# nj42: see mys8 # nj156: see shakB # nj522: see gfA # NK1 (M. Nirenberg) location: 3-{72}. references: Kim and Nirenberg, 1989, Proc. Nat. Acad. Sci. USA 86: 7716-20. phenotype: Homeobox gene expressed in embryos in several types of striated muscle cells and in some cells in the ventral ner- vous system. Fewer transcripts were detected in the central nervous systems (CNS) of larvae, pupae, and adults. No tran- scripts were detected in 0-3 hour embryos. cytology: Located at 93E3-5 close to NK3 and NK4. molecular biology: Sequence analysis of cloned cDNA and genomic DNA (7,609 nonoverlapping bp) revealed four exons. One major species of poly A+ RNA from embryos 2.9 kb in length was detected. NK1 protein contains 661 amino acid residues and it is rich in S, A, P, and H. The amino acid sequence of the homeobox is closely related to the H-40 homeobox of the honey- bee, Apis millifera (Walldorf, Fleig, and Gehring, 1989, Proc. Nat. Acad. Sci. USA 86: 9971-75) and chicken CHox3 homeobox (Rangini et al., 1989, Gene 76: 61-74). NK1 protein contains alternating repetitive, H/P residues (a paired repeat similar to those of prd and bcd proteins), and contains regions rich in H/Q, S/P, S/T, repetitive A, and repetitive G residues. NK1 also contains an acidic domain before the homeobox. Intron 3 is located within the homeobox between codons for homeobox amino acid residues 44 and 45. Homeobox genes cloned from monkey and rat DNA contain homeobox amino acid sequences identical to that of NK1 (52 amino acid residues compared). # NK2 (M. Nirenberg) location: 1-{0.0}. references: Kim and Nirenberg, 1989, Proc. Nat. Acad. Sci. USA 86: 7716-20. Nakayama, Nakayama, Kim, and Nirenberg, unpublished. phenotype: NK2 is a homeobox gene whose expression starts at the blastoderm stage during cell membrane formation (2.5- 3.25-hour embryos) in the region that gives rise to the ven- tral nervous system. NK2 transcripts detected in the ventral nervous system at later stages of embryonic development. NK2 transcripts also found in the midgut starting at 12 hours of embryonic development and thereafter during embryonic develop- ment. NK2 mRNA also found in larvae and pupae but the abun- dance of the mRNA is lower than that of embryos. NK2 mRNA is expressed in the central nervous system of the adult. cytology: Located at 1C. molecular biology: Sequence analysis of NK2 cDNA and part of the cloned genomic DNA (3033 nonoverlapping bp) showed that NK2 is a homeobox gene with two exons. NK2 is a basic protein with 723 amino acid residues and relatively high levels of A, S, H, G, and P with localized regions of alternating acidic and basic amino acid residues, and with regions of abundant S/T and P, or H, Q, and P, with repetitive A residues, pest sequences, an acidic domain, and an alternating H/A repeat. Northern analysis revealed one species of poly A+ RNA 3.5 kb in length. # NK3 (M. Nirenberg) location: 3-{72}. references: Kim and Nirenberg, 1989, Proc. Nat. Acad. Sci. USA 86: 7716-20. Webber, Kim, Guo, and Nirenberg, unpublished. phenotype: Homeobox gene expressed transiently during embryonic development in some mesodermal cells (foregut and hindgut vis- ceral muscle cells). NK3 poly A+ RNA was not detected in 0- 3-hour embryos, but was found in low abundance in RNA from 3- 6-hour embryos. The abundance was maximum in RNA from 6-12- hour embryos and then declined during further embryonic development. cytology: Located at 93E1-3 close to homeobox genes NK4 and NK1. molecular biology: Genomic DNA fragments were cloned that con- tain both NK3 and NK4 homeobox genes. NK3 and NK4 homeobox regions are separated by approximately 7.5 kb in genomic DNA. Sequence analysis of cloned NK3 cDNA and genomic DNA revealed two exons separated by a short intron. NK3 protein consists of 374 amino acid residues and contains S/T rich regions and several regions rich in acidic and basic amino acid residues. Northern analysis revealed one species of NK3 poly A+ RNA, approximately 1.5 kb in length. # NK4 (M. Nirenberg) location: 3-{72}. references: Kim and Nirenberg, 1989, Proc. Nat. Acad. Sci. USA 86: 7716-20. Rajni, Kim, Guo, and Nirenberg, unpublished. phenotype: The NK4 homeobox gene is first expressed in 3-hour embryos; no NK4 mRNA is detected in embryos at earlier stages of development. NK4 mRNA is detected only in mesodermal cells. The transcripts are most abundant in 3-9-hour embryos; the mRNA decreases in abundance thereafter. cytology: Located at 93E1-3 close to homeobox genes NK3 and NK1. molecular biology: The homeobox sequences of NK4 and NK3 are separated in genomic DNA by approximately 7.5 kb. Sequence analysis of cloned NK4 cDNA and genomic DNA revealed three exons. NK4 is a basic protein (41,192 Mr ) with 371 amino acid residues, and has relatively high levels of S, Q, A, and P. NK4 protein contains a homeobox that is not closely related to any known homeobox protein, contains pest sequences, Q repeats, and regions with abundant H and Q, or S, T, and P. One major species of poly A+ RNA was detected, 1.7 kb in length. # nkd: naked cuticle location: 3-47.3. origin: Induced by ethyl methanesulfonate. references: Jurgens, Kluding, Nusslein-Volhard, and Wieschaus, 1983, DIS 59: 157-58. Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. Arias, Baker, and Ingham, 1988, Development 103: 157-70. phenotype: Denticle bands partially deleted. Embryonic lethal. Terminal phenotype partly due to cell death after germ band shortening (Martinez-Arias). alleles: Six ethyl-methanesulfonate-induced alleles. allele synonym ref ( comments ________________________________________ nkd1 nkd6J 2 weak allele nkd2 nkd7E 2 strong allele nkd3 nkd7H 2 strong allele nkd4 nkd9G 2 nkd5 nkd9H 2 nkd6 nkdYE88 1 ( 1 = Carrol and Scott, 1986, Cell 45: 113-26; 2 = Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. cytology: Located in 75D-76B; uncovered by T(Y;3)L131DL14P = T(Y;3)75D1;76B5-10 (Nusslein-Volhard). # nmd: no mitochondrial derivative (M. Fuller) location: 2-. discoverer: Wolf, 1988. origin: Recovered in a single P-element screen by Berg, McKearn and Spradling. The male sterile mutation has not yet been shown to be associated with the insert. synonym: ms(2)ry4. references: Wolf, Madder, Bonneville and Fuller, unpublished. phenotype: Recessive male sterile. Onion stage early sperma- tids in homozygous males either lack or have only tiny mito- chondrial derivatives. Flagellar axonemes elongate without mitochondrial derivatives. Mitochondria present in polar pri- mary spermatocytes, but degenerate prior to meiosis in mature primary spermatocytes. Females are fertile. cytology: The transposable element is inserted at 31. # no action potential: see napts # no bridge: see nob # no distributive disjunction: see nod # no mitochondrial derivative: see nmd # no object fixation: see nof # no ocelli: see noc # no ocelli; narrow eyes: see none # no on-transient: see non # no receptor potential A: see norpA # no wings: see ap3 # nob: no bridge (J.C. Hall) location: 1-12. origin: Induced by ethyl methanesulfonate. discoverer: Heisenberg. references: Heisenberg, Borst, Wagner, and Byers, 1985, J. Neu- rogenet. 