# na: narrow abdomen location: 1-45.2. origin: X ray induced. discoverer: H. M. Miller, 34c. references: 1934, DIS 2: 9. 1935, DIS 4: 9. Hardy, Lindsley, Livak, Lewis, Sivertsen, Joslyn, Edwards, and Bonaccorsi, 1984, Genetics 107: 591-610. phenotype: Abdomen long and cylindrical in both sexes. Viabil- ity low; female fertility low. Ovaries in juvenile condition (Brehme). RK2. cytology: Placed in 12E1-13A5 on the basis of its inclusion in Df(1)KA9 = Df(1)12E1;13A5. #*na2 origin: Ultraviolet induced. discoverer: Edmondson, 51g. references: 1952, DIS 26: 60. phenotype: Like na. RK2. # Na-CP: Na-channel-protein location: 2-{107}. references: Ashburner. phenotype: Structural gene for sodium-channel protein. cytology: Placed in 60E. # nac: neuronally-altered-carbohydrate (F. Katz) location: 3-{48}. origin: Induced by ethyl methanesulfonate. references: Katz, Moats, and Jan, 1988, EMBO J. 7: 3471-77. phenotype: Mutants show alteration or loss of a normally neuron-specific glycoconjugate; staining by anti-HRP antibo- dies in imaginal and adult neural tissue is eliminated. At 25 the mutant flies are viable and fertile; nac/nac females, how- ever are sterile at 18. Under heat stress (37 for five minutes) they show abnormal jittery behavior. Developmental abnormalities, including defects in the assembly of the omma- tidia and in the formation of the wing, appear at 18 in the homozygous offspring of heterozygous parents. Maternal effect embryos show loss of the anti-HRP glycan determinant and are lethal. cytology: Located in 84F4-84F12. # naked cuticle: see nkd # nanos: see nos # napts: no action potential (J.C. Hall; M. Kernan) location: 2-56.2. origin: Induced by ethyl methanesulfonate. references: Wu, Ganetzky, Jan, Jan, and Benzer, 1978, Proc. Nat. Acad. Sci. USA 75: 4047-51. Wu and Ganetzky, 1980, Nature (London) 286: 814-16. Kauvar, 1982, Mol. Gen. Genet. 187: 172-73. Jackson, Wilson, Strichartz and Hall, 1984, Nature 308: 189- 91. Ganetzky, 1984, Genetics 108: 897-911. Kyriacou and Hall, 1985, Nature (London) 314: 171-73. Burg and Wu, 1986, J. Neurosci. 6: 2968-76. O'Dowd and Aldrich, 1988, J. Neurosci. 8: 3633-43. Stern, Kreber, and Ganetzky, 1990, Genetics 124: 133-43. Elkins and Ganetzky, 1990, J. Neurogenet. 6: 207-19. Nelson and Wyman, 1990, J. Neurobiol. 21: 453-69. Budnick, Zhong, and Wu, 1990, J. Neurosci. 10: 3754-68. phenotype: Larvae or adults become rapidly paralyzed when exposed to 37 and rapidly recover on return to lower tempera- tures. Rearing stocks chronically at room temperature or above causes napts to "adapt" such that higher temperatures (> 40) are required for paralysis (Kyriacou and Hall, 1985). Experi- ments involving one-time rearing at low temperature caused napts to paralyze at relatively low temperatures (Nelson and Wyman, 1990). Axonal conduction (but not synaptic transmission) fails in larvae at high temperatures (Wu et al., 1978; Wu and Ganetzky, 1980), but action potentials in the giant fiber (GF) pathway of adults are not blocked at tempera- tures up to 43 (Elkins and Ganetzky, 1990; Nelson and Wyman, 1990), though the latency from brain stimulation to response of thoracic muscles are aberrantly long, even at low tempera- tures (Nelson and Wyman, 1990), and this long-latency disap- pears as the temperature is raised to 35 (Elkins and Ganetzky, 1990). "Following frequency" of napts thoracic muscle responses (re. GF pathway stimulation) reduced at elevated temperatures, an effect which can be reversed by injection of 4-amino-pyridine (Nelson and Wyman, 1990). At permissive tem- peratures, refractory period for elicitation of a series of action potentials is abnormally long (Ganetzky and Wu, 1980); at these low temperatures, napts suppresses effects of "hyperexcitability" mutations such as Sh, bas, bss, eas, Hk, kdn, and tko (Ganetzky and Wu, 1982, Genetics 100: 597-614). napts is unconditionally lethal (Ganetzky and Wu, 1980) in a double mutant with parats1 (death occurring during 1st larval instar) and the viability of other para; napts combinations is poor (Ganetzky, 1984); two doses of para+ (in males) suppresses high-temperature paralysis of napts (Stern et al., 1990). In mosaic experiments, cuticular clones of parats1 in a napts background (after low-temperature development) have non-functioning sensory cells, probably due to lack of nerve conduction which, however, did not cause any anatomical abnor- malities involving the central projections of these sensory neurons (Burg and Wu, 1986). Another developmental study, examining larval nerve terminal innervating body-wall muscles (Budnik et al., 1990), showed slight reduction in the extent of branching caused by napts at permissive temperature; the increase in branching (and higher than normal number of vari- cosities on motor-neurites) induced by an eag Sh double mutant was suppressed by napts (re. low-temperature rearing). napts in combination with tipE leads to poor viability at permissive temperature for both mutants (Ganetzky, 1986, J. Neurogenet. 3: 19-31; Jackson, Wilson, and Hall, 1986, J. Neurogenet. 