, 5 10 kb deficiency ( 1 = Kankel and Lipshitz, 1981, Proc. 7th Int. Symp. Div. Biophys. The Taniguchi Foundation (Y. Hotta, ed.). pp. 215-38; 2 = Lipshitz and Kankel, 1985, Dev. Biol. 108: 56-77; 3 = Niklas and Cline, 1983, Genetics 103: 617-31; 4 = Schalet, 1986, Mutat. Res. 163: 115-44; 5 = Watanabe and Kankel, 1990, Genetics 126: 1033-44. | vcb = viable contrast blind. cytology: Placed in 6E2-4 based on its inclusion in Df(1)Sxl-bt = Df(1)6E2;7A6 but not Df(1)HA32 = Df(1)6E4-5;7A6. molecular biology: Isolated (Watanabe and Kankel, 1990) by walking distally from clone mapping to 6E4-5. Walk crosses distal breakpoints of Df(1)HA32 (= ogre+) and of Df(1)Sxl-bt (= ogre-), which are 70 kb apart. Five transcripts from this interval were detected on Northern blots of RNA from embryos and larvae; one mRNA of 2.9 kb was reduced in abundance in larvae hemizygous for ogre1; precise mapping of the ogre5 deletion indicated it would be missing at least part of this 2.9 kb transcript (and two other RNAs, including an 1.35 kb species). Transformation with a 12.5 kb genomic fragment, which should include the source of the 2.9 kb mRNA, rescues ogre-associated lethalities and the optic lobe abnormalities that can be seen in pharate adults expressing ogre1; these transformants, in an ogre5 genetic background, exhibits res- toration of the entire 2.9 kb, but only part of the 1.35 kb mRNA. cDNAs were cloned from embryonic libraries, and sequencing of the largest insert (2.45 kb) indicated that it can encode the entire protein, a 362-amino-acid polypeptide; features of the conceptual translation product include a puta- tive membrane spanning region and a potential glycosylation site; there were no significant similarities, in data bases, to the ogre sequence. # okr: okra (T. Schupbach) location: 2-1. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female sterile; homozygous females lay eggs which are of variable shapes; in the most extreme cases, the eggs are longer than normal, more pointed at the posterior end, and lack dorsal appendages, resembling eggs produced by the dom- inant female-sterile mutation Fs(2)D. alleles: Two, okrRU = okr1, okrWS = okr2. ojos castanos: see cast # ol-2: see sp # olfactory: see olf # olfactory pathway: see mbmC # olfactory-trap-abnormal: see ota # olfA: olfactory-A (J.C. Hall) location: 1-21.0 (from cytology; maps between ct and sn meioti- cally). origin: Induced by ethyl methanesulfonate. references: Rodrigues and Siddiqi, 1978, Proc. Indian Acad. Sci. B 87: 140-60. Rodrigues, 1980, Development and Neurobiology of Drosophilia (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York, pp. 361-69. Venard and Pichon, 1984, J. Insect Physiol. 30: 1-5. Venard, Antony, and Jallon, 1989, Neurobiology of Sensory Sys- tems (Singh and Strausfeld, eds.). Plenum Press, New York, pp. 377-85. Ayyub, Paranjape, and Siddiqi, 1990, J. Neurogenet. 6: 243- 62. phenotype: Larvae and adults are relatively poorly repelled by aldehydes (Rodrigues, 1980; benzaldehyde usually employed in the relevant Y-tube/olfactometric tests); strongest allele, in this regard is olfAx1, and yet it still detects these odorants (Ayyub et al., 1990). Responses to ethyl acetate, acetone, acetic acid, and ethanol are normal (first of these tested in adults and larvae, the latter three only in larvae). In odor-induced jump assay, mutants show about half-normal fre- quency of such responses (Ayyub et al., 1990). Electroanten- nogram recordings from adults indicate somewhat reduced response to benzaldehyde, but normal ones to butanol and butyl acetate (Venard and Pichon, 1984). The physiological defect seen, with benzaldehyde as the stimulus, involves a biphasic dose-response curve (Venard et al., 1989), as if there are two kinds of antennal receptors for this substance, only one of them being affected by olfA. alleles: allele discoverer ref ( _____________________________ olfAx1 Rodrigues 1 olfAx6 Rodrigues 1 olfAx8 Rodrigues 1 olfAx11 Rodrigues 1 olfAx24 Ayyub 2 olfAx25 Ayyub 3 ( 1 = Rodrigues, 1980, Development and Neurobiology of Droso- phila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York, pp. 361-69. 2 = Ayyub, Paranjape, and Siddiqi, 1990, J. Neurogenet. 6: 243-62. cytology: Maps to 7B8-D1 (Ayyub et al., 1990), based on its inclusion in the region of overlap of Dp(1;2)sn+72d = Dp(1;2)6C;7C9-D1 and Dp(1;3)sn13a1 = Dp(1;3)7A8;8A5 and its complementation by Df(1)ct268-42 = Df(1)7A5-6;7B8-C1. other information: Original group of these mutations reported initially by Rodrigues and Siddiqi (1978), but not then noted as "olfA" (see Rodrigues, 1980, and subsequent references listed above). olfA alleles complement the closely linked olfC and olfE mutations. # olfB: olfactory-B (J.C. Hall) location: 1-{0.5}. origin: Induced by ethyl methanesulfonate. discoverer: Rodrigues. references: Rodrigues and Siddiqi, 1978, Proc. Indian Acad. Sci. B 87: 147-60. Rodrigues, 1980, Development and Neurobiology of Drosophilia (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York, pp. 361-69. Ayyub, Paranjape, Rodrigues, and Siddiqi, 1990, J. Neurogenet. 6: 243-62. phenotype: Similar phenotype to olfA (Rodrigues, 1980), but subnormal responses of larvae or adults to aldehydes [benzal- dehyde and formaldehyde plus salicilaldehyde as well (Ayyub et al., 1990)] seen only after rearing at 28 (permissive tempera- ture in these tests, first performed by Rodrigues, 1980, extended by Ayyub et al., 1990, was 22). Larvae and adults grown at non-permissive temperature normal in responses to ethyl acetate, acetic acid, ethanol and acetone (Ayyub et al., 1990). Physiological responses of antennae to aldehydes briefly noted to be normal by Siddiqi [1984, Genetics, New Frontiers (Chopra, Sharma, Joshi, and Bansal, eds.). Oxford and IBH Publishing Co., New Delhi, Vol. III, pp. 243-61]. alleles: One mutant allele, olfBx4. cytology: Maps to 2B17-C2 (Ayyub et al., 1990), based on com- plementation by Df(1)w-vco (2C1;3C5) but not by Dp(1;3)wvco (2B17-C1;3C5-6;77D3-5;81). other information: Complements olfA, olfE, and olfF. The one extant mutant allele, now known as olfBx4, originally reported by Rodrigues and Siddiqi (1978), but not then called olfB (see Rodrogues, 1980). # olfC: olfactory-C (J.C. Hall) location: 1-21.0. (from cytology, meiotically maps between cv and sn, closer to the latter). origin: Induced by ethyl methanesulfonate. discoverer: Rodrigues. references: Rodrigues and Siddiqi, 1978, Proc. Indian Acad. Sci. B 87: 147-60. Rodrigues, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York, pp. 361-69. Tompkins and Hall, 1981, Z. Naturforsch 36c: 694-96. Mane, Tompkins, and Richmond, 1983, Science 222: 419-21. Venard and Pichon, 1984, J. Insect Physiol. 30: 1-5. Curcillo and Tompkins, 1987, Behav. Genet. 17: 81-86. Venard, Antony, and Jallon, 1989, Neurobiology of Sensory Sys- tems (Singh and Strausfeld, eds.). Plenum Press, New York, pp. 377-85. Ayyub, Paranjape, Rodrigues, and Siddiqi, 1990, J. Neurogenet. 