2: 1-20. Bouhouche and Vaysse, 1991, J. Neurogenet. phenotype: Protocerebral bridge between left and right sides of adult brain seems disintegrated into two or more glomeruli; fiber number in interhemispheric commisure of white pupa reduced; learning is poor in "arena paradigm" tests of adults, using sugar and odorants (Heisenberg et al., 1985); larval learning test using electric shocks and odorants gave approxi- mately half the normal score (Heisenberg, unpublished). Locomotor activity of mutant adults is abnormal (spontaneous walking speed, regarding forward strides of legs, is slow), and in flight, there is reduced frequency of flight starts, altered "object response" and reduced occurrences of "body saccades" (Heisenberg). Adults exhibit aberrant habituation of proboscis-extension reflex (Bouhouche and Vaysse, 1991). alleles: One mutant allele, called nobKS49. cytology: Placed in 4F5-12 (Heisenberg). # noc: no ocelli location: 2-{50}. discoverer: Ashburner. references: Ashburner, Angel, Detwiler, Faithfull, Gubb, Har- rington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91. Ashburner, Aaron, and Tsubota, 1982, Genetics 102: 421-35. Ashburner, Tsubota, and Woodruff, 1982, Genetics 102: 401- 20. Ashburner and Harrington, 1984, Chromosoma 89: 329-37. Chia, Carp, McGill, and Ashburner, 1985, J. Mol. Biol. 186: 689-706. Gubb, Roote, Harrington, McGill, Durrant, Shelton, and Ash- burner, 1985, Chromosoma 92: 116-23. McGill, Chia, Karp, and Ashburner, 1988, Genetics 119: 647- 61. phenotype: The genetic complexity of noc is indicated by phenotypic as well as molecular data (McGill et al., 1988). Mutants are characterized by partial or complete absence of ocelli and their associated bristles. Strong noc alleles lack all three ocelli and have fewer interocellar microchaetae; ocellar and interocellar bristles are absent; anterior pos- talar and notopleural bristles may not be present; postverti- cal bristles are crooked, an adventitious pair often occurring between a normal pair. Weak alleles may overlap wild type in phenotype, the flies having smaller ocelli and an aberrant pattern of interocellar microchaetae. Male and female homozy- gotes are viable and fertile. Penetrance and expressivity is stronger in males and in flies that emerge later. While a homozygous deletion of the entire noc region is lethal, distal or proximal regions can be homozygously deleted without caus- ing lethality. Some noc alleles and deficiences are lethal with In(2L)Scorv1, whose 2L breakpoint lies within noc, while other alleles are viable with the Sco inversion. alleles: Mutants and rearrangements are listed in the table. noc deficiencies are described in the rearrangement section. allele origin discoverer ref ( phenotype cytology mol. biol | ____________________________________________________________________________ noc2 EMS Tsubota 1, 2, 5-8 weak In(2L)35B1-2; -62 to -68 36D3 noc3 / ray Tsubota 2, 5-7 very weak noc4 / / ray Harrington 1, 5-8 strong In(2LR)35B1-2; -109 to -117 41 noc6 / / ray Harrington 7 strong noc7 / ` / ray Harrington 1, 6-8 weak In(2LR)35A1-4; -77 to -80 40 noc14 / / ray Harrington 7 weak noc15 / ray Harrington 7 weak noc18 EMS Spoerel 5, 7 weak noc19 / EMS Spoerel 5, 7 weak noc21 / ray McGill strong noc56.1 EMS noc56.3 EMS nocTE35A spont Ising 2-4, 5-8 very strong TE35A -108 insertion - [Sco] X ray Krivshenko 3, 8 antimorph Tp(2;2) -24.6 to of noc ? -107.8 ( 1 = Ashburner, Aaron, and Tsubota, 1982, Genetics 102: 421-35; 2 = Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91; 3 = Ashburner, Detwiler, and Woodruff, 1983, Genetics 104: 405-31; 4 = Ashburner and Harrington, 1984, Chromosoma 89: 329-37; 5 = Ashburner, Tsubota, and Woodruff, 1982, Genetics 102: 401- 20; 6 = Chia, Carp, McGill, and Ashburner, 1985, J. Mol. Biol. 186: 689-706; 7 = Gubb, Roote, Harrington, McGill, Durrant, Shelton, and Ashburner, 1985, Chromosoma 92: 116-23; 8 = McGill, Chia, Karp, and Ashburner, 1988, Genetics 119: 647-61. | From the molecular map of the wild-type noc-Adh region (McGill et al., 1988); coordinate 0 an EcoRI restriction site 1321 bp to the left of the start of transcription of the larval Adh transcript; "+" values to the right, "-" values to the left. / Lethal or semilethal with In(2LR)Scorv. ` Inversion in T(Y;2)60D7-F. - Synonym: TE146. Phenotype of Sco enhanced by deletion and suppressed by duplication of the noc gene (McGill et al., 1988). cytology: Placed in 35B1-2 on the basis of its inclusion in Df(2L)A178 = Df(2L)35B1-2;35B2-3 but not in Df(2L)A48 = Df(2L)35B2-3; 35D5-7. molecular biology: The DNA region associated with noc can be defined by the mapping of breakpoints of noc mutants which locate noc approximately between -117 and -62 kb on the molec- ular map of the wild-type noc - Adh region (McGill et al., 1988). If, however, Sco (a rearrangement in which the noc gene has been transposed from 35B to 35D) is considered to be an antimorphic allele of noc and is included in the locus, the noc region will be enlarged and will be located approximately between -117 and -24.6 kb. This region, almost 100 kb in estimated total length, is not thought to be continuous, but to be functionally divided into at least three components, the two distal ones (nocA and nocB) resulting in a mutant pheno- type when deleted and the proximal one (nocC) resulting in a noc+ phenotype when deleted (McGill et al., 1988). Breakpoints of Sco revertants are only found in nocB and nocC. Tp(2;3)Mpe, which shows a noc+ rather than a noc phenotype over deletions for the entire noc locus, has its 2L breakpoint between nocA and nocB (McGill et al., 1988). # nod: no distributive disjunction (R.S. Hawley) location: 1-36. references: Baker and Carpenter, 1972, Genetics 71: 255-86. Carpenter, 1973, Genetics 73: 393-428. Wright, 1973, Mol. Gen. Genet. 122: 101-18. 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. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. Zhang and Hawley, 1990, Genetics (submitted). phenotype: Females homozygous for nod alleles exhibit high fre- quencies of meiotic chromosome loss and nondisjunction at meiosis I. Most nod-induced nondisjunctional events involve nonexchange chromosomes. For example, in nod/nod females non- disjunction frequencies for the always nonexchange fourth chromosomes approaches 90% (the vast majority of gametes are nullo-4 ova), whereas nonexchange X chromosomes apparently disjoin at random. Both the frequency of exchange and the disjunction of exchange bivalents was shown to be normal in nod/nod females. Thus, with respect to its role in meiosis, the nod+ function appears to be limited to the distributive segregation system. Based on an analysis of secondary nondis- junction in noda/noda females, Carpenter concluded that the nod defect does not impair the process of partner choice within the distributive system, but rather specifically impairs the disjunctional process. Nonexchange chromosomes derived from noda/noda mothers also undergo nondisjunction, and presumably loss, at meiosis II. In addition, chromosomes derived from noda/noda mothers are mitotically unstable. nod-induced mitotic chromosome loss is restricted to maternal nonexchange chromosomes and does not exert any discernable effect on meiosis in males or on mitotic chromosome stability (Baker et al., 1978). Although none of the existing nod alleles is lethal or female sterile, the dosage-sensitive antimorphic mutation l(1)TW6 (Wright, 1973) is argued to be allelic to nod on the basis of three lines of evidence. First, l(1)TW6/+ females display a meiotic phenotype that is virtually identical to that exhibited by noda/noda females. Second, the two loci map to the same position on the X chromo- some (Wright, 1973; Baker). Third, a /-ray induced revertant of l(1)TW6 was shown to be a recessive nod allele (New and Hawley). alleles: allele origin synonym ref ( comments ____________________________________________ noda EMS mei254 1, 2 nod1 / rays nodb1 4 induced in FM7a nod2 / rays nodb9 4 induced in FM7a nod3 / rays nodb17 4 induced in FM7a nod4 / rays nodb27 4 induced in FM7a nod5 / rays nodb29 4 induced in FM7a nod6 / rays nodb34 4 induced in FM7a nod7 / rays nodbd 4 induced in FM7a Associated with In(1)10C;15D-E nod8 EMS l(1)TW6 3 ( 1 = Baker and Carpenter, 1972, Genetics 71: 255-86; 2 = Carpenter, 1973, Genetics 73: 393-428; 3 = Wright, 1973, Mol. Gen. Genet. 