3: 1-17). napts is, at permissive temperature, hypersensi- tive to blocking effects of tetrodotoxin (TTX) on action potentials (Ganetzky and Wu, 1980); brain membrane extracts of napts, assayed at low or high temperatures, have subnormal levels of tetrodotoxin (Kauvar, 1982) or saxitoxin (Jackson et al., 1984) binding activity; the latter study reports that there are no qualitative alterations of this binding activity (kd is normal). Cultured neurons from napts larvae are 4 to 5-fold more resistant than wild-type cells to killing effects of veratridine, irrespective of temperature (22 vs 35) (Suzuki and Wu 1984, J. Neurogenet. 1: 225-38), but TTX has no effects on these mutant cells, whose general growth charac- teristics are also normal (Wu, Suzuki and Poo, 1983, J. Neu- rosci. 3: 1888-99). The mutation does not seem to modify the expression of sodium currents in embryonic neurons (O'Dowd and Aldrich, 1988, J. Neurosci. 8: 3633-43). Exposure of napts males to high temperature causes arrest of oscillator underly- ing rhythmic component of courtship song (Kyriacou and Hall, 1985); in experiments on conditioned courtship, napts males learn normally but have shortened memory spans, and napts suppresses Sh-induced decrements in courtship learning (Cowan and Siegel, 1984, J. Neurogenet. 1: 333-44; 1986, J. Neuro- genet. 3: 187-201). alleles: allele origin synonym discov/ref ( comments ___________________________________________________________________ napts1 | EMS 2 temperature-sensitive paralysis when homo- or hemizygous; male viable when homozygous; lethal with parats1 napts2 HD naphd9 1 fails to complement napts1 paralysis; no P element insertion male viable when homo- zygous napts3 EMS nap1-1 1 fails to complement napts1 paralysis; male viable when homo- zygous napts4 EMS nap10-1-1 1 fails to complement lethality of napts1 in parats1 background; male viable when homo- zygous napts5 EMS nap20-4-1 1 fails to complement lethality of napts1 in parats1 background; male viable when homo- zygous nap6 EMS nap17-1 1 temperature-sensitive paralysis with napts1; male viable when homozygous nap7 / / ray fails to complement napts1 paralysis; male lethal when homozygous or with mle; homozygous females not temperature sensitive naprv1 / ray naptsrev1 1 male lethal in homo- zygotes or with mle; homozygous females not temperature sensitive; reduction in temperature sensitivity with napts1 and parats1 ( 1 = Kernan and Ganetzky; 2 = Wu, Ganetzky, Jan, Jan, and Benzer, 1978, Proc. Nat. Acad. Sci. USA 75: 4047-51. | Homozygous nap1 flies paralyzed at lower temperature than nap1/Df(2R)nap flies (Kernan and Ganetzky). Paralysis of homozygotes suppressed by para+ duplications (Stern and Ganetzky). / T(2;3)nap7 = T(2;3)42A2-7;80-81. cytology: Located in 42A2-8, since uncovered by Df(2R)nap9 (R. Kreber). molecular biology: Locus cloned by Kuroda, Kernan, Kreber, Ganetzky, and Baker. Molecular analyses of nap and mle indi- cate that the same open reading frame encodes mle+, nap+ and napts activities. other information: The paralysis of nap is not complemented by mle alleles, thus nap appears to be allelic to mle (Kuroda, Kernan, Kreber, Ganetzky, and Baker). Germline transformation and analysis of mutations also show that napts is a gain-of- function mutation of mle. # narrow: see nw # narrow abdomen: see na # narrow-Blade: see nwB # narrow-Dominant: see nwD # narrow eye: see ney # narrow scoop: see nrs # nbA: night blind A (J.C. Hall) location: 1-36.6. synonym: nonB; omp18; P18. references: Heisenberg and Gotz, 1975, J. Comp. Physiol. 98: 217-241. Heisenberg and Buchner, 1977, J. Comp. Physiol. 117: 127-62. Heisenberg, 1979, Handbook of Sensory Physiology (H. Autrum, ed.). Springer-Verlag, Berlin, Vol. 7, pp. 665-79. Bulthoff, 1982, Biol. Cybernet. 45: 63-70. 1982, DIS 58: 31. Kulkarni and Hall, 1987, Genetics 115: 461-75. Homyk and Pye, 1988, J. Neurogenet. 5: 37-48. phenotype: Higher than normal light-intensity thresholds needed for optomotor or phototactic responses (Heisenberg and Gotz, 1975). More specifically, high-acuity optomotor responses (ability to respond to relatively narrow moving stripes) rela- tively normal, but high-sensitivity flies (ability to respond to moving stimuli in dim light conditions) are impaired, hence, a "night-blind" phenotype (Heisenberg). In "slow phototaxis/Y-tube" tests (using ordinary white fluorescent light), mutant adults were extremely subnormal and in fact preferred the dark-arm of the Y (Kulkarni and Hall, 1987). Light-on and light-off transient spikes of electroretinogram reduced in amplitude, possibly absent (Heisenberg, 1979; Homyk and Pye, 1989). Weak orientation to spots in Y-maze test (Bulthoff, 1982). nbA mutation may define an essential gene, because nbA3/l(1)11Aa1 heterozygotes lack ERG transients (Homyk and Pye) and are severely defective in phototaxis (Kul- karni and Hall, 1987). alleles: allele origin discoverer synonym ______________________________________________ nbA1 EMS Heisenberg nbAH18; opm18 nbA2 EMS Heisenberg nbAH47; opm47 nbA3 Eichenberger nbAEE171; ldg cytology: Placed in 11A2. Consistent with the non- complementation of l(1)11Aa1 is that nbA3 has its ERG (Homyk and Pye, 1989) and phototaxis (Kulkarni and Hall, 1987) defects uncovered by In(1)A78, In(1)A97, or Tp(1;1)A101, which have common breakpoints in 11A2 and fail to complement