6: 243-62. phenotype: Adults show poor responses to acetates and acetone, and have dimished responses to some alcohols, in tests involv- ing Y-tube olfactometer (Rodrigues, 1980). Odor-induced jump assays on olfCx3 and olfCx17 adults (Ayyub et al., 1990) gave results paralleling those using olfactometer (whereby these mutants are in one of two different "acetate defective" categories; see alleles). Larvae respond abnormally to acetetes and normally to aldehydes (Rodrigues, 1980). Elec- troantennograms (EAGs) recorded from adults show olfC to exhi- bit diminished responses of olfactory receptors to acetates (Venard and Pichon, 1984) and to 2-butanone as well (Venard et al., 1989). Similar physiological [Siddiqi, 1984, Genetics: New Frontiers (Chopra, Sharma, Joshi, and Bansal, eds.). Oxford and IBH Publishing Co., New Delhi, Vol. III, pp. 243- 61], and also behavioral (Rodrigues, 1980), experiments involving pairs of odorants, e.g. ethyl and iso-amyl acetate, suggested more than one independent "channel" for the recep- tion of these substances. In SEM observations (Venard et al., 1989) mutant antenna seems to have normal number and distribu- tion of the three kinds of sensilla on the anterior face of the funiculus (from where EAGs recorded). Electrophoresis of triton extracts of antennae generates an extra band of esterase activity in olfC, which is found in neither wild-type nor in mutant thoraces and abdomens (Venard et al., 1989). olfC males fail to have their courtship of wild-type males inhibited by high concentrations of volatile compounds (unlike normal males, which are inhibited). Mutant males court other males with abnormally high vigor yet court females with sub- normal intensity (Tompkins et al., 1981). Further studies showed that the mutant courts immature males vigorously (as do wild-type males), and this wanes as the courtee ages, but not to the same extent as in normal pairings; the inappropriately high levels of olfC courtships directed at maturing males includes all sex behaviors except attempted copulation (Cur- cillo and Tompkins, 1987). An inability of mutant males to discriminate between recently mated and virgin females was reported by Mane et al. (1983), who also showed that olfC males can detect, 6 hours post insemination, a difference between females mated to Est-60 males vs. males carrying a non-null allele of this gene (the latter kind of mated females were said to be relatively inhibitory to male courtship); these experiments suggested that the enzyme encoded by Est-6 turns a "pre-anti-aphrodisiac" compound, cis-vaccenyl acetate, which is transferred from males to females during copulation into a further, or the actual aphrodisiac, cis-vaccenyl alcohol; some elements of such results and inferences (Mane et al., 1983) have been called into question (Vander Meer, Obin, Zawistowski, Sheehan, and Richmond, 1986, J. Insect Physiol. 32: 681-86; Scott and Richmond, 1987, J. Insect Physiol. 33: 363-69) but argued by others [Ferveur, Cobb, and Jallon, 1989, Neurobiology of Sensory Systems (Singh and Strausfeld, eds.). Plenum Press, New York, pp. 377-85, pp. 397-409] to still have force, at least insofar as an anti-aphrodisiac role for cis-vaccenyl acetate goes. alleles: allele discoverer comments _________________________________________________________ olfCx2 Rodrigues reduced attraction to both ethyl and iso-amyl acetate olfCx3 Rodrigues reduced attraction to both ethyl and iso-amyl acetate olfCx5 Rodrigues normal response to ethyl acetate; reduced to iso-amyl acetate olfCx10 Rodrigues like olfCx2 and olfCx3 olfCx13 Rodrigues not mentioned anymore by Ayyub et al. (1990) olfCx14 Ayyub like olfCx5 olfCx17 Ayyub like olfCx5 cytology: Maps to 7D1-6 (Ayyub et al., 1990); olfCx3 and olfCx17 uncovered by Df(1)C128 = Df(1)7D1;7D5-6. other information: Originally isolated (Rodrigues and Siddiqi, 1978) in the same "then-unnamed" manner as olfA, olfB and olfD (the latter = sbl). olfCx3 over olfC deletion behaves with same poor responses to acetates as does homozygous mutant; however, olfCx17 female hemizygotes defective in responses to both ethyl and iso-amyl acetates, whereas, this allele in homozygous females allows for normal responses to ethyl ace- tate. Mutagenesis of olfCx17 led to some strains with "stronger" acetate-based olfactory deficit than the starting mutant. In one of these called olfCx17-1a, responses to iso- amyl acetate worse than in olfCx17, and the new strain also shows reduction in responses to benzaldehyde; both of these abormalities covered by Dp(1;2)sn+72d = Dp(1;2)6C;7C9-D1 and uncovered by Df(1)ct-J4 = Df(1)7A2-3;7C1, apparently placing this novel genetic defect in 7A2-C1, a region separate from olfC. # olfD: see sbl # olfE: olfactory-E (J.C. Hall) location: 1-{21.0}. origin: Induced by ethyl methanesulfonate. discoverer: Ayyub. references: Hasan, 1989, J. Genet. 68: 139-46. Ayyub, Paranjape, Rodrigues, and Siddiqi, 1990, J. Neurogenet. 6: 243-62. Hasan, 1990, Proc. Nat. Acad. Sci. USA 87: 9037-41. phenotype: Larvae and adults show reduction in responses to benzaldehyde in petri-plate-based and Y-tube olfactometric assays, respectively. In odor-induced-jump assay (using ben- zaldehyde), mutants jump less than half as often as normal flies. allele: There is one extant allele, olfEx26. cytology: Best estimate of location is 7C9;7D1 (Ayyub et al., 1990; Hasan, 1989, 1990). The gene is covered by Dp(1;2)sn+72d = Dp(1;2)7B1;8A5. It is also covered by Dp(1;3)sn13a1 = Dp(1;3)6C5;7C9;79E and uncovered by Df(1)C128 = Df(1)7D1;7D5-6, rearrangements that overlap according to molecular data. molecular biology: Cloned by Hasan (1989, 1990) using chromo- somal walking beginning with sn-region probes. Southern-blot mapping of proximal breakpoint of Dp(1;3)sn13a1 and the distal breakpoint of Df(1)C128 defines a 25 kb interval that includes olfE (see cytology). A 5.4 kb transcript detected with a probe relatively near (but distal to) the 7D9 breakpoint of Dp(1;3)sn13a1, is believed to represent olfE mRNA (Hasan, 1990). This transcript is found throughout the life cycle; it is in the head and bodies of adults. Another mRNA of 1.7 kb hybridizes to probes that detect the 5.4 kb transcript. A 14 kb genomic fragment that includes the 5.4 kb transcript partially rescued olfactory defects. In jump assays, more normal phenotypes were obtained, when the DNA insert was homozygous; in Y-tube tests, homozygosity was required for any appreciable rescue. other information: olfE complements olfA, olfB, and olfF. The closely-linked mutants olfA and olfE are both impaired in their responses to benzaldehyde. # olfF: olfactory-F (J.C. Hall) location: 1-{1}. origin: Induced by ethyl methanesulfonate. discoverer: Ayyub. references: Ayyub, Paranjape, Rodrigues, and Siddiqi, 1990, J. Neurogenet. 