122: 101-18. 4 = Zhang and Hawley, 1990, Genetics (submitted); cytology: Placed in 10C2-3 by deficiency mapping. molecular biology: nod cloned and sequenced (Zhang, Knowles, Goldstein, and Hawley, 1990, Cell 62: 1053-62). 2.4 kb tran- script found in meiotically-active ovaries; not found in males. N-terminal domain of predicted protein shows amino acid similarity to the mechano-chemical domain of kinesin heavy chain. # nofA: no object fixation A (J.C. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. synonym: S100. references: Gotz, 1980, Development and Neurobiology of Droso- phila (Siddiqi, Babu, Hall, and Hall, ed.). Plenum Press, New York, pp. 391-407. Bulthoff, 1982, DIS 58: 31. 1982, Biol. Cybernet. 45: 63-70. 1982, Biol. Cybernet. 45: 71-77. phenotype: Poor orientation in tests involving fixation on objects or movements to and from in a "choice" experiment between two identical objects (i.e., flies in an arena). Nor- mal response to spots in a Y-maze test. Mutants make rapid continuous changes in their visual gaze instead of sporadic changes as in wild type. alleles: One mutant allele, called nofAS100 (Heisenberg and Wolf, 1979, J. Comp. Physiol. 130: 113-30). # nofC: see norpA # nofD (J.C. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. references: Bulthoff, 1982, DIS 58: 31. 1982, DIS 58: 32-33. 1982, Biol. Cybernet. 45: 63-70. 1982, Biol. Cybernet. 45: 71-77. phenotype: Poor orientation to objects, including spots in Y- maze test; electroretinogram normal. alleles: One mutant allele, nofDB11. # nofE: see sol16 # nofF (J.C. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. references: Bulthoff, 1982, DIS 58: 31. 1982, Biol. Cybernet. 45: 63-70. phenotype: Same phenotype as nofD or nofE. alleles: One mutant allele, nofFS71. # nofG (J.C. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. references: Bulthoff, 1982, DIS 58: 31. phenotype: Same basic phenotype as nofA in relation to visual objects. Electroretinogram normal. alleles: One mutant allele, nofGS13. # nofI (J.C. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. references: Bulthoff, 1982, DIS 58: 32-33. 1982, Biol. Cybernet. 45: 63-70. phenotype: Poor orientation to spots in Y-maze test. Eye color brownish; screening pigment in photoreceptors disrupted. Irregularities in pattern of rhabdomere endings. Electrore- tinogram normal. alleles: One mutant allele, nofIB3. # nofK (J.D. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. references: Bulthoff, 1982, DIS 58: 32-33. 1982, Biol. Cybernet. 45: 63-70. phenotype: Same phenotype as nofI. alleles: One mutant allele, nofKB6. # nofL (J.C. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. references: Bulthoff, 1982, DIS 58: 32-33. 1982, Biol. Cybernet. 45: 63-70. phenotype: Same phenotype as nofI. alleles: One mutant allele, nofLB7. # non-claret disjunctional: see ncd # nonA: no on or off transient-A (J.C. Hall) location: 1-52.3 (Pak); 1-56 (Heisenberg) (the former location more consistent with Kulkarni et al., 1988, and with cytol- ogy). origin: Induced by ethyl methansulfonate. synonym: Positive spike II group (Benzer); x14 (Pak), opm2 (Heisenberg). references: Hotta and Benzer, 1970, Proc. Nat. Acad. Sci. USA 67: 1156-63. Pak, Grossfield, and Arnold, 1970, Nature 227: 518-20. Heisenberg, 1971, DIS 46: 68. 1972, J. Comp. Physiol. 80: 119-36. Heisenberg and Gotz, 1975, J. Comp. Physiol. 98: 217-41. Heisenberg and Buchner, 1977, J. Comp. Physiol. 117: 127-62. Bulthoff, 1982, Biol. Cybernet 45: 63-70, 71-77. Kulkarni, Steinlauf, and Hall, 1988, Genetics 118: 267-85. Wheeler, Kulkarni, Gailey, and Hall, 1989, Behav. Genet. 19: 503-28. Jones and Rubin, 1990, Neuron. 4: 711-23. Besser, Schnabel, Wieland, Fritz, Stanewsky, and Saumweber, 1990, Chromosoma, in press. phenotype: Defective optomotor responses and phototaxis, with the former being especially defective (Heisenberg, 1972; Heisenberg and Buchner, 1977; Kulkarni et al., 1988). Poor orientation behavior in Y-maze (Bulthoff, 1982a, b). nonA5 flies exhibit specific lack of responses to front-to-back mov- ing visual stimuli, whereas reaction to back-to-front motion is intact (Heisenberg, 1972). Physiologically, there are reduced or absent light-on and light-off transient spikes in electroretinogram, whereas photoreceptor potential is normal (Hotta and Benzer, 1970; Pak et al., 1970; Heisenberg, 1971; Kulkarni et al., 1988; Jones and Rubin, 1990). Larval visual response (re negative phototaxis) normal [Hotta and Keng, 1984, Animal Behavior: Neurophysiological and Ethological Ap- proaches (Aoki et al., eds.). Springer-Verlag, Berlin, pp. 49-60]. Courtship song is abnormal, as influenced by one, possibly two, mutant alleles; nonA9 (originally diss) males produce abnormal song, regarding pulses relatively late in trains of such song sounds (each one resulting from a bout of wing vibration); the abnormalities are polycyclicity (Kulkarni et al., 1988) and anomalous intra-pulse frequency components (Wheeler et al., 1989); pulses early in trains, or throughout short ones, are nearly normal; courtship hum sounds manifest irregular sine waves, though their fundamental frequencies are normal (Wheeler et al., 1989). nonA9 by itself is also an optomotor-defective/ERG-abnormal mutant (Kulkarni et al., 1988) and fails to complement other mutant alleles with regard to these visual phenotypes (Rendahl, Kulkarni, and Hall, unpublished); but these heterozygotes, in a homozygous tra genetic background, sing normally (with the possible exception of nonA2/nonA9, Rendahl et al., unpublished), as do males hem- izygous for alleles isolated as visual mutants. alleles: allele discoverer synonym comments ___________________________________________________________ *nonA1 Benzer nonABS18 nonA2 Pak nonAP14 does not complement nonA9 song defects nonA3 Pak nonAP49 complements nonA9 song defects nonA4 Pak nonAP60 complements nonA9 song defects nonA5 Heisenberg nonAH2, opm2 *nonA6 Heisenberg nonAH17 *nonA7 Heisenberg nonAH48 *nonA8 Heisenberg nonA530 nonA9 Steinlauf diss isolated as song mutant cytology: Placed in 14C1-2, by in situ hybdridization, using a cDNA probe (von Besser et al., 1990). Covered by Dp(1;2)r+75c = Dp(1;2)14B13;15A9;35D-E; not included in Df(1)81k21e = Df(1)14C1-2;15A5 (Jones and Rubin, 1990, Neuron. 