l(1)11Aa lethals (Homyk and Pye; Lefevre, 1981). Hence, nbA maps to 11A2. Included in Df(1)RC29, a cytologically invisi- ble deletion that removes l(1)11Aa, gd, tsg, and fw (see Kul- karni and Hall, 1987, and Homyk and Pye, 1989 for further details). other information: The ldg (lamina-degeneration) designation for one of the alleles of this gene (nbA3) turned out to be a misnomer. nbA was also once called nonB (no-on-transient-B) [Pak, 1975, Handbook of Genetics (King, ed.). Plenum Press, New York, Vol. 3, pp. 703-33], but this designation was sub- sequently dropped. Possible complexity of the genes in the 11A2 region is suggested by the failure of not only nbA, but also the very closely linked cac courtship song mutation to complement l(1)11Aa and the (lethal) breakpoints in 11A2 (Kul- karni and Hall, 1987; also see cytology). cac seems otherwise unrelated to nbA (Kulkarni and Hall, 1987), in that this song mutant has normal vision (behaviorally and physiologically), nbA males sing normally, and the two kinds of mutation comple- ment each other for both phenotypes (tested in a homozygous tra background, with regard to courtship song). # nc2: see haync2 # nc3: see ms(3)nc3 # nc4: see wrl # nc16: see mrn # nc32: see ms(3)nc32 # ncd: non-claret disjunctional location: 3-100.7 (to the left of ca). origin: Induced by ethyl methanesulfonate. references: Davis, 1969, Genetics 61: 577-24. Sequeira, Nelson, and Szauter, 1989, Genetics 123: 511-24. Yamamoto, Komma, Shaffer, Pirrotta, and Endow, 1989, EMBO J. 8: 3543-52. Endow, Henikoff, and Niedziela, 1990, Nature (London) 345: 81-83. McDonald and Goldstein, 1990, Cell 61: 991-1000. phenotype: Disjunction in homozygous females abnormal; incidence of nondisjunction of all chromosome pairs in the first meiotic division and of meiotic and early-cleavage mitotic loss of maternally inherited chromosomes is high. X- chromosome recombination normal among both regular and excep- tional progeny. Behavior of nonhomologues correlated; doubly disomic and doubly nullosomic ova more frequent than expected (Davis). Similar in action to ca of D. simulans (Sturtevant, 1929, Z. Wiss. Biol. Abt. A 135: 323-56). Two thirds of mitotic loss of chromosomes in progeny of ncd mothers takes place in the first zygotic division; one third takes place subsequently. The majority of X-chromosome loss (85-95%) is of the maternally inherited X but there is also appreciable loss of the paternally inherited X as well (Sequeira et al.). Somatic loss of X and 4 correlated (Portin, 1978, Heredity 41: 193-203). Cytological description of meiotic behavior in D. simulans ca females (Wald, 1936, Genetics 21: 264-81) includes abnormal first meiotic spindle, second meiotic arrest, and dispersal of chromosomes into multiple micronu- clei; micronuclei also observed in ncd females (Roberts). Spindles frequently multipolar in first meiotic division (Puro) and in early-embryo nuclear divisions, and nuclei remain close together in center of egg (Kimble and Sandstedt, 1981, Genetics 978: s97). Kimble and Church (1981, J. Cell Sci. 62: 301-18) observed four classes of metaphase 1 confi- gurations: (1) two or more spindles (2) abnormally wide spindles with widely separated bivalents (3) unipolar spin- dles, and (4) normal spindles; the first three comprise 80% of configurations. Approximately 20% of eggs of ncd1 females asymmetrical or with more than two appendages (Kimble and Church). Hinton and McEarchen (1963, DIS 37: 90) reported a haploid-diploid mosaic. ncd ovaries transplanted into normal host behave autonomously (Roberts, 1962, DIS 36: 120). Chro- mosome segregation normal in ncd males. alleles: Most ncd mutations recovered simultaneously with ca mutations; the double mutants are designated cand in the claret entry; they are caused by a single lesion affecting both transcription units, and are inseparable. allele origin synonym ref ( comments ___________________________________________________________ ncd1 X ray 2 recovered as cand; 2.6 kb deletion ncd2 EMS 3 recovered as ca+; no 2.6 kb deletion ncd3 / ray cand2 4 recovered as cand3 ncd4 / ray cand3 4 recovered as cand4 ncd5 HD ca3-1 5 recovered as cand5; 2.6 kb deletion ncd6 HD ca22-8 5 recovered as cand6; 2.6 kb deletion ncd7 spont caCm 5 recovered as cand7; 2.6 kb deletion ncd8 HD caP3 5 recovered as cand8; 2.6 kb deletion ncdD | EMS NCD 1 slight dominant effect ( 1 = Kennison; 2 = Lewis and Gencarella, 1952, Genetics 37: 600-01; 3 = O'Tousa and Szauter, 1980, DIS 55: 119; 4 = Sequeira, Nelson, and Szauter, 1989, Genetics 123: 511-24; 5 = Yamamoto, Komma, Shaffer, Pirrotta, and Endow, 1989, EMBO J. 8: 3543-52. | Discoverer: Steiner. cytology: Using in situ hybridization, ncd was placed in 99B8- 10 by Yamamoto et al. (1989) and in 99B-C by McDonald and Goldstein (1990). molecular biology: Region cloned in an 160-kb chromosome walk from 99C6-8 to 99B8-10 (Yamamoto et al., 1989); the presumed ncd gene was later cloned and identified by PCR (McDonald and Goldstein, 1990). Transformation with a 0.9-kb fragment that contains the site of insertion of the P element in ca34 res- cues the ncd phenotype. This fragment hybridizes to a 2.2-kb mRNA that is abundant in adult ovaries but not