6: 243-62. phenotype: Compared to wild-type flies, olfF adults require a higher concentration of benzaldehyde for detection in Y-tube olfactometer (e.g. no response at a dilution of 10-5, which readily repels wild-type flies). Mutant shows normal responses to acetates, propionic acid and butanol. olfF/Df(1)w-vco females are fertile. alleles: There is one extant allele, olfFx267. cytology: Located in 2E1-3C2 since uncovered by Df(1)64c18 = Df(1)2E1-2;3C2. other information: olfF complements olfA, olfB, and olfE. # olive-2: see sp # olvD: see dpD #*om: ommatidia location: 1-0.1 (to the right of sc). origin: X ray induced in (or with) ac3. discoverer: Muller. references: Muller, Prokofyeva, and Raffel, 1935, Nature 135: 253-55. Muller, 1935, DIS 3: 30. phenotype: Ommatidia disarranged, giving a slight eye roughness difficult to classify. RK3. cytology: Thought by Muller to be in or very close to 1C1. # omb: optomotor-blind (J.C. Hall) location: 1- {7.5}. origin: Induced by ethyl methanesulfonate. discoverer: Heisenberg. synonym: ombH31; opm31. references: Heisenberg, Wonneberger, and Wolf, 1978, J. Comp. Physiol. 124: 287-96. Blondeau and Heisenberg, 1982, J. Comp. Physiol. 145: 321-29. Bausenwein, Wolf, and Heisenberg, 1986, J. Neurogenet. 3: 87-109. Pflugfelder, Schwartz, Roth, Poeck, Sigl, Kerscher, Jonschker, Pak, and Heisenberg, 1990, Genetics 126: 91-104. phenotype: Adults expressing omb1, the only allele studied in phenotypic detail, are impaired in optomotor turning responses in tests involving tethered or freely moving flies (Heisenberg et al., 1978; Blondeau and Heisenberg, 1982; Kulkarni, Stein- lauf, and Hall, 1988, Genetics 118: 267-285; Dushay, Rosbash, and Hall, 1989, J. Biol. Rhythms 4: 1-27). The mutant is also aberrant in orientation to vertical stripe (Heisenberg et al., 1978). More detailed examination of "yaw torque" optomo- tor responses show that omb1 is restricted in responses to stimulation of "frontal visual field", with mutant behavior summarized as retaining "object responses" but missing "large field responses" (Bausenwein et al., 1986). The mutant is relatively normal in "lift/thrust" response to vertical pat- tern movement and in regard to landing response elicited by front-to-back horizontal motion. Slow phototaxis, using Y- tube, was markedly subnormal (Dushay et al., 1989). Giant arborizing fibers in lobula plate. Since isolation and the original histological examinations, anatomical abnormalities have become more pronounced, e.g., the optic lobes remain in "pre-imaginal" orientation in some omb adults, viz., long axis of medulla optic ganglia oriented more frontally than in wild-type (Blondeau and Heisenberg, 1982); other behavioral abnormalities: omb shows anomalous avoidance reaction, i.e., "antifixation" to objects in Y-maze test (Bulthoff, 1982, Biol. Cybernet. 45: 63-70); courting males exhibit diminished tracking responses of and turning responses to moving females (Cook, 1980, Biol. Cybernet. 37: 41-51; Tompkins, Gross, Hall, Gailey, and Siegel, 1982, Behav. Genet. 12: 295-307). Visual stimulus-induced metabolic activity in the optic lobes (monitored by distribution of radioactive 2-deoxyglucose) is normal, suggesting that basic structure and function of gan- glia distal to lobula plate is normal (Bulthoff and Buchner, 1985, J. Comp. Physiol. 156: 25-34). Without effect on locomotor activity rhythm (Helfrich, 1986, J. Neurogenet. 3: 321-43). alleles: Only one viable allele, omb1 (isolated as ombH31). A number of lethal rearrangements with breakpoints in 4C5-6 uncover omb along with other closely linked mutations. cytology: Placed in 4C5-6 based on its inclusion in Df(1)GA56 = Df(1)4C5-6;4D1 and Df(1)rb13 = Df(1)4C5-6;4D3-E1 but not Df(1)ovo6 = Df(1)4C5-6;4E2-3 or Df(1)ovo7 = Df(1)4C5-6;4E2-3 (Pflugfelder et al., 1990). Associated with In(1)omb = In(1)4C4-7;12D2-E1. molecular biology: Located in an 340-kb walk initiated from polytene bands microdissected from 4B-C (Pflugfelder et al., 1990). Seven omb- breakpoints identified in a 80-kb subseg- ment; in distal-to-proximal order, they are T(1;3)biD1, Tp(1;1)biD1 (which contains a 30 kb insert within the omb region), T(1;2)biD2, In(1)omb, Df(1)GA56, Df(1)rb13, and Df(1)rb5; these are spread over a distance of 80 kb. The distal breakpoint of Df(1)ovo7 (which is omb+) is 15 kb proxi- mal to that of Df(1)rb5 (which is omb- and was mapped within 4C5-6 by Southern blots, though no cytological breakpoints for it are given). Northern blot probes (Pflugfelder et al., 1990), encompassing all breakpoints that cause an omb pheno- type, detected two transcripts that could be associated with the omb function. T3 (6 kb) and T7 (an approximately 2-kb smear); the genomic sources of these RNAs are 80 kb apart; they are most prominent in mid-embryos, late L3, early pupae, and adults; another fainter transcript (T7 ), with a similar developmental profile, comes from a more proximal region to the right of the In(1)omb breakpoint. There are also several additional low-abundance embryonic/pupal transcripts that map between two relatively distal omb- breakpoints. Various cDNAs have been cloned, including those representing T3 and T7; the modest amount of sequencing done, as of Pflugfelder et al. (1990), revealed no significant matches. other information: Two EMS-induced lethals with no physically detectable lesions within the relevant portion of the walk noted above fail to complement bi, Qd, lac, omb, and l(1)bi, the designation applied to the lethality of several of the rearrangements in the region; these complementation groups overlap the distal 20 kb of the omb region. The lethals are designated l(1)omb282 and l(1)omb3198 by Pflugfelder et al. (1990), but the law of parsimony suggests that they be desig- nated l(1)bi1 and l(1)bi2, respectively. Other observations suggesting that the omb region is genetically complex (Pflug- felder et al., 1990) are exemplified by the fact that l(1)bi1/Qd females have lacquered wings. # ome: omega location: 3-36. origin: Induced by ethyl methanesulfonate. references: Chihara and Kimbrell, 1986, Genetics 114: 393-404. phenotype: In the presence of homozygous omega, larval cuticle protein 5 migrates more slowly, irrespective of the Lcp5 alleles present; migration of the residual Lcp5 bands also altered. omega+ product postulated to play a role in modify- ing the Lcp5 gene product. # oml: ommatidiless location: 1-31. origin: X ray induced. discoverer: Ritterhoff. references: Biggin, 1969, DIS 44: 49. phenotype: Expression varies from normally shaped eyes with displaced facets to complete absence of eyes; variable penetrance; ventral part of eye most often affected. 10% of flies show palps in epidermis that replaces missing eye tis- sue; 5% show reduced head, fused ocelli, and abnormal anten- nae. # omm: ommatoreductum location: 1-12.8. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1953. references: 1958, DIS 32: 72. phenotype: Some peripheral ommatidia absent, frequently in an irregular manner, giving a rough eye and a notched border. Shape of head abnormal; head bristles deranged or absent. Palps absent or deformed. Thoracic bristles deranged. Wings often unexpanded. Good viability and fertility in both sexes. RK2. other information: One allele each induced by CB. 1246, CB. 1522, CB. 1592, CB. 1528; two alleles induced by CB. 3026. # ommatidia: see om # ommatidiless: see oml # ommatoreductum: see omm #*On: Open location: 3-26. origin: X ray induced. discoverer: Tanaka, 36c26. references: 1937, DIS 7: 21. 