4: 711-23). molecular biology: Cloned from two very different starting points. Genetic one: beginning with a probe hybridizing to proximal 14B, and by walking in the proximal direction, the distal breakpoints of Dp(1;2)r+75c and Df(1)81k21e were localized at approximately +64 kb and +84 kb, respectively, on the coordinates of Steller (Jones and Rubin, 1990). Two over- lapping genomic fragments from a portion of this interval res- cued nonA5- and nonA9-associated ERG defects (Jones and Rubin, 1990) and the song defects of the latter as well (Rendahl et al., unpublished). Genomic probes from within the "rescuing region" detected 4-, 3-, and 2.8-kb transcripts (Jones and Rubin, 1990), which are relatively constant in abundance through the life cycle (though the last of these was at rela- tively lower concentrations in embryos; also see von Besser et al. for embryo results). Same kind of probes led to cDNAs (from adult head library), one of which when sequenced predicts a ca. 700-amino-acid-basic protein (Jones and Rubin, 1990) that contains "RNP" RNA binding motifs (von Besser et al., 1990). No homologies found in a data-base search. The gene was also cloned serendipitously by a completely indepen- dent method. A particular monoclonal antibody raised against embryonic chromatin (Frasch and Saumweber, 1989, Chromosoma 97: 272-81), which appears to react specifically with a pro- tein in polytene chromosome puffs, was used to isolate clones from an expression library (von Besser et al., 1990); the sequence of one such clone predicts the same protein as that described by Jones and Rubin. In situ hybridization to embryos with a cDNA probe detects fairly ubiquitous spatial expression of the transcript(s) (von Besser et al., 1990). This kind of expression is also seen using an anti-NONA mono- clonal antibody to stain sections throughout the life cycle (Rendahl, Jones, and Hall, unpublished), with the additional fact that the nervous system is included in the many tissues so expressing and that the subcellular localization appears to be nuclear. The gene comprises five exons and is transcribed from left to right. Analysis of the mRNAs expressed from nonA indicates the transcript complexity includes alternative splicings and protein products that differ in approximately 35 C-terminal amino acids (Jones and Rubin, 1990; von Besser et al., 1990). Truncation of both the predicted protein forms (I and II) by oligonucleotide directed mutagenesis followed by transformation, leads to no rescue of nonA ERG defects; whereas a stop codon that prematurely terminates only form II does so rescue (Jones and Rubin, 1990). other information: Mosaic analysis (Hotta and Benzer, 1970) suggested that ERG defects map to photoreceptors; but too few gynandromorphs were analyzed to rule out an optic-lobe "focus", which is more likely to be the focus for visual- movement-response abnormalities (especially those reported by Heisenberg, 1972). Two genomic clones, whose distal endpoints are just distal to nonA-rescuing DNA fragments, rescue each of two non-allelic lethals [l(1)14Cc, and l(1)14Ca] that map to the same cytogenetic interval as does nonA; transformation with overlapping genomic clones indicates an order from left to right of l(1)14Cc l(1)14Ca nonA (Jones and Rubin, 1990). Both lethals complement the ERG defects of nonA5 (Jones and Rubin, 1990) and complement the song abnormality of nonA9 (Kulkarni and Hall, unpublished). # nonB: see nbA # nonC (J.C. Hall) location: 1- (not localized). origin: Induced by ethyl methanesulfonate. references: Heisenberg, 1979, Handbook of Sensory Physiology (Antrum, ed.). Springer-Verlag, Berlin, Vol. VII/6A, pp. 665-79. Bulthoff, 1982, DIS 58: 31. 1982, Biol. Cybernet. 45: 63-70. phenotype: Defective phototaxis and optomotor responses; no light-on or light-off transients in electroretinogram, prob- ably due to defect in photoreceptor cells per se; abnormal orientation to spots in Y-maze test. alleles: Two mutant alleles, nonC1 (=X37), nonC2 (=X72). # none: no ocelli; narrow eyes location: 3-. discoverer: Shearn. references: Stark, Srivastava, Carlson, and Garment, 1984, DIS 60: 191-93 (fig.). phenotype: No ERG or deep pseudopupal in none/none flies. In the compound eye, corneal facets are fused and corneal hairs displaced, but corneal nipples are present. There is an all- glial cell mass in the peripheral retina and there are no rhabdomeres or optic cartridges as in the wild-type fly. In the ocellar area, only remnants of the ocellar lenslets can be observed. other information: none mutants resemble Gl mutants in regard to morphology of the compound eye (Harte and Kankel, 1982, Genetics 101: 477-501) and absence of an ERG. # nonpupariating 3: see npr3 # norpA: no receptor potential A (J.C. Hall) location: 1-6.5. origin: Induced by ethyl methanesulfonate. discoverer: Pak, Grossfield, and Arnold; Hotta and Benzer; Heisenberg (all independently). synonym: nofC; x12, x13, x16, x24. references: Hotta and Benzer, 1970, Proc. Nat. Acad. Sci. USA 67: 1156-63. Pak, Grossfield and Arnold, 1970, Nature (London) 227: 518- 20. Deland and Pak, 1973, Nature (London), New Biol. 244: 184-86. Pak, Ostroy, Deland, and Wu, 1976, Science 194: 956-59. Harris and Stark, 1977, J. Gen. Physiol. 69: 261-91. Ostroy, 1978, J. Gen. Physiol. 72: 717-32. Hotta, 1979, Mechanisms of Cell Change (Ebert and Okada, eds.). John Wiley, New York, pp. 169-82. Minke and Armon, 1980, Photochem. & Photobiol. 32: 553-62. Lo and Pak, 1981, J. Gen. Physiol. 77: 155-75. Matsumoto, O'Tousa, and Pak, 1982, Science 217: 839-41. Yoshioka, Inoue, and Hotta, 1983, Biochem. Biophys. Res. Comm. 111: 567-73. Inoue, Yoshioka, and Hotta, 1985, Biochem. Biophys. Res. Comm. 132: 513-19. Matsumoto and Pak, 1985, Neurobiology (Gilles and Balthazart, eds.). Springer-Verlag, Berlin, pp. 398-412. Banga, Bloomquist, Brodberg, Pye, Larrivee, Mason, Boyd, and Pak, 1986, Chromosoma 93: 341-46. Wilson and Ostroy, 1987, J. Comp. Physiol. 161: 785-91; 793- 98. Bloomquist, Shortridge, Schneuwly, Perdew, Montell, Steller, Rubin, and Pak, 1988, Cell 54: 723-33. Inoue, Yoshioka, and Hotta, 1988, J. Biochem. 103: 91-94. Zinkl, Maier, Studer, Sapp, Chen, and Stark, 1990, Vis. Neu- rosci. 5: 429-39. phenotype: Structural gene for phospholipase-C (PLC; specifi- cally, phosphatidyl inositol 4.5 biphosphate phosphodies- terase). norpA mutants are blind and have no (or reduced) light-elicited photoreceptor potentials (re: electroretino- grams) in the compound eyes and ocelli. Adults homozygous or hemizygous for severe alleles are completely blind, whereas those carrying weaker alleles have amplitude-subnormal ERGs induced by light (Ostroy and Pak, 1974, BBRC 59: 960-66; Wil- son and Ostroy, 1987a). Light-induced behavior (negative pho- totaxis) of larvae also absent under influence of severe alleles [Markow, 1981, Behav. Neur. Biol. 31: 348-53; Hotta and Keng, 1984, Animal Behavior: Neurophysiological and Etho- logical Approaches (Aoki et al., eds.). Springer-Verlag, Ber- lin, pp. 49-60]. A decrease in the amount of rhodopsin occurs under influence of severe alleles (Ostroy, 1978), though this was largely blocked when the mutant flies were reared and kept in constant darkness (Zinkl et al., 1990), and precedes an age-dependent degeneration of adult photoreceptors (Wilson and Ostroy, 1987b), which is accentuated at high temperatures (Zinkl et al., 1990). Severe mutants show no pigment granule migration with light adaptation (Lo and Pak, 1981). Electro- physiological as well as behavioral phenotypes are present in the youngest flies tested, long before the degenerative changes become apparent. There are zipper-like membrane spe- cializations on plasmalemma of norpA retinula cells (Alawi, Jennings, Grossfield, and Pak, 1972, Adv. Exp. Med. Biol. 24: 1-21; Stark, Sapp, and Carlson, 1988, J. Neurogenet. 