in the ovary- minus carcasses nor in males. The transcript is absent in ncd1 and ncd7, but is presents in ncd2, ca1, and ca34. The 2.2-kb mRNA is transcribed from right to left and its 5 end is very close to that of a transcription unit on the opposite strand that generates a 7.4-kb mRNA thought to encode the ca product. All five ncd ca chromosomes tested have the same or similar 2.6-kb deletions for the 5 region shared by the two transcription units: ncd2, which is ca+, fails to show the deficiency, and is presumed to be a point mutation. Nucleo- tide and putative nucleic acid transcripts have been obtained by Endow et al. (1990) and McDonald and Goldstein (1990). The cDNA is 2294 nucleotides in length, has a single open reading frame, and is predicted to encode a 75,795-dalton protein 685 amino acids in length (McDonald and Goldstein, 1990). The amino acid sequence shows significant similarity in its carboxy-terminal domain to the motor amino-terminal domain of kinesin heavy chain (Endow et al., 1990; McDonald and Gold- stein, 1990), but the non-motor domains of the proteins encoded by ncd and Kin are not similar. Biochemical proper- ties of the presumed ncd protein were tested and found to be similar to those of kinesin, suggesting that ncd encodes a kinesin-like protein. # ncn: nurse cell number location: 3-68. origin: Induced by ethyl methanesulfonate. discoverer: Nusslein-Volhard. synonym: ncn-I. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. phenotype: Female sterile; no eggs laid. Follicles have increased numbers of nurse cells and are often tumorous. alleles: ncn018 and ncn077. # nd: see N # ndl: nudel location: 3-17. synonym: mat(3)2; mel(3)5. references: Rice, Ph.D. Thesis, Yale University. Anderson and Nusslein-Volhard, 1984, Nature 311: 223-27. phenotype: Maternal effect mutation producing totally dorsal- ized embryos. Spacing of transverse stripes of ftz protein altered in mutant embryos (Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32). alleles: ndl1 through ndl7 recovered as ndl046, ndl093, ndl111, ndl133, ndl169, ndl260, and ndlrm2. # Ndw: Nicked wing location: 3-87.2. origin: Treatment with DNA of nuclear polyhedrosis virus from Galleria melonella. references: Shandala, 1985, Tsitol. Genet. 19: 179-83. phenotype: Homozygous lethal. Wings nicked in heterozygotes. Maximum penetrance of wing phenotype at 16, minimum at 28; TSP in larval period. #*ne: nicked eye location: 2- (not located). references: Kiil, 1946, DIS 20: 66. phenotype: Eye margin nicked. Overlaps wild type. RK3. other information: Probably an allele of L. # ne: see fs(1)ne #*Ne: Nelson's mutant location: 3-31. references: Gowan and Nelson, 1942, Science 96: 558-59. Gowan, 1961, Sex and Internal Secretions (Young and Corner, eds.). The Williams and Wilkins Co., Baltimore, Vol. 1, pp. 27-28. Belote and Lucchesi, 1980, Genetics 96: 165-86. phenotype: Female progeny from Ne mothers are embryonic lethals. # neb: nebbish (M. Fuller) location: 2- discoverer: Wolf, 1988. origin: Recovered in a single P-element screen by Berg, McKearn and Spradling, but has not yet been shown to be associated with the insert. synonym: sl(2)ry3. references: Wolf and Fuller, unpublished. phenotype: Recessive late lethal. Some homozygotes survive until the pupal period, but very few eclose. Squash prepara- tions of pupal testes reveal that the mitochondrial derivative (nebenkern) fails to elongate during spermatid differentia- tion. Flagellar axonemes are assembled. Onion stage early spermatids appear normal. # nec: necrotic location: 2-{56}. references: Ashburner. cytology: Placed in 43A1-3. neither inactivation nor afterpotential: see nina # Nelson's mutant: see *Ne # nesher: see nr net: net Edith M. Wallace, unpublished. # net: net location: 2-0.0. phenotype: Wing veins form plexus-like net; first posterior cell between L3 and L4 widens toward tip; branch missing from posterior crossvein; all veins fused at base of wing, like bi. According to Waddington [1940, J. Genet. 41: 75-139 (fig.)], spaces form between epithelial layers owing to inadequate con- traction during pupal period; spaces later fuse and form extra veins (Diaz-Benjumea, Gonzalez-Gaitan, and Garcia-Bellido, 1989, Genome 31: 612-19). RK1. alleles: Six net alleles [not including Df(2L)net62] are described in the following table. allele discoverer origin ref ( cytology ___________________________________________________________________ net1 Bridges,31c10 spont 1, 2, 5, 7 Df(2L)21A1;21B4-5 *net2 Braun,1937 spont 1 *net3 Williams,56f spont 1, 8 *net4 Meyer,56c spont 1, 6 net18 | X ray 4 In(2LR)21B3;42C-D1 + terminal df? net38j Ives spont 3 ( 1 = CP627; 2 = Golubovsky, Kulakov, and Korochkina, 1978, Genetika 14: 294-305; 3 = Ives, 1968, DIS 43: 64; 4 = Koro- chkina and Golubovsky, 1978, DIS 53: 197-200; 5 = Lewis, 1945, Genetics 30: 137-66; 6 = Meyer, 1956, DIS 30: 77; 7 = Waddington, 1940, J. Genet. 