1937, DIS 8: 11. phenotype: Wings spread. Homozygous viable. RK2. #*op: opaque location: 1-50. origin: X ray induced. discoverer: H. M. Miller, 33k. references: 1934, DIS 2: 9. 1935, DIS 3: 14. 1935, DIS 4: 10. phenotype: Wings opaque and whitish, usually divergent and slightly convex. Viability and fertility good in male, poorer in female. RK3. # opa: odd paired location: 3-48. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. Nusslein-Volhard, Kluding, and Jurgens, 1985, Cold Spring Har- bor Symp. Quant. Biol. 50: 145-54. phenotype: Deletes alternate metasegments, as defined by a line separating the anterior from the posterior parts of the ante- rior compartments; portions of denticle bands of T2, A1, A3, A5, and A7 and naked cuticle of T3, A2, A4 and A6 missing. Pattern of Ubx protein distribution in the double-sized units reveals them to be composite, the anterior half being derived from an odd-numbered parasegment and the posterior half from an even-numbered parasegment (read metasegment) (Ingham and Martinez-Arias, Nature 324: 592-97). Without discernable effect on ftz expression (Carrol and Scott, 1980, Cell 45: 113-26). However, exhibits loss of en product with a consequent increase in Ubx expression in even-numbered parasegments (Martinez-Arias and White, 1988, Development 102: 325-38). alleles: Nine ethyl methanesulfonate-induced alleles, opa1- opa9, isolated as 5H, 7N, 9C, 9O, 13D, E8, IIC, IIP, and T (Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69). cytology: Placed in 82A-E; between autosomal breakpoints of T(Y;3)J17 = T(Y;3)Xhy+;82A and T(Y;3)D107 = T(Y;3)h7;82E. # opaque: see op #*opb: opaque broad location: 1-28.3. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1955. references: 1959, DIS 33: 88. phenotype: Short, broad, and opaque wings with slightly convex or concave membranes. Slightly brownish eye color. Legs short with long segments frequently bowed. Abdomen slightly abnormal in shape; genitalia deformed. Males fertile; viabil- ity about 10% wild type. Females sterile. RK3. # Open: see On #*oph: ophthalmopedia location: 2-45. origin: Spontaneous. discoverer: Gordon, 1934. references: 1936, J. Genet. 33: 25-60. 1941, DIS 14: 39. phenotype: In extreme form, an appendage grows from eye; in less extreme form, eye is kidney shaped. Expression sensitive to genetic and environmental modification. Effect caused by enlargement and abnormal folding of eye-forming portion of optic disk in late larvae [Waddington and Pilkington, 1943, J. Genet. 45: 44-50 (fig.)]. Disc development autonomous in reciprocal transplants with wild type (Abaturova and Ginter, 1968, Genetika 4(11): 58-64); partial oph disks display reduced mutant development when transplanted into wild-type hosts (Ginter and Abaturova, 1969, Genetika 5(10): 38-43). RK3. # opht: ophthalmoptera location: 1-5. origin: Spontaneous. references: Ouweneel, 1970, Genetica 41: 1-20. phenotype: A semidominant enhancer of ld and Dfdr and perhaps other eye-shape mutants. In the presence of opht, flies bear- ing the above mutants produce wing-like outgrowths in the eye. Expression more extreme at 17 than at 29; temperature sensi- tive period in second- and third-instar larvae (Postelthwaite, 1974, Dev. Biol. 36: 212-17). # Ophthalmoptera: see Opt # opm2: see nonA # opm3: see rdgA12 # opm4: see rdgA13 # opm5: see rdgA14 # opm8: see tH8 # opm9: see rdgA15 # opm10: see rdgA16 # opm14: see rdgA17 # opm18: see nonB or nbA # opm24: see tH24 # opm37: see elf # opm47: see nbA # opm52: see norpA # Opt: Ophthalmoptera location: 2-68 (based on progeny testing of 32 Bl-c recom- binants from OptB/Bl c females). phenotype: A homeotic modifier of ey2 and possibly other small-eye mutants (e.g., eyD/+). In the presence of Opt, ey2 flies exhibit protrusions of wing tissue from the region of the eye; development is normal at 17, but homeotic transforma- tion is observed at 29; the temperature-sensitive period is during the second larval instar [Postlethwait, 1974, Dev. Biol. 36: 212-17 (fig.)]. Protrusions from the anterior por- tion of the eye have the triple row of bristles characteristic of the anterior wing margin; the fronto-orbital region of the head produces bristles with bracts characteristic of the costa in the proximal wing (Postlethwait). alleles: allele origin discoverer synonym ref ( comments ______________________________________________________ OptB EMS Bacher, 1966 3 OptG spont eyopt 1, 2 ( 1 = Garcia-Bellido, 1969, DIS 44: 52 2 = E. Goldschmidt and Lederman-Klein, 1958, J. Hered. 49: 262-66; 3 = Lewis and Bacher, 1969, DIS 44: 48. other information: Allelism not tested; assumed from similarity of phenotype and location on the second chromosome. # optic ganglia-reduced: see ogre # optomotor: see opm # optomotor-blind: see omb # or: orange location: 2-106.7 [0.3 unit to the right of sp based on 11 recombinants among 3317 flies (Ives, 1967, DIS 43: 400)]. phenotype: Eye color bright orange. or/pd wild type (Von Halle). 5% normal complement of drosopterin; implanta- tion of phenylalanine crystals in pupal abdomen one day before eclosion results in bright red eye with a four-fold increase in drosopterin content (Schwinck, 1969, Genetics 61: s53). RK1. alleles: or45a and or49h weaker alleles than or1 and or66k (Schwinck, 1969, DIS 4: 46). allele origin discoverer ref ( _________________________________________ or1 spont Mossige, 1942 2 or45a spont Ives, 45a 1 or49h spont Ives, 49h31 1 or66k spont Schwinck, 66k20 3 ( 1 = Ives, 1951, DIS 25: 70; 2 = Mosssige, 1950, DIS 24: 61; 3 = Schwinck, 1964, DIS 44: 46. # ora: see ort Double mutant ort1 ninaE1 described as oraJK84; components separable by recombination. # ora transientless: see ort # ord: orientation disruptor (R.S. Hawley) location: 2-103.5. origin: Induced by ethyl methanesulfonate. references: Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 352-434. Mason, 1976, Genetics 84: 545-72. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. Goldstein, 1980, Chromosoma 78: 79-111. phenotype: In females homozygous for ord, exchange is strongly reduced. In both males and females, ord causes a dramatic increase in both reductional and equational nondisjunction as assayed genetically. In male meiosis, Goldstein observed abnormal sister-chromatid associations during prophase as well as precocious sister-chromatid separation, followed by random disjunction during anaphase I. "The bulk of the first divi- sion misbehavior consists of sister chromatids' disjoining from one another, a process which normally occurs only during the second meiotic division" (Goldstein). ord also elevates the frequency of mitotic chromosome misbehavior (Baker et al., 1978). "A substantial proportion of this mitotic instability can be accounted for by a hypothesis in which ord causes precocious sister-chromatid separation, followed by random disjunction, in somatic as well as germline cells" (Gold- stein). Thus the ord locus likely specifies a function required for sister-chromatid cohesion during most or all cell divisions. cytology: Placed in 59B-D by Mason (1976). Further confined to 59D4-10 by deficiency analysis (Miyazaki and Orr-Weaver). # ort: ora transientless (J.C. Hall) location: 2-66.4. origin: Induced by ethyl methanesulfonate. references: Koenig and Merriam, 1977, DIS 52: 50-51. O'Tousa, Leonard, and Pak, 1989, J. Neurogenet. 