5: 49-59). Microvillar membranes of the photoreceptor-cell rhabdomeres are severely depleted in six-day-old norpA7 adults [Hirosawa and Hotta, 1982, The Structure of the Eye (Holli- field, ed.). Elsevier, New York, pp. 45-53]. norpA mutants show polypeptide differences with respect to eye proteins on 1-d or 2-d gels [Ostroy and Pak, 1973, Nature (London) 243: 120-21; Hotta, 1979]. The mutation blocks light-induced phosphorylation of three eye-specific proteins (Matsumoto et al., 1982); one of these proteins has been identified as R1-6 opsin (Nichols and Pak); blockage of this phosphorylation is most complete in severely blind norpA alleles, less so in norpA alleles with measurable ERGs. Phospholipid kinase (diglyceride kinase) activity is nearly absent in norpA mutants, as is phosphorylation of the photoreceptor phospholi- pid, phosphatidic acid (Yoshioka et al., 1983). Hydrolysis of phosphatidyl-inositol 4.5-biphosphate, liberation of the ino- sitol triphosphate product, and activity of PLC are only 2-3% normal (Inoue et al., 1985, 1988), under the influence of a severe allele (norpA7) and are about 10% of normal in norpA9, decreasing another five-fold (as does heat-sensitive blind- ness) after shift to 28 (Inoue et al., 1985, 1988). so (sine oculis) removes about 90% of PLC activity, whereas a norpA mutation can remove substantially more (Inoue et al., 1985; Yoshioka, Inoue, and Hotta, 1985, J. Biochem. 97: 1251-54); this would seem to jibe with the provisional demonstration, by in situ hybridization, of a low level of norpA expression (however, this was not shown to be specifically a gene pro- duct) in the optic lobes and central brain (Bloomquist et al., 1988). alleles: allele discoverer synonym ref ( comments | _____________________________________________________________ norpA1 Bulthoff norpAB1 3, 4 / norpA2 Bulthoff norpAB2 3, 4 / norpA3 Bulthoff norpAB5 3, 4 / norpA4 Bulthoff norpAB8 3, 4 Group II / norpA5 Bulthoff norpAB9 3, 4 Group II / norpA6 Bulthoff norpAB10 3, 4 Group II / norpA7 Benzer norpAEE5 2, 7 Group II norpA8 Benzer norpAJM11 norpA9 Benzer norpAKO50 8 Ser ? -> Phe; Gly ? -> Ser temperature- sensitive allele norpA10 Benzer norpAKS85 norpA11 Benzer norpAKS115 norpA12 Benzer norpASB37 norpA13 Heisenberg norpAH3 Group III norpA14 Heisenberg norpAH4 Group II norpA15 Heisenberg norpAH5 Group IV norpA16 Heisenberg norpAH9 Group I norpA17 Heisenberg norpAH10 Group II norpA18 Heisenberg norpAH14 Group III norpA19 Heisenberg norpAH19 Group II norpA20 Heisenberg norpAH21 Group III norpA21 Heisenberg norpAH23 Group IV norpA22 Heisenberg norpAH26 Group III norpA23 Heisenberg norpAH27 Group IV norpA24 Heisenberg norpAH28 Group II norpA25 Heisenberg norpAH30 Group II norpA26 Heisenberg norpAH33 Group III norpA27 Heisenberg norpAH35 Group I norpA28 Heisenberg norpAH39 Group II norpA29 Heisenberg norpAH43 Group III norpA30 Heisenberg norpAH44 Group II norpA31 Heisenberg norpAH52 2, 5, 8 Ser ? -> Tyr opm52 temperature- sensitive allele norpA32 Heisenberg norpAH54 Group III norpA33 Pak norpAP12; x12 2, 9-11 Group III norpA34 Pak norpAP13; x13 2, 10, 11 Group II norpA35 Pak norpAP16; x16 2, 11 Group III norpA36 Pak norpAP24 1, 2, 10 Group I norpA37 Pak norpAP39 Group I norpA38 Pak norpAP40 Group II norpA39 Pak norpAP41 Group I norpA40 Pak norpAP42 Group III norpA41 Pak norpAP45 Group III norpA42 Pak norpAP46 Group II norpA43 Pak norpAP47 Group IV norpA44 Pak norpAP51 Group III norpA45 Pak norpAP54 Group III norpA46 Pak norpAP55 Group I norpA47 Pak norpAP57 Group IV norpA48 Pak norpAP64 Group III norpA49 Pak norpAP70 Group II norpA50 Pak norpAP71 Group II norpA51 Pak norpAP76 Group III norpA52 Pak norpAP78 Group III norpA53 Pak norpAP79 Group III norpA54 Pak norpAP81h 2 norpA55 ` norpAsuI 6 Group II norpA56 ` norpAsuII 6, 12 Group IV norpA57 ` norpAsuIII 6 Group II ( 1 = Banga, Bloomquist, Brodberg, Pye, Larrivee, Mason, Boyd, and Pak, 1986, Chromosoma 93: 341-46; 2 = Bloomquist, Shor- tridge, Schneuwly, Perdew, Montell, Steller, Rubin, and Pak, 1988, Cell 54: 723-33; 3 = Bulthoff, 1982, DIS 58: 31; 4 = Bulthoff, 1982, DIS 58: 32; 5 = Deland and Pak, 1973, Nature (London) New Biol. 244: 184-86; 6 = Harris and Stark, 1977, J. Gen. Physiol. 69: 261-91; 7 = Hirosawa and Hotta, 1982, The Structure of the Eye (Hollifield, ed.) Elsevier, New York, pp. 45-53; 8 = Hotta and Masai, 1991, J. Neurogenet., in press; 9 = Ostroy and Pak, 1973, Nature (London), New Biology 243: 120-21; 10 = Ostroy and Pak, 1974, Biochim. Biophys. Acta 368: 259-68; 11 = Pak, Gross- field, and Arnold, 1970, Nature (London) 227: 518-20; 12 = Stark, Chen, Johnson, and Frayer, 1983, J. Insect Phy- siol. 29: 123-31. | Alleles classified arbitrarily into four groups based on the electroretinogram amplitudes: I = no ERG; II = very small (<3mV) ERG, even with high intensity stimuli; III = intermediate ERG; IV = ERG ampli- tudes approaching that of wild type ERGs when intense stimuli are used. / Fixation defective; isolated on basis of poor orientation to spots in a Y-maze test and originally designated nofC muta- tions (Bulthoff, 1982). Exhibit defective visual response in a freely walking test. ERG's light sensitivity severely reduced and there are no light-on or light-off transient spikes. ` Recovered as allele specific suppressors of rdgB9 (Harris and Stark, 1977, see also Stark, Chen, Johnson, and Frayer, 1983, J. Insect Physiol. 29: 123-31). cytology: Located at 4B6-C1 by in situ hybridization (Bloom- quist et al., 1988); lies between the cytologically indistin- guishable distal breakpoints of Df(1)rb41 and Df(1)biD2 at 4B6-C1. molecular biology: Gene cloned and sequenced (Bloomquist et al., 1988). Encodes a 7.5 kb RNA expressed in the head. Putative norpA protein of 1095 amino acid residues shows extensive sequence similarity to a phospholipase C (PLC) amino acid sequence from bovine brain (Bloomquist et al., 1988). Report of a decrement in an eye-specific diacylglyceride kinase activity (diacylglyceride being produced as a result of PLC action) in norpA (Yoshioka, Inoue, and Hotta, 1984, Biochem. Biophys. Res. Comm. 119: 389-95) is not readily explainable by other enzymatic studies of the mutant, which are consistent with the clone and sequence data. Note that the PLC decrements are correlated with physiological severi- ties of various norpA mutations, whereas DGK reductions are not (Inoue et al., 1988). other information: norpA mutations have been used to assess the role of "basic vision " in complex behaviors such as courtship and circadian rhythms. Initiation of courtship and beginning of mating are prolonged in mutant males (Markow and Manning, 1980, Behav. Neur. Biol. 29: 276-80; Tompkins, Gross, Hall, Gailey, and Siegel, 1982, Behav. Genet. 12: 295-307), but norpA females appear to mate more readily than normal females (Tompkins et al., 1982; Markow and Manning, 1982, DIS 58: 104-05). Blind norpA adults can respond to light changes, with regard to their cyclically changing locomotor activity in 12h:12h light:dark (LD) cycles, and in terms of being entrained to exhibit free-running circadian rhythms of activity after transfer from LD to constant darkness (Konopka, 1980, Neurosci. Abstr. 6: 706; Dushay, Rosbash, and Hall, 1989, J. Biol. Rhythms 4: 1-27); yet, the free running periodicities were about 1 hour shorter than control values (Dushay et al., 1989). Experiments involving turning on per- gene expression in adult photoreceptors, which requires expo- sure (of wild-type) to light-dark transition, is normal in two severe norpA's (Zerr, Hall, Rosbash, and Siwicki, 1990, J. Neurosci. 