41: 75-139; 8 = Williams, 1956, DIS 30: 79-80. | Terminal deficiency tentative. cytology: Placed in region 21A1-B5 on the basis of its associa- tion with Df(2L)net62 = Df(2L)21A1;21B4-5. #*neu: neuter location: Autosomal. origin: Spontaneous. discoverer: Travers, 1955. references: Clarke, 1957, DIS 31: 80. phenotype: Homozygous female intersex; homozygous male normal. RK3. other information: Not an allele of ix (Maynard Smith). # neu: neuralised (J.C. Hall) location: 3-50. origin: Induced by ethyl methanesulfonate. references: Lehmann, Dietrich, Jimenez, and Campos-Ortega, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 226-29. Lehmann, Jimenez, Dietrich, Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 62-74. Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. Campos-Ortega, 1985, Trends Neurosci. 8: 245-50. Hartenstein and Campos-Ortega, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 210-21. phenotype: Homozygous lethal, with hyperplasia of neural com- ponents at the expense of epidermal components as seen in other neurogenic lethal mutations (N, bib, mam, etc.); neu mutations cause especially strong neural hypertrophy; also aberrant imaginal disc development when expressed in mosaic clones (Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32). N+ duplications reduce the neu neural hypertro- phy, while neu+ duplications have no effect on N defects (De la Concha, Dietrich, Weigel, and Campos-Ortega, 1968, Genetics 118: 499-508). alleles: allele origin discoverer synonym _________________________________________________________ neu1 EMS Nusslein-Volhard, Wieschaus neu9L119 neu2 EMS Nusslein-Volhard, Wieschaus neu11B116 neu3 EMS Nusslein-Volhard, Wieschaus neu12H56 neu4 X ray neu21.1 ( neu5 EMS Bremer neuaL119 neu6 EMS De la Concha neuEK1 neu7 EMS De la Concha neuEK2 neu8 EMS De la Concha neuEK3 neu9 EMS De la Concha neuEK4 neu10 EMS De la Concha neuEK5 neu11 EMS Nusslein-Volhard, Wieschaus neuIF65 neu12 EMS Nusslein-Volhard, Wieschaus neuIN94 neu13 EMS Nusslein-Volhard, Wieschaus neuIIIA83 neu14 EMS neuKE2 neu15 X ray De la Concha neuXK1 neu16 X ray Knust neuXK2 ( Recovered as revertant of the enhancing effect of E(spl) on spl. Does not complement other neu alleles. cytology: Placed between 86C1-2 and 86D8 (Lehmann et al., 1983) since it is uncovered by Df(3R)cu = Df(3R)86C1-2;86D8 (Ash- burner, Angel, Detwiler, Faithfull, Gubb, Harrington, Little- wood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91); also placed in 85C based on cytology of In(3R)neuXK2 = In(3R)85C;87D5-14;90E-F (Campos-Ortega, 1985). # neural disrupted: see nrd # neuralized: see neu Neurogenic-element-binding transcription factor: see Ntf # Neuroglian: see Nrg # Neuron-specific: see Nsp # neuronally-altered-carbohydrate: see nac # neuter: see *neu #*ney: narrow eye location: 1- (rearrangement). origin: X ray induced. discoverer: Becker, 1950. references: 1952, DIS 26: 69. phenotype: Homozygote has narrow eyes halfway between B and wild type. Heterozygote usually normal. RK1A. cytology: Associated with In(1)ney = In(1)10A;16D. #*ni: nicked location: 3-40 (35 to 45). origin: Spontaneous. discoverer: Neel, 41c26. references: 1942, DIS 16: 51. phenotype: Small notches or nicks in wing tips of 60-90% of homozygous males and 80-100% of homozygous females. RK3. #*ni2: nicked on chromosome 2 location: 2- (not located). origin: Spontaneous. discoverer: Travers, 1955. references: Clarke, 1957, DIS 31: 80. phenotype: Wing tips deeply emarginated between L2 and L4 and occasionally between L4 and L5. Penetrance and viability good. RK3. # nicked: see ni # nicked on chromosome 2: see ni2 # nicked eye: see ne # Nicked wing: see Ndw # night blind A: see nbA # ninaA: neither inactivation nor afterpotential A (J.C. Hall; B.H. Shieh) location: 2-1.4. references: Pak, Conrad, Kremer, Larrivee, Schinz, and Wong, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York, pp. 331-46. Larrivee, Conrad, Stephenson, and Pak, 1989, J. Gen. Physiol. 78: 521-45. Homyk, Pye, and Pak, 1981, Genetics 100: s30. Stephenson, O'Tousa, Scavarda, Randall, and Pak, 1983, The Biology of Photoreceptors (Cosens and Vince-Prue, eds.). Cambridge University Press, England, pp. 471-95. Zuker, Mismer, Hardy, and Rubin, 1988, Cell 53: 475-85. Shieh, Stamnes, Seavello, Harris, and Zuker, 1989, Nature (London) 338: 67-70. Schneuwly, Shortridge, Larrivee, Ono, Ozaki, and Pak, 1989, Proc. Nat. Acad. Sci. USA 86: 5390-94. phenotype: Strong blue light leads to anomalously small degree of photoreceptor inactivation, and the prolonged depolarizing afterpotential PDA (seen after such treatment of wild-type photoreceptor cells) degrades rapidly following blue-light exposure reaching baseline levels within a few seconds; only the six outer photoreceptors (R1-R6) in each eye facet are aberrant physiologically (Larrivee et al., 1981). Rhodopsin levels are much lower than normal in these outer cells; altered gene dosage of ninaA+ does not effect changes in rho- dopsin levels; ninaA's mutant phenotypes are not suppressed by feeding on retinoid (e.g. vitamin A-enriched) media. alleles: With respect to defective PDA, ninaA2 > ninaA1 > ninaA3. allele origin discoverer synonym molecular biology ______________________________________________________ ninaA1 EMS Pak ninaAP228 Trp208 -> stop ( | ninaA2 EMS Pak ninaAP263 Gln87 -> stop ( ninaA3 EMS Pak ninaAP269 His227 -> Leu ( ninaA4 EMS Ondek Asn58 -> Lys ninaA5 EMS Ondek Arg60 -> Pro ninaA6 EMS Ondek Arg76 -> Stop ninaA7 EMS Ondek Gly88 -> Asp ninaA8 