6: 41-52. phenotype: Electroretinogram lacks on-transient, and shows either no off-transient or a delayed one, occurring 100-150 milliseconds after the light coincident photoreceptor poten- tial is elicited. Rhodopsin levels, prolonged depolarizing afterpotentials, and rhabdomere structure are normal in R1-6 photoreceptors of ort eyes, unlike the case of ninaE single or double mutants (see allele tables of ort and ninaE). alleles: allele discoverer synonym ref ( comments ________________________________________________________ ort1 Koenig ora 1, 2 recovered as double mutant with ninaE1 called ninaEJK84 ort2 Hardy, Orevi ortUS1471 2 and Merriam ort3 Hardy, Orevi ortUS1606 2 and Merriam ort4 Hardy, Orevi ortUS2525 2 and Merriam ort5 Hardy, Orevi ortUS6096 2 and Merriam ort6 Pak ortP306 2 ( 1 = Koenig and Merriam, 1977, DIS 52: 50-51; 2 = O'Tousa, Leonard, and Pak, 1989, J. Neurogenet. 6: 41-52. cytology: Located at 92A4-B1 (O'Tousa et al., 1989). Uncovered by Df(3R)12 = Df(3R)92A4-11;92D2-8; complemented by Df(3R)B16 = Df(3R)92A11-B1;92E10-F2. other information: ort1 has been placed to the left of ninaE1 by recombinational separation of the two genes (O'Tousa et al., 1989) as well as by cytological location. (For further discussion of these genes, see ninaE). # orthodenticle: see otd # os: outstretched small eye location: 1-59.2. origin: X ray induced. discoverer: Abrahamson, 1953. synonym: odsy. references: Verderosa and Muller, 1954, Genetics 39: 999. phenotype: Wings held virtually at right angles to body. Eyes small and rounded. os/oso has wing effect but eyes normal. os/oss has eye effect but wings normal. RK1. cytology: Localized to 17A5-6 (Laughnan). other information: Originally considered two separate loci, od: outstretched and sy: small eye, Muller proposed a single gene based on the recovery of a mutant with both phenotypes, which was not resolvable into two components by recombination as well as on the failure to recover recombinants between od and sy in trans heterozygotes (Verderosa and Muller). # osbdw: outstretched small eye-bending wings origin: X ray induced. discoverer: Halfer, 1960. synonym: bdw. phenotype: Wings divergent and drooping, size and shape normal. Males sterile. RK2A. cytology: Associated with T(1;3)osbdw = T(1;3)16E;80C. oso: outstretched small eye-outstretched Edith M. Wallace, unpublished. # oso: outstretched small eye-outstretched origin: X ray induced. discoverer: Muller, 1930. synonym: od. references: 1930, J. Genet. 22: 303 (fig.). 1935, DIS 3: 30. Verderosa and Muller, 1954, Genetics 39: 999. phenotype: Wings extremely divergent, often at right angles to body. oso/oss is wild type. RK1. # oss: outstretched small eye-small eye origin: Spontaneous. discoverer: Bridges, 19g3. synonym: sy. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 236. phenotype: Eyes small and rounded, high on the head but not bulging. RK1. # osa: osa (J.A. Kennison) location: 3-60.0. origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1983. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Isolated as a dominant suppressor of the antenna to leg transformation in Pc2 AntpNs double heterozygotes. Also acts as a dominant suppressor of AntpNs, Pc and Pcl alleles. Recessive embryonic lethality associated with all alleles. Also fails to complement In(3R)Antprv1 for viability. alleles: Four from ethyl methanesulfonate and three from P-M hybrid dysgenesis. cytology: 90B1-90D1 based on its inclusion within the tran- sposed segment of Tp(3;3)S462 = Tp(3;3)64C-E;89D1-2;90D1 but not within the transposed segment of Tp(3;1)bxd111 = Tp(3;1)4D;89E;90B2 and its failure to complement In(3R)Antprv1 = In(3R)81F;90B-C. #*osh: outshifted location: 1-33.0 (no crossover with v in 997 chromosomes). origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1955. references: 1958, DIS 32: 73. phenotype: Wings shortened and often slightly divergent. Body and wings pale in color. Eyes somewhat smaller and browner than normal. Viability and fertility good in both sexes. RK2. # osk: oskar location: 3-48 (distal to p and hb). references: Lehmann and Nusslein-Volhard, 1986, Cell 47: 141- 52. phenotype: Homozygous females normally viable and fecund; homozygous males fertile. Embryos produced by homozygous females lack pole plasm and fail to produce pole cells; abdom- inal region remains unsegmented and eventually dies. Temperature-sensitive period for the germ-line effect is the last six hours of oogenesis and for abdominal development the last twelve to fourteen hours (osk8). Homozygous osk germ cells autonomous in pole cell transplants. Polar cytoplasm from unfertilized eggs or normal embryos capable of rescuing pole cell formation if injected at the posterior extremity of the early embryo and abdominal segmentation, to the extent of producing viable but sterile adults, if injected into the pos- terior half of preblastoderm embryos. Embryos produced by homozygous BicD; osk females are indistinguishable from those produced by osk alone suggesting that osk+ product is required for the formation of bicaudal embryos; also required for the early anterior-posterior gradient of hb expression (Tautz, 1988, Nature 332: 181-84). alleles: Nine ethyl-methanesulfonate-induced alleles. allele synonym comments ______________________________________________ osk1 osk54 osk2 osk84 strong allele osk3 osk88 osk4 osk123 osk5 osk150 osk6 osk166 strong allele osk7 osk255 hypomorphic allele osk8 osk301 hypomorphic allele temperature sensitive osk9 osk346 strong allele cytology: Placed in 85B based on its inclusion in Df(3R)p-XT26 = Df(3R)85A3;85C1-2 and Df(3R)p-XT103 = Df(3R)85A2;85C1-2 but not in Df(3R)p-XT118 = Df(3R)84F;85B1 (Lehmann and Nusslein- Volhard, 1987, Dev. Biol. 119: 402-17). # osp: outspread (M. Ashburner) location: 2-50.1 [0.01 cM to the left of Adh (Detwiler)]. references: Woodruff and Ashburner, 1977, Genetics 92: 117- 132. Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Lit- tlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91. phenotype: Wings held out at 45 to body axis. Strong alleles, and homozygous deficiencies show, in addition, a "tenting" of the wings so that they resemble those of arc. Df(2L)osp homozygous viable and fertile, though viability reduced in crowded cultures. alleles: allele origin discoverer ref ( cytology __________________________________________________________________ osp1 EMS? E. H. Grell osp3 / ray Detwiler Tp(2;3)35B3-4;36C11;98E2-3 osp4 EMS Harrington 1 osp6 EMS Harrington 1 osp7 EMS Harrington 1 osp8 EMS Harrington osp16 EMS Detwiler osp19 EMS Detwiler osp22 EMS Detwiler In(2L)35B3;35D3-5 osp24 EMS Detwiler osp25 EMS Detwiler osp27 EMS Detwiler osp35 / ray Detwiler osp40 / ray Detwiler osp59 / ray Detwiler In(2L)35B3;35B3-6 osp76e EMS Littlewood 1, 2 osp77e EMS Littlewood 1, 2 osp80.1D DEO | Detwiler 2 osp83 / ray Detwiler osp90 / ray Detwiler T(2;3)35B2-3;89B9-11 osp104 / ray Detwiler osp201 / ray Detwiler ospCH62 EMS O'Donnell ospCH63 EMS O'Donnell osppb3 X ray Kaufman T(2;3)35B2-3;82E2-8;89A9-10 ospMpl X ray Shelton ( 1 = Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186; 2 = Ashburner, Faithfull, Littlewood, Richards, Smith, Velissariou, and Woodruff, 1980, DIS 55: 193-95. | diepoxyoctane. cytology: Placed in 35B2-3. other information: Probably the gene immediately to the left of Adh. # Osw: Outspread wing location: 3- (between Tb and ca). references: Sequeira, Nelson, and Szauter, 1989, Genetics 123: 511-24. phenotype: Wings held out (Ganetzky). # ot: outheld location: 1-65.7. references: 1958, DIS 32: 73. phenotype: Wings held horizontally; inner margin slightly cut away in many males. Ocellar bristles usually absent or reduced; effect variable. Hairs sparse, especially in poste- rior midthoracic region. Males sterile; viability about 20% wild type. RK3. cytology: Placed in 19A5 on the basis of its inclusion in Df(1)16-2-19 = Df(1)19A5;19D3 but not in Df(1)mal10 = Df(1)19A5-6;19E1. (see also Schalet, Lefevre, and Singer, 1970, DIS 45: 165). alleles: allele origin discoverer synonym ref ( comments _______________________________________________________ ot1 TEM Fahmy, 1952 1 viable ot2 EMS Lefevre l(1)DC711 2 lethal ot3 EMS Lefevre l(1)VA132 2 lethal ( 1 = Fahmy, DIS 32: 73; 2 = Lefevre and Watkins, 1986, Genetics 113: 869-95. # ota1: olfactory-trap-abnormal-1 (J.C. Hall) location: 1-43. origin: Induced by ethyl methanesulfonate. references: Woodard, Huang, Sun, Helfand, and Carlson, 1989, Genetics 123: 315-26. phenotype: Poor odor responses in tests involving an olfactory trap; entry into such traps was subnormal when odorant was food medium or ethyl acetate. Phenotype also subnormal in odor-induced jump responses (using ethyl acetate, propionic acid, or benzaldehyde as stimulant). Electroretinogram abnor- mal; very weak light induced depolarization and no light-on or light-off transients. cytology: Maps to 12A6-13A5, owing to coverage of both olfac- tory and ERG defects by Dp(1;f)LJ9. # ota2: olfactory-trap-abnormal-2 (J.C. Hall) location: 1-between y and cv (nearer to former). origin: Induced by X-rays or ethyl methanesulfonate. references: Woodard, Huang, Sun, Helfand, and Carlson, 1989, Genetics 123: 315-26. phenotype: Abnormal trap-entry kinetics (cf. ota1), with food medium or ethyl acetate as stimulant (ota21 isolated using former, ota22 using latter). In odor induced jump tests ota21 responded normally to ethyl acetate, propionic acid, and ben- zaldehyde; but ota22 gave subnormal responses to the first two of these stimulants. ERG normal (both alleles). alleles: Two alleles, ota21 (X-rays) and ota22 (formerly ota4). Allelism determined only by trap-entry behavior of the double heterozygote, i.e. no mapping data on ota22. cytology: Proximal to 1B14, because ota2 not covered by y2Y61l (duplicated from X distal tip to the site just noted). # Ota3: Olfactory-trap-abnormal-3 (J.C. Hall) location: 1-( not localizable; see other information). origin: Induced by ethyl methanesulfonate. references: Woodard, Huang, Sun, Helfand, and Carlson, 1989, Genetics 123: 315-26. phenotype: Abnormal trap-entry kinetics with ethyl acetate as stimulant (cf. ota1). In odor-elicited jump tests, subnormal responses occurred to ethyl acetate and propionic acid but not to benzaldehyde. ERG normal. Uppercase-ness of this gene's symbol stems from at least partial dominance associated with Ota3/+ females' trap-entry behavior. other information: A map position for Ota3 was not indicated by testing segregants from y cv v f/Ota3 heterozygotes. Genetic origin of Ota3 may be more complicated; Ota3 phenotype may not be the result of a single X-linked mutation. # ota5: olfactory-trap-abnormal-5 (J.C. Hall) location: 1-unlocalized. origin: Induced by ethyl methanesulfonate. references: Woodard, Huang, Sun, Helfand, and Carlson, 1989, Genetics 123: 315-26. phenotype: Males exhibit abnormal trap-entry kinetics with ethyl acetate as stimulant; not as subnormal (in these behavioral tests) as are the other ota genes. In odor- elicited jump tests with ethyl acetic or propionic acid as stimuli, however, ota5 shows the same degree of impairment as ota22, and like ota22, shows normal jump responses to benzal- dehyde. ERG normal. Homozygous ota5 females behaved normally in the behavioral tests described. # ota7: olfactory-trap-abnormal-7 (J.C. Hall) location: 1-between y and cv (nearer to former). origin: Induced by ethyl methanesulfonate. references: Woodard, Huang, Sun, Helfand, and Carlson, 1989, Genetics 123: 315-26. phenotype: Abnormal trap-entry kinetics (cf. ota1) with ethyl acetate as stimulant. This phenotype is semi-dominant, as indicated from similar testing of ota7/+ females. Odor- induced jump responses normal. ERG abnormal. The photorecep- tor potential begins anomalously to decay to baseline soon after normal light-on transient appears; then renewed (cornea-negative) depolarization is observed (all of these dynamics observed during 0.5 second stimulus). Finally, a normal light-on transient is observed. The abnormal ERG phenotype, which co-segregates with subnormal trap-entry kinetics, is recessive. cytology: Located proximal to 1B14, because the recessive ERG abnormality is not covered by y2Y61l. # otd: see oc # otu: ovarian tumor (R. King) location: 1-23.2. references: King, Bahns, Horowitz, and Larramendi, 1978, Int. J. Insect Morphol. Embryol. 7: 359-75. King and Riley, 1982, Dev. Genet. 3: 69-89. King, Mohler, Riley, Storto, and Nicolazzo, 1986, Dev. Genet. 7: 1-20. King and Storto, 1988, BioEssays 8: 18-24. Mulligan, Mohler, and Kalfayan, 1988, Mol. Cell. Biol. 8: 1481-88. phenotype: Homozygous females defective in proliferation, dif- ferentition, or maturation of the germ line, depending on the level of activity of the particular allele. So-called quies- cent alleles (QUI) produce ovarioles lacking in germ cells; oncogenic alleles (ONC) produce cystocytes that continue dividing and form tumors; differentiated alleles (DIF) produce chambers containing only "pseudonurse" cells (PNCs) or nurse cell/oocyte (NC/O) syncytia. In these, transport of nurse cell cytoplasm to the oocyte is inhibited and chambers are arrested at a pseudo-12 stage [Bishop and King, 1984, J. Cell Sci. 67: 87-119 (fig.)]. Mutant nurse cells that fail to pump their cytoplasm into the oocytes are also unable to form a system of actin microfilament bundles in their cortical cytoplasm during stage 10B (Storto and King, 1988, Dev. Genet. 