10: 2749-62). Pressure injections of PLC into eye during ERG recordings does not ameliorate defective norpA phy- siology (Zinkl et al., 1990). Rhabdomere turnover rhodopsin cycling rhythms (Stark, Sapp, and Schilly, 1988, J. Neurocy- tol. 17: 499-509) are damped or absent in norpA (Zinkl et al., 1990). # nos: nanos location: 3-66.2. origin: Induced by ethyl methanesulfonate. discoverer: Lehmann. references: Nusslein-Volhard, Frohnhofer, and Lehmann, 1987, Science 238: 1675-81. Lehmann, 1988, Development 104 (Suppl.): 17-27. Hulskamp, Schroder, Pfeifle, Jackle, and Tautz, 1989, Nature (London) 338: 629-32. Irish, Lehmann, and Akam, 1989, Nature (London) 338: 646-48. Struhl, 1989, Nature (London) 338: 741-44. phenotype: Maternal-effect lethal. Mutant embryos lack abdomi- nal segments, but have normal pole cells and pole plasm; no posterior activity in pole plasm. Transport or diffusion of the nos gene product from the posterior of the embryo seems to be essential for development of the wild-type abdominal pat- tern. Presence of the nos protein represses the activity of of the gene product encoded by the hb maternal transcript in the posterior half of the embryo (Hulskamp et al., 1989; Irish et al., 1989; Struhl, 1989). Eggs deficient for both hb and nos, when fertilized by hb+ sperm, develop into normal embryos and subsequently into viable flies. alleles: Four alleles, three strong and one weak (Wang and Leh- mann, 1989). cytology: Located in 91F-92A. molecular biology: nos has been cloned (Lehmann) and a maternal transcript identified (Wang and Lehmann, 1989). # Not upheld: see Mhc16 # Notch: see N # Notch 2: see N-b # Notch b: see N-b # Notch Xasta: see NX # notchoid: see nd under N # notchy: see ny # Notopleural: see Np Np: Notopleural From Bridges, Skoog, and Li, 1936, Genetics 21: 788-95. #*Np: Notopleural location: 2-58.7 to 60.2 (between cn and en; inseparable from blo). origin: Spontaneous. discoverer: Nichols-Skoog, 33b20. references: Bridges, Skoog, and Li, 1936, Genetics 21: 788-95 (fig.). Li, 1936, Peking Nat. Hist. Bull. 11: 39-48. phenotype: Notopleural, humeral, presutural, and pretarsal bristles shorter and blunter than normal. Wings short and broad. Female produces few or no progeny. Viability fair. Development retarded. More extreme at 19 than at 25, also more extreme in female. Lethal over T(2;3)dp. Homozygous lethal. RK2A. cytology: Locus lies between 44F1 and 45E2 on the basis of its association with Df(2R)Np = Df(2R)44F1-2;45E1-2 (Bridges). # npr1: see BRC # npr2: see BRC # npr3: nonpupariating 3 location: 1-65.8. origin: Induced by ethyl methanesulfonate. synonym: l(1)npr-3; l(1)d.deg.12. references: Kiss, Bencze, Fodor, Szabad, and Fristrom, 1976, Nature (London) 262: 136-38. Kiss, Szabad, and Major, 1978, Mol. Gen. Genet. 164: 77-83. Kiss, Szabad, Belyaeva, Zhimulev, and Major, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York and London, pp. 163-81. phenotype: Male lethal; continues development through larval stage, but does not purpariate. Imaginal discs are very small and structureless; ring glands are normal in size on eighth to tenth day of larval life. Puparium formation can be induced by implantation of wild-type ring glands. # nr: nesher location: 2-28.3 (26.5 cM to left of Bristle). origin: Isolated from isofemale lines carrying eagle that were derived from natural populations in California. references: Prout and Green, 1986, DIS 63: 169. phenotype: Identical to eg; nr and eg combined are eg in pheno- type. # nrd: neural disrupted location: 2- {7}. origin: Differential screen of genomic clones using cDNA probes prepared from neural and non-neural cells. references: Neumann and Mahowald. phenotype: Embryonic lethal typified by an enlarged brain, irregular ventral nerve cord formation, and disorganized peri- pheral ganglia; these defects first appear in 10-12 hour embryos and include a delay in germband contraction and a failure of head involution. The CNS of mutant embryos fails to complete the normal condensation that leads to compact paired cerebral hemispheres and a ventral ganglion. In late mutant embryos, the brain, which has protruded dorsally through a hole in the cuticle, remains extended and flattened against the vitelline membrane and the ventral neuromeres are extended posteriorly; discontinuities or thinnings of the ven- tral nerve cord can frequently be observed. Normal develop- ment of the mouth parts and cephalopharyngeal apparatus is disrupted. cytology: Located in 23A1-3 by in situ hybridization of cloned DNA. molecular biology: Gene (selectively expressed in neural cells) cloned; 2.3 kb transcript obtained both maternally and in 10- 18 hour old embryos. Transcript remains in larval, pupal, and adult stages. Non-neural specific 1.3 and 0.9 kb RNAs are transcribed off the opposite strand. The 2.3 kb transcript is expressed in neural cultures as well as in vivo. # Nrg: Neuroglian location: 1-23.6. synonym: l(1)7Fa. references: Bieber, Snow, Hortsch, Patel, Jacobs, Traquina, Schilling, and Goodman, 1989, Cell 59: 447-60. Hortsch, Bieber, Patel, and Goodman, 1990, Neuron. 4: 697- 709. phenotype: Encodes a protein that is likely to play a role in neural and glial cell adhesion in the developing Drosophila embryo. Widely expressed in the embryo, particularly on the surfaces of a large subset of neurons and glia that interact with and adhere to one another along the dorsal surface of the developing CNS and within the peripheral nerve roots; the pro- tein can be detected along neuronal axons, but not cell bodies. Three polypeptides of 155, 167, and 180 kd are detected on Western blots; deglycosylation experiments reduce these to a single 155 kd band; removal of N-linked high- mannose oligosaccharides causes a shift to about 162 kd. It is also expressed in a number of non-neuronal tissues such as trachea, hindgut, salivary gland and muscle. Recessive alleles are embryonic lethals and show little or no evidence of Neuroglian expression; the overall structure of the CNS and PNS, and in particular the peripheral nerve roots and CNS axon pathways develop in a relatively normal way in lethal embryos. alleles: Neuroglian has been identified with a previously iso- lated lethal mutation of which ten alleles have been described. allele origin discoverer synonym ref ( comments ________________________________________________________________________________ Nrgl1 X ray Lefevre l(1)HC280 3 T(1;3)4A;7E;80-81? Nrgl2 X ray Lefevre l(1)HC293 3 In(1)6D-E1;7F3-4 Nrgl3 X ray Lefevre l(1)HF336 3 Nrgl4 X ray Lefevre l(1)RA35 1, 3 amorphic allele; In(1)6E;7F1 Nrgl5 EMS Lefevre l(1)EC255 4 Nrgl6 EMS Lefevre l(1)EF435 4 Nrgl7 EMS Lefevre l(1)VA142 1, 4 hypomorphic allele Nrgl8 EMS Lefevre l(1)VA321 4 Nrgl9 spont Schalet l(1)17-145 Nrgl10 EMS Digan l(1)B4 2 ( 1 = Bieber, Snow, Hortsch, Patel, Jacobs, Traquina, Schil- ling and Goodman, 1989, Cell 59: 447-60; 2 = King, Mohler, Riley, Storto, and Nicolazzo, 1986, Dev. Genet. 7: 1-20; 3 = Lefevre, l981, Genetics 99: 461-80; 4 = Lefevre and Watkins, 1986, Genetics 113: 869-95. cytology: Placed in 7F by in situ hybridization; by deficiency analysis placed in the region common to Df(1)KA14 = Df(1)7F1- 2;8C5 and Df(1)RA2 = Df(1)7D10;8A4-5. molecular biology: A Neuroglian-specific antibody was used to screen an embryonic cDNA expression library; cDNA's corresponding to a 5.1 kb transcript were recovered and local- ized to 7F on polytene chromosomes. Encodes two different proteins by tissue-specific alternative splicing, which differ in their cytoplasmic domains; the longer form is restricted to the surface of neurons in the CNS and some support cells in the PNS. The shorter form is more widely expressed in other cells and tissues. Northern blots probed with sequences specific to each of the polypeptides reveal transcripts of 5.5 kb for the short form and 5.7 and 7.6 kb for the long form. Sequence analysis reveals that Neuroglian is an integral mem- brane glycoprotein that is a member of the immunoglobulin superfamily. The extracellular portion of the protein con- sists of six immunoglobulin C2-type domains followed by five fibronectin type III domains. It is closely related to ver- tebrate neural adhesion molecules, most extensively to mouse L1. # nrs: narrow scoop location: 1-54.2. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1959, DIS 33: 88. phenotype: Wings narrow and slightly shorter than normal; fre- quently scooped. Slightly thinner bristles. Eyes large and dull red. Eye and body colors darken with age. Viability and fertility good in male; fertility low in female. RK2. # Nrt: Neurotactin (J.C. Hall) location: 3-{45}. origin: Molecular cloning, starting with monoclonal-antibody screening of expression library. references: de la Escalera, Bockamp, Moya, Piovant, and Jimenez, 1990, EMBO J. 9: 3593-3601. Barthalay, Hipeau-Jacquotte, de la Escalera, Jimenez, and Piovant, 1990, EMBO J. 9: 3603-09. Hortsch, Patel, Bieber, Traquina, and Goodman, 1990, Develop- ment 110: 1327-40. phenotype: Three monoclonal antibodies selected because of binding to presumptive imaginal neurons within the larval cen- tral nervous system (CNS) (de la Escalera et al., 1990) and an additional one found by virtue of binding to neuronal surfaces in embryos (Hortsch et al., 1990) detected the same ca. 135 kd protein on Western blots of homogenates from embryos, late larva, and pupae. The membrane-bound material is called neu- rotacin (NRT) because of its expression at points of interneu- ronal cell contact. Antibody staining (de la Escalera et al., 1990, Hortsch et al., 1990) shows concentration of the protein in dorsal and ventral portions of embryonic blastoderm (where staining appears cell surface-limited), all over gastrulating embryos (although Hortsch et al., 1990, imply a somewhat more restricted expression pattern), in the "proliferating" CNS (including neuroblasts and their progeny) of stage 10-11 embryos, and in regions of contact between neuroblasts. In visceral mesoderm (stage 13), non-neuronal expression dimin- ishes, although it is seen on fat body cells and the "dorsal vessel"; intense staining continues in embryonic CNS (but is relatively weak in axons of motor neurons); PNS expression is evident as well (seemingly restricted to sensory cells that send out multiple dendritic projections, and, in fact, PNS cell-body signals are weaker than on dendrites); cell-surface expression apparent in the various expressing tissues during mid-embryogenesis; in early L1, NRT signals decay but reappear in CNS (in optic formation centers and in neuron clusters and associated axons in ventral cord); the protein's expression persists in imaginal neurons through mid-pupal stage, wanes as such cells complete maturation, and is undetectable in adults. L3 imaginal discs are NRT positive (e.g. on developing chordo- tonal neurons of leg discs and in developing photoreceptor cells plus their axons, posterior to the morphogenetic fur- row). Cell culture studies, including electron-microscope observations (Barthalay et al., 1990), suggest further that NRT is a "contact molecule" between neurons or epithelial cells; there is uniform expression along intercellular contact areas; non-adhesive Schneider-2 cells, transfected with Nrt cDNA, do not become self adhesive, but these cells bind to a subpopulation of embryonic cells. cytology: Placed in 73C1-2 by in situ hybridization (de la Escalera et al., 1990; Hortsch et al., 1990). Embryos defi- cient for this region do not stain with anti-NRT monoclonal antibodies (de la Escalera et al., 1990; Hortsch et al., 1990). molecular biology: cDNAs cloned from expression libraries (de la Escalera et al., 1990; Hortsch et al., 1990). Such clones, when used in Northern blots, detected three or more tran- scripts, whose expression patterns are different during the course of embryogenesis (Hortsch et al., 1990), and which exhibit a later "peak" in early pupae (de la Escalera et al., 1990); the larger RNA species appear to be so because of more 3 untranslated nucleotides (de la Escalera et al., 1990). In situ hybridizations (Hortsch et al., 1990) revealed temporal/spatial expression patterns similar to those seen immunohistochemically. Sequencing of a complete cDNA (de la Escalera et al., 1990; Hortsch et al., 1990) predicts an 846- amino-acid polypeptide [which would, as a core protein, be ca. 93 kd, though actual measurements of its size indicate 120 kd (Barthalay et al., 1990)]. There is one predicted transmem- brane region, and details of which monoclonal antibodies can stain simple whole-mounted embryos vs. permeabilized ones (de la Escalera et al., 1990), as well as biochemical analyses (epitope mapping), using antibodies raised against Nrt-fusion protein constructs (Hortsch et al., 1990), are consistent with the protein's being inserted into membranes, with the N- terminus cytoplasmic and the C-terminus extracellular. Data- base comparisons (de la Escalera et al., 1990; Hortsch et al., 1990) indicate similarity of portion of NRT's extracellular domain to cholinesterases, including product of Drosophila Ace locus; this NRT region is also similar to Drosophila glutactin and to rat thyroglobulin. NRT apparently lacks the "landmark" serine residue that would indicate it to have actual esterase activity (Hortsch et al., 1990). other information: Embryos homozygous for either of the two Nrt- deletions used by de al Escalera et al. (1990) [Df(3L)st-k10 = Df(3L)73A3-4;73D1-2 and Df(3L)73A11-B1;73D1-2] do not exhibit any "extra" gross abnormalities of the CNS. Deletion of regions just distal to Nrt [i.e. Df(3L)st100.62 = Df(3L)72F3-7;73B3 or Df(3L)st-e5 = Df(3L)?;73A9-10] leads to defects in axonal patternings (because of the absence of the abl and dab genes in 73B, cf. Gertler, Bennet, Clark, and Hoffman, 1989, Cell 58: 103-113), but the further removal of Nrt+ does not make this phenotype worse (de la Escalera et al., 1990). # Ns: see AntpNs # Ntf: Neurogenic element binding transcription factor location: 2-{83}. synonym: Elf-1: Element I binding activity. references: Bray, Burke, Brown and Hirsh, 1989, Genes Dev. 3: 1130-45. Dynlacht, Attardi, Admon, Freeman, and Tjian, 1989, Genes Dev. 3: 1677-88. phenotype: Gene encodes at least three isoforms of a protein that binds to upstream sequences of Ddc, en, ftz, and Ubx. The proteins share epitopes as recognized by two monoclonal antibodies. Expression first detected in 4-to-8 hour embryos, peaking from 8 to 12 hours and declining from 12 to 16 hours; NTF protein detected in nuclei of ectodermal derivatives; seen in all epidermal cells and changing subsets of neurons in the developing central nervous system. cytology: Placed in 54F1-2 by in situ hybridization. molecular biology: Protein purified by DNA-affinity chromatog- raphy using promoter sequences derived from Ddc, Ubx, or both. Three prominent polypeptides recovered (140, 120, and 83 kd); the purified proteins shown to bind to specific neurogenic control regions upstream from Ddc, ftz, and Ubx by DNA foot- printing and to stimulate transcription of these genes in vitro. Northern blots of embryonic RNA detect mRNA's of 7.4 and 10.6 kb. cDNA clones isolated by screening an expression library either with monoclonal antibody (Bray et al.) or with synthetic oligonucleotides (Dynlacht et al.). Three different cDNA's identified by Bray et