EMS Ondek Gly89 -> Asp ninaA9 EMS Ondek Gly89 -> Ser ninaA10 EMS Ondek Gly96 -> Glu ninaA11 EMS Ondek Gly98 -> Ser ninaA12 EMS Ondek Glu110 -> Lys ninaA13 EMS Ondek Lys112 -> stop ninaA14 EMS Ondek Gly125 -> Asp ninaA15 EMS Ondek Met126 -> Ile ninaA16 EMS Ondek Asn128 -> Tyr ninaA17 EMS Ondek Asn134 -> His ninaA18 EMS Ondek Gln137 -> His ninaA19 EMS Ondek Gln137 -> Leu ninaA20 EMS Ondek Gln137 -> stop ninaA21 EMS Ondek Trp147 -> stop ninaA22 EMS Ondek Gly156 -> Asp ninaA23 EMS Ondek intron ninaA24 EMS Ondek intron ninaA25 EMS Ondek Asp174 -> stop ninaA26 EMS Ondek Pro179 -> Leu ninaA27 EMS Ondek Cys188 -> Tyr ninaA28 EMS Ondek Pro200 -> Leu ninaA29 EMS Ondek stop -> Cys ? ( Schneuwly, Shortridge, Larrivee, Ono, Ozaki, and Pak, 1989, Proc. Nat. Acad. Sci. USA 86: 5390-94. | Shieh, Stamnes, Seavello, Harris, and Zuker, 1989, Nature 338: 67-70. cytology: Placed in 21D4-E2, by in situ hybridization (Shieh et al., 1989). Included in Df(2L)ast4 = Df(2L)21D1-2;21E1-2 but not Df(2L)ast6 = Df(2L)21E1-2;21E2-3. molecular biology: ninaA has been cloned, the nucleotides sequenced, and deduced amino acid sequences determined (Shieh et al., 1989; Schneuwly et al., 1989). It encodes a 237-amino acid protein with 40% sequence identity to the vertebrate cyclosporin A-binding protein, cyclophilin, that is involved in the activation of T-lymphocytes. Cyclophilin shown to be a peptidylprolyl cis-trans-isomerase that catalyzes rate- limiting steps in the folding of a number of proteins in vitro. # ninaB (J.C. Hall) location: 3-53.5. references: Pak, 1979, Neurogenetics: Genetic Approaches to the Nervous System (Breakfield, ed.). Elsevier/North- Holland, New York, pp. 67-99. Stephenson, O'Tousa, Scavarda, Randall, and Pak, 1982, The Biology of Photoreceptors (Cosens and Vince-Prue, ed.). Cam- bridge University Press, England, pp. 471-95. phenotype: Superficially like ninaA in aberrant visual physiol- ogy, but all eight photoreceptors in each eye facet affected by ninaB; can be restored to wild-type phenotype by dietary supplement of retinal but not by other retinoids. alleles: allele origin synonym ___________________________ ninaB1 EMS ninaBP315 ninaB2 EMS ninaBP319 ninaB3 EMS ninaBP360 cytology: Located in 87D14-F12 based on inclusion in Df(3R)l26c = Df(3R)87D14-E1;87F11-12 (Kremer, Wong, Pak). # ninaC (J.C. Hall) location: 2-22. origin: Induced by ethyl methanesulfonate. references: Pak, 1979, Neurogenetics; Genetic Approaches to the Nervous System (Breakfield, ed.). Elsevier/North- Holland, New York, pp. 67-99. Stephenson, O'Tousa, Scavarda, Randall, and Pak, 1982, The Biology of Photoreceptors (Cosens and Vince-Prue, ed.). Cam- bridge University Press, England, pp. 471-95. Matsumoto, Pye, Isono, and Pak, 1983, Neurosci. Abstr. 9: 325. Matsumoto, Isono, Pye, and Pak, 1987, Proc. Nat. Acad. Sci. USA 84: 985-89. Montell and Rubin, 1988, Cell 52: 757-72. Stowe and Davis, 1990, Cell Tissue Res. 260: 431-34. phenotype: Basic physiological and rhodopsin-depleted pheno- types like those of ninaB or ninaD mutants, except that ampli- tude of prolonged depolarizing afterpotential and rhodopsin levels are not so severely depressed, and these phenotypes cannot be rescued by vitamin A (or other retinoid) feeding. Decreased rhodopsin content is due to reduction in diameter of the rhabdomeres; the microvilli are shorter than normal and have reduced cytoskeletal electron-dense regions (Matsumoto et al., 1983). In particular, the central axial filament of the microvillus is absent (ninaC5) or greatly reduced (ninaC2, ninaC3). Actin immunoreactivity retained in the villi of flies homozygous for these alleles (Stowe and Davis). The mutant phenotype can be rescued using P-element mediated germ line transformation. alleles: At least ten ethyl-methanesulfonate-induced alleles. allele synonym comments _____________________________________________________ ninaC1 ninaCP216 ninaC2 ninaCP221 decrease in concentration and mobility of the 4.8 kb RNA ninaC3 ninaCP225 decrease in concentration of the 4.8 kb RNA ninaC4 ninaCP230 ninaC5 ( ninaCP235 decrease in concentration of the 3.6 and the 4.8 kb RNA ninaC6 ninaCP238 ninaC7 ninaCP239 ninaC8 ninaCP240 ninaC9 ninaCP262 ninaC10 ninaCP266 ( Appears to be null allele. cytology: Located in 28A1-3; included in synthetic deletion constructed using T(Y;2)R147 = T(Y;2)BSXhj;27E and T(Y;2)R50 = T(Y;2)h1-2;28B. molecular biology: The ninaC gene was cloned, sequenced and the eye-specific amino-acid sequences deduced (Montell and Rubin, 1988). The locus was expressed as two extensively overlapping mRNAs of 3.6 and 4.8 kb found in late pupae and adults; the RNAs code for a 132 kd protein (made up of 1135 amino acids) and a 174 kd protein (made up of 1501 amino acids) found in the rhabdomeres of the photoreceptor cells. Near the N ter- minus of both proteins is a putative protein kinase domain joined to a domain homologous to the globular head of the myo- sin heavy chain. The upstream DNA region contains an eleven- base-pair region in common with ninaE and Rh2 (Mismer, Michael, Laverty, and Rubin, 1988, Genetics 120: 173-80). other information: ninaC appears to be inseparable from Sp (2- 22.0), though no ninaC mutations cause Sternopleural-like defects. # ninaD (J.C. Hall) location: 2-57. origin: Induced by ethyl methanesulfonate. references: Pak, 1979, Neurogenetics: Genetics Approaches to the Nervous System (Breakfield, ed.). Elsevier/North-Hol- land, New York, pp. 67-99. Stephenson, O'Tousa, Scavarda, Randall, and Pak, 1982, The Biology of Photoreceptors (Cosens and Vince-Prue, ed.). Cam- bridge University Press, England, pp. 471-95. Johnson and Pak, 1986, J. Gen. Physiol. 