9: 91-120). The proportions of ovarioles with the different phenotypes appear to reflect the level of function of the par- ticular allele; homozygotes are less severely affected than hemizygotes (80% of ovarioles of females carrying otu1, otu4, otu5, or otu7 in combination with an otu deficiency lack germ cells, whereas 5% of the ovarioles of homozygotes lack germ cells); similarly, the levels of function of certain alleles decline as the developmental temperature is raised. Thus otu1 behaves like a DIF allele at 18, an ONC allele at 23, and a QUI allele at 28. The ovarian tumors which give the mutant gene its name are made up of large numbers of single cystocytes and small numbers of clones of 2-4 interconnected cells [King, 1979, Int. J. Insect Morphol. Embryol. 8: 297-309 (fig.)]. Most cystocytes undergo complete cytokinesis, and there are defects in the construction and functioning of the polyfusomal system during the cycles of cystocyte divisions [Storto and King, 1989, Dev. Genet. 10: 70-86 (fig.)]. Drosophila nurse cells normally undergo nine or ten cycles of DNA replication (Mulli- gan and Rasch, 1985, Histochemistry 82: 233-47), and the chromatids dissociate so that each nucleus is filled with a jumbled mass of oligotene threads. In otu PNCs, the chroma- tids remain in register, generating banded polytene chromo- somes [Dabbs and King, 1980, Int. J. Insect Morphol. Embryol. 9: 215-29 (fig.)]. Homologues pair and rearrangement confi- gurations can be discerned [King, Riley, Cassidy, White, and Paik, 1981, Science 212: 441-43 (fig.)]. The largest polytenes have undergone 12 cycles of endonuclear replication (Rasch, King, and Rasch, 1984, Histochemistry 81: 105-10). The banding pattern of PNC polytenes is similar to that of the polytenes from larval salivary gland cells (Sinha, Mishra, and Lakhotia, 1987, Chromosoma 95: 108-16; Heino, 1989, Chromo- soma 97: 363-73). At 25, otu11 behaves as an ONC allele, the cells dividing to form tumors, but at 18, homozygous females produce oocytes that reach a pseudo-14 stage, contain beta yolk spheres and can undergo early embryogenesis. In the case of DIF alleles such as otu4, females generate pseudo-12 eggs which lack beta yolk spheres and never initiate development. When otu11 is combined with alleles from the QUI class such as otu2, the heteroallelic females are sterile. Heteroalleles between otu11 and certain DIF alleles show various degrees of fertil- ity [Storto and King, 1987, Roux's Arch. Dev. Biol. 196: 210-21 (fig.)]. otu11/otu14 females are fully fertile although the nurse cells, unlike those of wild-type females, contain banded chromosomes (Storto and King, 1988). Oocyte differentiation is destabilized in certain otu alleles; for example, the presumptive oocytes in about 20% of otu7 homozygotes resemble nurse cells in their polytenization, although they lag behind the remaining nurse cells by at least one replication cycle [King, Rasch, Riley, O'Grady, and Storto, 1985, Histochemistry 82: 131-34 (fig.)]. Germ line autonomy has been demonstrated for otu3, otu4, and otu7 (Wieschaus, Audit, and Masson, 1981, Dev. Biol. 88: 92-103; unpublished work cited in King et al., 1986). alleles: 21 alleles are listed in the following table. Heteroallelic combinations usually produce intermediate pheno- types, but some show partial complementation. allele origin discoverer synonym ref ( comments ____________________________________________________________________ otu1 EMS Gans fs(1)A231 1, 2, 3 oncogenic otu2 EMS Mohler fs(1)14-97 2, 3, 4 quiescent otu3 EMS Gans fs(1)A116 1, 2, 3 oncogenic otu4 EMS Mohler fs(1)13-1994 2, 3, 4 differentiated otu5 EMS Mohler fs(1)11-1037 2, 3, 4 differentiated otu6 EMS Engstrom fs(1)209 2 quiescent otu7 EMS Engstrom fs(1)1304b 2 differentiated otu8 EMS Engstrom fs(1)1396 2 quiescent otu9 EMS Mohler fs(1)12-3266 2, 4 differentiated otu10 EMS Mohler fs(1)12-4474 2, 4 quiescent otu11 EMS Mohler fs(1)14-334 2, 4 oncogenic otu12 EMS Mohler fs(1)12C-129 2, 4 quiescent otu13 EMS Mohler fs(1)13F-3 2, 4 oncogenic otu14 EMS Vyse fs(1)4077 2 differentiated otu15 EMS Digan fs(1)A3 2 quiescent otu16 EMS Digan fs(1)1001 2 quiescent otu17 EMS Digan fs(1)1401 2 quiescent; 2 kb deletion otu18 | P insert Mohler otuP1 5 oncogenic otu19 P insert Mohler otuP2 5 oncogenic otu20 | P insert Mohler otuP3 5 normal otu21 | P insert Mohler otuP4 5 oncogenic ( 1 = Gans, Audit, and Masson, 1975, Genetics 81: 683-704; 2 = King, Mohler, Riley, Storto, and Nicolazzo, 1986, Dev. Genet. 7: 1-20; 3 = King and Riley, 1982, Dev. Genet. 3: 69-89; 4 = Mohler and Carroll, 1984, DIS 60: 236-41; 5 = Mulligan, Mohler, and Kalfayan, 1988, Mol. Cell. Biol. 8: 1481-88. | P-elements in otu18, otu20, and otu21 are of molecular sizes 2.9, 0.6, and 0.5 kb, respectively (Kalfayan, Walsh, Ousley, and Nishiharu, unpubl.). cytology: Placed in 7F1 based on its inclusion in Df(1)KA14 = Df(1)7F1-2;8C6 and its mapping genetically 0.4 cM to the left of l(1)7Fa10 which is also placed in 7F1 (King et al., 1986). molecular biology: Identification of otu sequences based on the insertion of transposable sequences in the same EcoRI restric- tion fragment of a lambda clone from 7F1 into each of four hybrid-dysgenesis-induced otu alleles and the correlation between excision of these sequences and restoration of fertil- ity in revertants of otu18 and otu19. otu17 contains a dele- tion of 2 kb in the restriction fragment distal to the frag- ment altered in the insertional alleles (Mulligan et al., 1988). The otu gene is at least 4.6 kb long and is subdivided into seven introns and eight exons. The first and sixth introns are large (534 and 583 b, respectively); the others range in size from 53 to 68 b. The first exon specifies an untranslated leader which contains the ribosomal binding sites. The otu gene encodes at least two ovary-specific and four testis-specific mRNAs. The major ovarian message is 3.2 kb, while a minor message is 4.0 kb. The 3.2 kb mRNA, which is transcribed from exons 2 through 8, specifies a proline- rich protein, 811 amino acids long. Exons 2-6 encode segments of 76, 33, 51, and 46 amino acids, respectively. The largest exon (number 7) encodes 415 amino acids, while the eighth exon specifies 58 amino acids at the carboxyl end of the protein and a trailer which contains the binding site for the polyadenylating enzyme (Mulligan et al., 1988; Steinhauer, Walsh, and Kalfayan, 1989, Mol. Cell. Biol., 9: 5726-32). # Out cold: see Ocd # outer rhabdomeres absent: see ort1 ninaE1 # outheld: see ot # outshifted: see osh # outspread: see osp # Outspread wing: see Osw # outstretched small eye: see os #*ov: oval location: 1-17.5. discoverer: Steinberg, 37h15. phenotype: Eyes somewhat oval and quite rough. RK1. # ovaless: see ovl # ove: overetherized location: 2- (not located). origin: Spontaneous. discoverer: Plaine and Aubele, 64b. references: 1965, DIS 40: 36. phenotype: Wings held vertically within 1 hr after eclosion, vibrate feebly but are incapable of supporting flight. Move- ments of first two pairs of legs uncoordinated. Viable and fertile although ove male often unsuccessful in mating with ove+ female. RK2. # Overflow: see DlOf # overlapping complementation complex: see BRC #*ovi: ovioculus location: 1-0.9. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1953. references: 1958, DIS 32: 73. phenotype: Eyes small, egg shaped, and rough. Wings spread or elevated to varying degrees; edges incised, especially inner margin. Eclosion slightly delayed. Males sterile. Viability 20-60% wild type. RK2. #*ovl: ovaless location: 2- (not located). origin: Spontaneous. discoverer: Bridges, 21a3. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 232. phenotype: Rough eyes. Males fertile; females entirely sterile. Small groups of cells in place of ovaries; ducts and genitalia normal. Abdomen of female grayish and translucent. RK3. # ovo: ovo (B. Oliver) location: 1-10.2. references: Mohler, 1977, Genetics 85: 259-72. Busson, Gans, Komitopoulou, and Masson, 1983, Genetics 105: 309-25. Komitopoulou, Gans, Margaritis, Kafatos, and Masson, 1983, Genetics 105: 897-920. Perrimon and Gans, 1983, Dev. Biol. 100: 365-73. Perrimon, 1984, Genetics 108: 927-39. Mohler and Carrol, 1984, DIS 60: 236-41. Oliver, Perrimon, and Mahowald, 1987, Genes Dev. 1: 913-23 (Fig.). Mevel-Ninio, Mariol, and Gans, 1989, EMBO J. 8: 1549-58. phenotype: All ovo alleles fully penetrant for female steril- ity; no male function for ovo+ known. Lack of zygotic activity results in complete absence of germ-line cells in adult female; reduction in numbers of germ cells first evident during early gastrulation. Homozygotes for weaker alleles produce germ cells, but oogenesis defective; egg chambers may degenerate prior to vitellogenesis or proceed through oogenesis and be oviposited, depending on allele; laid eggs are permeable to neutral red and never develop. Heterozygotes for two of the dominant alleles phenotypically similar to homozygotes for weak recessive alleles. Ovarian tumors formed in females carrying ovoD3 in heterozygous combination with the hypomorphic alleles, e.g., ovoD1rv20, or with fs(1)A1621. The ovoD2 mutation is partially suppressed by many Sxl alleles. ovoD1/+ females produce no eggs; extensively utilized in the selection of ovo+ germ-line clones. alleles: Recessive alleles, mostly recovered as revertants of dominant alleles, usually but not always, simultaneously mutant for svb or lzl; some svb alleles also simultaneously mutant for ovo; ovo proximal to svb and distal to rg by defi- ciency analysis. Many revertants are homozygous lethal owing to their being simultaneously mutant for svb. The lzl eye phenotype is cold sensitive and semi-dominant. Most rever- tants are amorphic in that, when tested in heterozygous combi- nation with ovoD1rv22 or ovoD1rv23, they have atrophic ovaries, with no egg chambers observable. allele origin discoverer synonym ref ( comments | ____________________________________________________________________________ ovoD1 EMS Komitopoulou fs(1)K1237 2 antimorph; germ- cell arrest ovoD2 EMS Komitopoulou fs(1)K1103 2 antimorph; per- meable eggs ovoD3 EMS Komitopoulou fs(1)K155 2 antimorph; per- meable eggs ovoD1rv1 EMS Oliver ovoD1rE1 4 svb ovoD1rv2 EMS Oliver ovoD1rE2 4 svb ovoD1rv3 EMS Oliver ovoD1rE3 4 svb ovoD1rv4 EMS Oliver ovoD1rE4 4 svb ovoD1rv5 EMS Oliver ovoD1rE5 4 ovoD1rv6 EMS Oliver ovoD1rE6 4 svb ovoD1rv7 / ray Perrimon ovoD1rG2 4 svb ovoD1rv8 / ray Perrimon ovoD1rG3 4 svb ovoD1rv9 / ray Perrimon ovoD1rG4 4 svb ovoD1rv10 / ray Perrimon ovoD1rG5 4 svb; In(1)4E1-2; 5A1-6 ovoD1rv11 / ray Perrimon ovoD1rG8 4 svb ovoD1rv12 / ray Perrimon ovoD1rG9 4 svb ovoD1rv13 / ray Oliver ovoD1rG10 4 svb ovoD1rv14 / ray Oliver ovoD1rG11 4 svb ovoD1rv15 / ray Oliver ovoD1rG12 4 svb ovoD1rv16 / ray Oliver ovoD1rG14 4 svb; regains ovo+ function ovoD1rv17 / ray Oliver ovoD1rG19 4 svb ovoD1rv18 / ray Oliver ovoD1rG20 4 svb ovoD1rv19 / ray Oliver ovoD1rG21 4 svb ovoD1rv20 / ray Oliver ovoD1rG23 4 svb; probably hypo- morphic ovoD1rv21 / ray Oliver ovoD1rG25 4 svb ovoD1rv22 spont Gans lzlG 1, 4 lzl ovoD1rv23 spont Oliver ovoD1rS1 4 ovoD1rv24 spont Gans ovoD1rS14 3 lzl; gypsy at 0.9 kb ovoD1rv25 spont Gans ovoD1rS22 3 lzl; gypsy at 0.9 kb ovoD1rv26 spont Gans ovoD1rS32 3 gypsy at 0.9 kb ovoD1rv27 spont Gans ovoD1rS35 3 lzl; gypsy at 0.9 kb ovoD1rv28 spont Gans ovoD1rS36 3 gypsy at 0.9 kb ovoD1rv29 spont Gans ovoD1rS37 3 gypsy at 0.9 kb ovoD1rv30 spont Gans ovoD1rS38 3 lzl; gypsy at 0.9 kb ovoD1rv31 spont Gans ovoD1rS78 3 lzl ovoD1rv32 spont Gans ovoD1rS80 3 svb ovoD1rv33 spont Gans ovoD1rS85 3 ovoD1rv34 spont Gans ovoD1rS86 3 ovoD1rv35 spont Gans ovoD1rS88 3 ovoD1rv36 spont Gans ovoD1rS89 3 ovoD1rv37 spont Gans ovoD1rS124 3 lzl; gypsy at 0.9 kb; 0.6 kb deletion at insertion site ovoD1rv38 P Gans ovoD1rHD71 3 svb ovoD1rv39 P Gans ovoD1rHD72 3 lesion in 4.0 to 4.9 kb ovoD1rv40 P Gans ovoD1rHD81 3 svb; 5-kb insert in 1.1 to 3.6 kb ovoD1rv41 P Gans ovoD1rHD82 3 svb ovoD1rv42 P Gans ovoD1rHD90 3 svb ovoD1rv43 P Gans ovoD1rHD91 3 svb; copia at 1.3 kb ovoD1rv44 P Gans ovoD1rHD93 3 svb ovoD1rv45 P Gans ovoD1rHD101 3 svb ovoD1rv46 P Gans ovoD1rHD104 3 svb ovoD1rv47 Gans 31 3 DNA lesion in 1.1 to 3.6 kb ovoD1rv48 Gans 51 3 DNA lesion in 1.1 to 3.6 kb ovoD1rv49 Gans 81 3 DNA lesion in 1.1 to 3.6 kb ovoD1rv50 Gans 118 3 DNA lesion in 1.1 to 3.6 kb ovoD1rv51 Gans 119 3 DNA lesion in 1.1 to 3.6 kb ovoD1rv52 Gans 121 3 DNA lesion in 1.1 to 3.6 kb ovoD3rv53 spont Gans ovoD3rS54 3 gypsy at 0.9 kb ovoD3rv54 spont Gans ovoD3rS57 3 gypsy at 0.9 kb ovoD3rv55 spont Gans ovoD3rS58 3 gypsy at 0.9 kb ovoD3rv56 spont Gans ovoD3rS59 3 copia at 0.9 kb ovoD3rv57 / ray Oliver ovoD3rG1 svb ovoM1 EMS Mohler ovorM1 4 hypomorph; per- meable eggs ovoM2 EMS Mohler ovorM2 4 hypomorph; per- meable eggs ( 1 = Busson, Gans, Komitopoulou, and Masson, 1983, Genetics 105: 309-25; 2 = Komitopoulou, Gans, Margaritis, Kafatos, and Masson, 1983, Genetics 105: 897-920; 3 = Mevel-Ninio, Mariol, and Gans, EMBO J. 8: 1549-58; 4 = Oliver, Perrimon, and Mahowald, 1987, Genes Dev. 1: 913-23. | Mutant alleles associated with ovoD revertants; coordinates from chromosomal walk of Mevel-Ninio et al.; origin desig- nated as SalI site just to the left of the gypsy insert of ovoD1rv30; positive values to the right. cytology: Placed in 4E2 based on its inclusion in Df(1)ovo6 = Df(1)4C5-6;4E2-3 and Df(1)bi-DL3 = Df(1)3C7-12;4E1-2 but not Df(1)bi-DL5 = Df(1)3C7-12;4E1-2 (Oliver). molecular biology: 32 kb of wild-type DNA containing ovo+ has been cloned, using the transposing element gypsy as a tag; the position of the ovo locus was limited distally on the molecu- lar map by the proximal breakpoint of Df(1)bi-D2 = Df(1)4B6- C1;4D7-E1 between coordinates -5 and -4 (Mevel-Ninio et al., 1989). Reversions of the dominant alleles ovoD1 and ovoD3 to recessive ovo alleles occurred in crosses to females carrying gypsy and the majority of these revertants carried insertions of gypsy and/or copia and other transposable elements; eleven spontaneous revertants contained a gypsy-element insert and one copia insert at coordinate 0.9; of the seven gypsy-induced revertants of ovoD1, four inserted in one orientation were associated with lzl mutations and the three inserted in the opposite orientation were not; gypsy-induced revertants of ovoD3 were lzl+ irrespective of orientation.