al. Presumed to arise as a result of alternative splicing; one of these encodes a polypeptide of 1063 residues and approximately 116 kd. The conceptual amino acid sequence contains several polyglutamine stretches (OPA repeats) in the N-terminal half; it shows no evidence of homeobox or zinc-finger domains; there is weak homology, however, to the helix-loop-helix motifs of myoD and myogenin. #*Nu: Nude location: 2- or 3- (rearrangement). origin: X ray induced. discoverer: Sutton, 41a27. phenotype: Many bristles missing from head and thorax; postscu- tellars, notopleurals, verticals, and postverticals usually present. Homozygous lethal. RK2A. cytology: Associated with T(2;3)Nu = T(2;3)24;36-37;39-40;73- 74;75-76;77-78;81-82;85-86;89-90. # nub: nubbin location: 2-47.0. origin: Spontaneous. discoverer: Mickey, 48e10. references: 1949, DIS 23: 61. phenotype: Wings very small, opaque, curved spoonlike up or down; inflated at eclosion. Wing margins interrupted. Only one vein (L2 or L3) present. Halteres somewhat reduced. Via- bility excellent. RK1. cytology: Placed in 33F1-5. Not included in Df(2L)64j = Df(2L)34E5-F1;35C3-D1 (E. H. Grell). # nub2 origin: Probably X ray induced. discoverer: R. F. Grell, 56f1. references: 1956, DIS 30: 71. phenotype: Wings small and spoonlike but less extreme than nub. Patches of dried blood on wings. Veins L1 to L4 almost indis- cernible; L5 and alula frequently absent. Viability and fer- tility excellent. RK1. # nub62d origin: X ray induced. discoverer: Seiger, 62d. references: 1963, DIS 37: 53. Abbadessa and Burdick, 1963, DIS 37: 54. phenotype: Wings very small and spoonlike. RK1. # Nuc: Nuclease location: 3-38.2. references: Angelosanto and Boyd, 1976, Genetics 83: s2. phenotype: Structural gene for a desoxyribonuclease active at alkaline pH and correlated with the appearance of a puff in the salivary glands of third instar larvae. alleles: Two electrophoretic variants, Nuc1, and Nuc2, were found in laboratory stocks. cytology: Located in 68D-70A (Y-autosome translocations); puff- ing activity correlated positively with level of DNase activity in salivaries during last 24 hours of larval develop- ment. # nuc1: nucleoside auxotroph 1 location: 2-104. synonym: pyr2. references: Naguib and Nash, 1976, Mol. Gen. Genet. 147: 13- 21. phenotype: Nucleoside auxotroph; responds to dietary ribonu- cleosides. alleles: nuc11 (= pyr2-1); nuc12 (= pyr2-2). # Nuclease: see Nuc # nucleoside auxotroph 1: see nuc1 # Nude: see Nu # nudel: see ndl # numb: numb location: 2- {35}. references: Uemura, Shepherd, Ackerman, Jan, and Jan, 1989, Cell 58: 349-60. phenotype: The numb gene must be able to function in the Droso- phila embryo in order for the peripheral sensory neurons to acquire their correct identity. In the mutants, the precur- sors of neurons and glial cells in the external sensory (es) organs are, for the most part, transformed into nonneural sup- port cells; some of the es organs are duplicated. Transforma- tion of neuron precursors into nonneural cells also occurs in the chordotonal (ch) organs. Precursors of the multiple den- drite (md) neurons undergo similar changes. Muscle develop- ment is abnormal in numb mutant alleles; some muscles are fewer in number than in wild type and show pattern changes (Uemura et al.). alleles: Three mutant alleles have been identified, all apparently nulls since the neuronal phenotype of homozygotes is indistinguishable from that of hemizygotes. allele origin molecular biology ___________________________________________ numb1 HD P-element at 30B numb2 DEB numb3 DEB cytology: Located in 30A-C since numb1 is not complemented by a deletion in this region; excision of the P-element at 30B leads to a reversion of the mutant phenotype. molecular biology: 50 kb of genomic DNA flanking the insertion of a transposon, pUChsneo, cloned by the plasmid rescue method and a chromosome walk. Two transcripts of 3.1 and 3.5 kb result from alternative splicing of numb, the first mRNA being maternal in origin and the second zygotic. cDNA clones from the 5' end of the maternal transcript and from the entire zygotic transcript have been sequenced. The zygotic DNA shows a single open reading frame. From these cDNA sequences, a 56 kd maternal protein and 61 kd zygotic protein have been predicted. Both maternal and zygotic products have putative zinc finger domains and are very basic. A 60 kd protein can be detected by anti-numb antibodies in very young (0-1 hr and 3-5 hr) numb+ embryos; a larger protein (65 kd) can be detected by this antibody in older numb+ embryos (11-13 hr and 15-17 hr). Homozygous numb1 embryos fail to show either pro- tein. Uemura et al. suggest that these proteins may be involved in nucleic acid binding. # Nup: see Mhc16 # nurse cell number: see ncn #*nw: narrow location: 2-79.6 (Rizki et al., 1980; see nwD); 2-79.3 (Doane and Clark, 1984; see nw2). phenotype: Wings long, narrow, and somewhat pointed. Low via- bility and fertility in both sexes. At 25C, may overlap wild type; at 19, nearly all flies approach wild type but have longer wings. RK2. alleles: allele origin discoverer ref ( _______________________________________________ *nw spont Bridges, 16b7 4 nw2 | spont Payne, 16l5 2, 4, 5 nwB X ray (?) P.H. Lewis, 1947 1 nwD X ray E.H. Grell, 59f 3, 6 ( 1 = Craymer, 1980, DIS 55: 197-200; 2 = Doane and Clark, 1984, DIS 60: 234; 3 = Grell, 1962, DIS 36: 37; 4 = Mor- gan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 227; 5 = Payne, 1924, Genetics 9: 327-42; 6 = Rizki, Rizki, and Grell, 1980, Wilhelm Roux's Arch. Dev. Biol. 188: 91-99. | Synonym: lance. cytology: Placed in 54A-55A. nw2: narrow 2 From Payne, 1924, Genetics 9: 327-42. # nw2 phenotype: Wings like nw, long, narrow, and somewhat pointed. Classification easier in females. Slight notching or tufting of marginal hairs on tip of wings. Both sexes nearly sterile. Ovaries tumorous at eclosion [King, Burnett, and Staley, 1957, Growth 21: 239-61 (fig.); King, 1964, Roy. Entomol. Soc. (London) Symp. Insect Reproduction, pp. 13-25]. Oogonia prol- iferate asynchronously within ovariole; follicle development inhibited [Beatty, 1949, Proc. R. Soc. Edinburgh, B 63: 249- 70 (fig.)]. RK2. # nwB: narrow-Blade phenotype: Wings of nwB/+ long and narrow; variable but does not overlap wild type. Female fertility reduced. Homozygote and nwB/nw2 heterozygote lethal. RK2. # nwD: narrow-Dominant phenotype: Wings of heterozygote longer and narrower than nor- mal. Expression variable and sometimes approaches wild type. Viability of nwD/+ low. Homozygous lethal, as is nwD/nw2. RK2. # NX: Notch Xasta location: 3- (between st and Dfd; 44.0-47.5). origin: X ray induced. discoverer: Ohnishi, 49l16. references: 1950, DIS 24: 61. 1951, DIS 25: 79. Schalet, 1960, DIS 34: 55. phenotype: Resembles Notch but more extreme. Homozygote resem- bles apXa. Viability of heterozygote fair; homozygote sem- ilethal. Enhanced by D1 and suppressed by H. Combination of NX and apXa produces small wings, like vg, and lower viabil- ity. RK2 as heterozygote. ny: notchy From Gruneberg, 1929, Biol. Zentralbl. 49: 680-94. # ny: notchy location: 1-32. origin: X ray induced. discoverer: Gruneberg, 28j29. references: 1929, Biol. Zentralbl. 49: 680-94 (fig.). 1934, DIS 2: 8. phenotype: Wing tips slightly nicked. Expression variable; overlaps wild type in some females and most males. Viability about 70% wild type. RK3. cytology: Placed in 10B5-18 based on its inclusion in Df(1)N71 = Df(1)10B5;10D4 but not Df(1)DA662 = Df(1)10B8;10D2.