88: 651-73. phenotype: Basic physiological and rhodopsin-depleted pheno- types like those of ninaB mutants (e.g. rhodopsin levels reduced in all three classes of photoreceptors); ninaD mutants can be rescued by dietary supplement of vitamin A and several other retinoids. Measurements of light-induced "quantum bumps" (the basic "units" of the photoreceptor potential) in ninaD2 (rhodopsin content, 10-2 X wild-type) showed these responses to be basically normal (implying that, since exten- sive inter-rhodopsin molecular interactions are likely to be extremely rare, such interactions are not necessary for gen- eration and adaptation of the bumps); yet, bump amplitudes approximately 4X normal (Johnson and Pak, 1986). alleles: Five ethyl-methanesulfonate-induced alleles. allele synonym _____________________ ninaD1 ninaDP245 ninaD2 ninaDP246 ninaD3 ninaDP258 ninaD4 ninaDP261 ninaD5 ( ninaDTH382 ( Smith, Shieh, and Zuker, 1990, Proc. Nat. Acad. Sci. USA 87: 1003-07. cytology: Placed in 36D1-E4 on the basis of its inclusion in Df(2L)H20 = Df(2L)36A8-9;36E3-4 and Df(2L)M-HS5 = Df(2L)36D1- E1;36F1-37A1. other information: Not the same gene as the very closely linked Arr1 (which produces a "phototransduction protein"); this was shown by sequencing coding exons of genomic DNA from ninaD2, ninaD3, and ninaD5, all of which exhibited wild-type arrestin sequences in these ORFs (Smith et al., 1990). # ninaE (J.C. Hall) location: 3-66.4. synonym: Rh1. references: Pak, 1979, Neurogenetics: Genetic Approaches to the Nervous System (Breakfield, ed.). Elsevier/North Hol- land, New York, pp. 67-99. Scavarda, O'Tousa, and Pak, 1983, Proc. Nat. Acad. Sci. USA 80: 4441-45. O'Tousa, Baehr, Martin, Hirsh, Pak, and Applebury, 1985, Cell 40: 839-50. Zuker, Cowman, and Rubin, 1985, Cell 40: 851-58. Pollack and Benzer, 1988, Nature (London) 333: 779-82. Johnson and Pak, 1986, J. Gen. Physiol. 88: 651-73. Stark and Sapp, 1987, J. Neurogenet. 4: 227-40. Zuker, Mismer, Hardy, and Rubin, 1988, Cell 55: 475-82. O'Tousa, Leonard, and Pak, 1989, J. Neurogenet. 6: 41-52. Washburn and O'Tousa, 1989. J. Biol. Chem. 264: 15464-66. phenotype: ninaE+ encodes the opsin moity of the major rhodop- sin, RH1, which occupies the rhabdomeres of the outer six pho- toreceptor cells R1-R6 in each ommatidium of the adult fly. This rhodopsin is also expressed in the larval light sensitive organs (Zucker et al., 1985; Pollack and Benzer, 1988). RH1 is a 39 kd basic protein (Pak and Nichols, 1985, J. Biol. Chem. 260: 12670-74). Homozygous ninaE mutants display severe depletion of rhodopsin from the outer photoreceptors, shown microspectrophotometrically and physiologically (Sca- varda et al., 1983; Johnson and Pak, 1986; also see below), as well as by absence of R1-6 staining with an anti-(Drosophila)- rhodopsin MAb (de Couet and Tanimura, 1987, Eur. J. Cell Biol. 44: 50-56). Electroretinograms demonstrate that the pro- longed depolarizing afterpotential (PDA) is absent; also, the sustained corneal-negative light-coincident response is reduced in some alleles and nearly wild type in amplitude in others. Physiological measurements of light-induced "quantum bumps" in three ninaE mutants (whose RH1 decrements range from 10-2 to 10-6 of wild-type) indicate that these responses-at the level of a given bump-are basically normal (implying that interactions among rhodopsin molecules are not likely to be critical for generation and adaptation of these "basic units" of photoreceptor potential (Johnson and Pak, 1986); bump amplitudes were higher than normal (more so in the more severe of the three mutants). Increased and decreased dosages of ninaE+ cause higher than normal and lower than normal rhodop- sin levels (Scavarda et al., 1983). Some mutants, when hetero- zygous to wild type, show less than 50% of the normal rhodop- sin level (e.g., ninaE7/+ yields 35% of the normal level); in heterozygotes of ninaE5, ninaE6, and ninaE7, the basic pho- toreceptor potential, as seen in electroretinograms, may be reduced. In mutant homozygotes, the cross-sectional area of rhabdomeres 1-6 is smaller than normal; in some mutants (ninaE1, ninaE3, ninaE7, and ninaE8), an age dependent, light-independent degeneration of R1-6 rhabdomeres (but not cell bodies) is observed; in the case of severe alleles like ninaE1 (see other information) or ninaE17, the rhabdomeres are present at eclosion, but degenerate rapidly thereafter (e.g., Stark and Sapp, 1987, O'Tousa et al., 1989); degeneration is cell autonomous in mosaics (Stark, Srygley, and Greenberg, 1981, DIS 56: 132-33). allele origin discoverer synonym ref ( comments __________________________________________________________________________________ ninaE1 EMS Koenig ninaEora 2, 4, 8 induced with ort1 as oraJK84; ca 10-6 normal RH1 level; Gin251 -> stop ninaE2 spont Engles ninaEENG 3, 5 4.2 kb insert; <1% normal transcript level ninaE3 EMS Pak ninaEP223 9 ninaE4 EMS Pak ninaEP228 9 ninaE5 EMS Pak ninaEP318 6, 8 3-13% normal RH1 level; normal transcript level; Pro120 -> Leu ninaE6 EMS Pak ninaEP322 7 RH1 undetectable ninaE7 EMS Pak ninaEP332 3, 6, 7, 8 <2% normal RH1 level; normal transcript level; Gly128 -> Arg ninaE8 EMS Pak ninaEP334 3, 7, 8 <1% normal RH1 level; normal transcript level; Thr283 -> Met; Trp289 -> Arg; Cys297 -> Ser ninaE9 | EMS Pak ninaEP352 1, 8 ca 10-6 normal RH1 level; Gin251 -> stop ninaE10 EMS Pak ninaEP353 ninaE11 EMS Pak ninaEP354 ninaE12 EMS Pak ninaEP361 ninaE13 EMS Pak ninaEP362 ninaE14 EMS Hardy, Orevi ninaERH7 ninaE15 EMS Hardy, Orevi ninaERH88 ninaE16 EMS Hardy, Orevi ninaEUS62 ninaE17 / ray O'Tousa ninaEO117 4 intragenic deletion ( 1 = Johnson and Pak, 1986, J. Gen. Physiol. 88: 651-73; 2 = Koenig and Merriam, 1977, DIS 52: 50-51; 3 = Leonard and Pak, 1984. Neurosci. Abstr. 10: 1032; 4 = O'Tousa, Leo- nard, and Pak, 1989, J. Neurogenet. 6: 41-52; 5 = O'Tousa, Baehr, Martin, Hirsh, Pak, and Applebury, 1985, Cell 40: 839-50; 6 = Scavarda, O'Tousa, and Pak, 1981, Neurosci. Abstr. 7: 61; 7 = Scavarda, O'Tousa, and Pak, 1983, Proc. Nat. Acad. Sci. USA 80: 4441-45; 8 = Washburn and O'Tousa, 1989, J. Biol. Chem. 264: 15464-66; 9 = Zuker, Mismer, Hardy, and Rubin, 1988, Cell 55: 475-82. | Same nonsense mutation and polymorphisms as ninaE1 (Washburn and O'Tousa, 1989). cytology: Placed in 92B6-7 based on its inclusion in Df(3R)o11 = Df(3R)92B5-6;92B7-8 (O'Tousa et al., 1985). molecular biology: Genomic clone isolated by cross homology to a bovine opsin-encoding cDNA (O'Tousa et al., 1985; Zuker et al., 1985). Opsin-encoding subclone identified by transforma- tion of ninaE mutant homozygotes. Nucleotide sequence con- tains an open reading frame interrupted by four introns with consensus splicing sequences; the conceptual amino acid sequence, which comprises 373 amino acids, indicates the pres- ence of seven putative membrane-spanning domains and several glycosylation sites. Probing of northern blots reveals the presence of an 1.5-1.7 kb eye-specific transcript, which is abundant throughout the depth of the retina (Pollock and Benzer, 1988). Three separable cis-acting control regions in the ninaE promoter extending from -120 to +61 have been iden- tified by Mismer and Rubin (1987, Genetics 116: 565-78), the first two appearing to be quantitative regulatory elements, the third affecting tissue-specificity of the promoter. There is an eleven-base-pair sequence in common with ninaC and Rh2 (Mismer, Michael, Laverty, and Rubin, 1988, Genetics 120: 173-80). The first two regions have the properties of enhancers required for normal promoter expression (Mismer and Rubin, 1989, Genetics 121: 77-87), although they do produce a ninaE expression pattern in a truncated Hsp70 promoter. As is the case for other opsins, putative phosphorylation sites are located near the C terminus of Drosophila RH1 protein; how- ever, removal of the relevant Ser and Thr residues by site- specific mutagenesis such that a premature termination codon is placed at amino-acid position 356, and transformation of that construct into a ninaE- host (Ozaki, Zuker, Pak, and Rubin, 1986, Neurosci. Abstr. 12: 639) led to light-induced physiological response of R1-6 indistinguishable from those of fully rescued control transformants (Zuker et al., 1988). The amount of rhodopsin phosphorylation in the engineered mutant was approximately half normal. other information: In one clean use of a ninaE variant to elim- inate responses of R1-6 photoreceptors, turn-on of per gene expression in nuclei of such cells (which requires exposures of the flies to light-dark transitions) was normal in ninaE17 (Zerr, Hall, Rosbash, and Siwicki, 1990, J. Neurosci. 10: 2749-62). A number of studies of this general sort have been carried out on the double mutant, ort ninaE (recovered as oraJK84); ort by itself is known to cause deficits in ERG light-on and light-off transient spikes (O'Tousa et al., 1989). The application of "ora" have usually been aimed at using it as a R1-6-removing tool for behavioral (e.g., Coombe, 1984, J. Comp. Physiol. 155: 661-72) or physiological (e.g., Stark, Schilly, Christianson, Bone, and Landrum, 1990, J. Comp. Physiol. 166: 429-36) experiments. Many of the abnor- malities, such as assessments of visual pigment content (most classically, Harris, Stark, and Walker, 1976, J. Physiol. 256: 415-39) are probably attributable to the ninaE component only; this includes an explicit demonstration that rhabdomere degeneration (Stark and Sapp, 1987, J. Neurogenet. 4: 227-40) is caused by ninaE (O'Tousa et al., 1989), similar to that caused by any other severe ninaE mutation. But certain effects of "ora" on visually mediated behaviors, such as decrements in male courtship (Markow and Manning, 1980, Behav. Neurobiol. 29: 276-80), the absence of blue-light influenced phototaxis (Willmund and Fischbach, 1977, J. Comp. Physiol. 118: 261-71), or the absence of R1-6-dependent optomotor responses (Heisenberg and Buchner, 1977, J. Comp. Physiol. 117: 127-62) could be affected by both factors.