# mi: minus location: 2-104.7. discoverer: Biddle, 28l. references: Bridges, 1937, Cytologia (Tokyo), Fujii Jub., Vol. 2: 745-55. phenotype: Bristles almost as small as hairs; hairs reduced in number and size. Body size small. Eclosion delayed. Viabil- ity low and erratic. Female entirely sterile; male fertile. RK2. cytology: Locus is in 59D6-E4 of salivary gland chromosome (Schultz) on the basis of its being between the right break- points of In(2R)bwVDe1 = In(2R)41B2-C1;59E2-4 and In(2R)bwVDe2 = In(2R)41A-B;59D6-E1. #*mib: miniature bristles location: 1-8.7. origin: X-ray induced. discoverer: Fahmy, 1956. references: 1959, DIS 33: 88. phenotype: Short, thin bristles. Body slightly darker than normal, particularly thorax and posterior border of tergites. Wings occasionally upheld and inner margins frequently incised. Male viable and sterile. RK3. # micro-oculus: see mo # Microcephalus: see Mc # microchaete: see mc # microptera: see mp # Microtubule associated protein-205 kd:: see Map205 # microwing: see mwg # mid: midline location: 2-16. references: Nusslein-Volhard, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. phenotype: Homozygous embryonic lethal; denticle bands defec- tive in ventral midline. alleles: allele origin synonym ref ( __________________________________________ mid1 EMS midIK 2 mid2 EMS midIIS 2 mid3 EMS midIIID 2 mid4 | EMS l(2)gdh-111 1 mid5 | EMS l(2)gdh-114 1 mid6 | EMS l(2)gdh-131 1 mid7 | EMS l(2)gdh-111902 1 mid8 X ray midh2 3 ( 1 = Kotarski, Pickert, and MacIntyre, 1983, Genetics 105: 371-86. 2 = Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82; 3 = Szi- donya and Reuter, 1989, Genet. Res 51: 197-208. | Allelism inferred from deficiency mapping, not complementa- tion mapping. cytology: Placed in 25D7-F3 based on its inclusion within the region of overlap between Df(2L)cl1 = Df(2L)25D7-E1;25E6-F3 and Df(2L)GpdhA = Df(2L)25D7-E1;26A8-9. # midget: see mgt # midgoid: see mdg # midgut amylase pattern: see map # midline: see mid # min: mini location: 2-90. references: Procunier and Tartof, 1975, Genetics 81: 515-23. Procunier and Dunn, 1978, Cell 15: 1087-93. phenotype: The locus encoding the genes for 5S RNA. Heterozy- gous deficiency for the region is normal in phenotype; how- ever, min mutants, although normal in phenotype when heterozy- gous or homozygous, express a phenotype indistinguishable from bb when hemizygous. Ordinarily, the haploid complement car- ries approximately 165 copies of 5S genes; in min-bearing chromosomes this number is reduced to approximately 80; according to Procunier and Tartof, this number is increased by compensation to 265 in hemizygotes for the normal allele. Eclosion of min hemizygotes delayed about two days; also show reduced viability which is more severe at 29 than at 25. alleles: min0 spontaneous (Procunier and Tartof). min1 and min2, induced by triethylenemelamine (Procunier and Dunn). cytology: Placed in 56E-F by in situ hybridization in one of the earliest uses of that technique (Wimber and Steffensen, 1970, Science 170: 639-41); Szabo notes two bands of label, at 56F1-2 and 56F6-7 (1974, J. Cell Biol. 63: 341). Also located between the breakpoints of T(Y;2)L139 = T(Y;2)56E and T(Y;2)L141 = T(Y;2)56F; T(Y;2)L62 = T(Y;2)56E-F is broken within the tandem array of sequences with approximately 80 copies on either side. molecular biology: Region contains a tandem array of 380-base- pair repeats, each comprising 120 base pairs of gene and 170 base pairs of spacer sequence; the spacer is 33% GC and the gene 57% GC (Hershey, Condad, Sodja, Yen, Cohen, Davidson, Ilgen, and Carbon, 1977, Cell 11: 585-98). Segments of tan- dem array cloned and restriction mapped (Artavanis-Tsakonas, Schedl, Tschudi, Pirrotta, Steward, and Gehring, 1977, Cell 12: 1057-67; Tschudi and Pirrotta, 1980, Nucleic Acid Res. 8: 441-51); variation in restriction maps attributable to variable numbers (4-7) of a tandemly repeated heptamer in the spacer region plus occasional other restriction site polymor- phisms. In addition some strains appear to have a continuous array of repeats, whereas others appear to contain a segment with a number of restriction sites that separates the array into two subsegments of approximately equal size (Junakoric, 1980, Nucleic Acid Res. 8: 3611-22). Nucleotide sequence and proposed secondary structure of 5S RNA provided by Behnamon and Jordan (1976, FEBS Lett. 62: 146-46) and Thompson, Weg- nez, and Hearst (1981, J. Mol. Biol. 147: 417-36). Following heat shock, 5S RNA synthesis is reduced and an abnormal pro- duct with 55 extra nucleotides appended to the 3' end appears instead; may be a precursor that does not get processed (Rubin and Hogness, 1975, Cell 6: 207-13). Linker-scanning mutation studies reveal five regions important for normal transcrip- tion; one between -39 and -26, presumably involved in polym- erase binding, and four internal sequences at 3-18, 37-44, 48-61, and 79-98 (Sharp and Garcia, 1988, Mol. Cell. Biol. 8: 1266-74). # min: see mnb # miniature: see m # miniature blistered: see mbs # miniature bristles: see mib # minibrain: see mnb # minus: see mi # minus bar: see mb # Minute-producer: see T(1;4)M-pro # minute chaetae: see mch # Minute ( ): see M( ) # minutelike: see ml # Mio: see DrMio # Mir: Mirabile (M. Muskavitch) location: 3- (rearrangement). origin: X ray induced. discoverer: Muskavitch. phenotype: Mirror-image duplication of tergite structure. Microchaetae are eliminated from the anterior portion of the tergite and replaced by a duplication consisting of an anteri- orly oriented row of macrochaetae and the darkly pigmented cuticle normally found in the posterior portion of the ter- gite. Fat body and oenocytes underneath the tergite are also duplicated with mirror-image symmetry (Madhavan and Madhavan). alleles: Original allele dominant and revertable by X ray mutagenesis suggesting that this allele constitutes a gain- of-function mutation. Animals heterozygous for any one of seven independent X- ray-induced revertant alleles, designated Mirrv1 through Mirrv7, and a wild-type allele exhibit wild- type tergite structure. cytology: Associated with T(1;3)Mir with the new order 1 - 20F|81F - 64C|94A - 81F|94A-100F; 20F|64C - 61A (Gelbart). Analysis of segregation behavior of the phenotype in relation to the components of an X ray-induced detachment of T(1;3)Mir indicates that the mutation maps to the third chromosome. other information: Not allelic to disembodied, hedgehog, pointed, rhomboid or shrew as assessed on the basis of lethal complementation tests employing representative alleles of these five loci. #*mis: misproportioned location: 1-1.3. origin: Induced by 1:4-dimethanesulfonoxybut-2-yne (CB. 2058). discoverer: Fahmy, 1951. references: 1938, DIS 32: 71. phenotype: Abdomen deformed: in male, large and broad; in female, tergites abnormal and hairs disarranged. Wings shor- tened in both sexes. Bristles thin. Body color rather pale. Eclosion slightly delayed. Male viability and fertility nor- mal; female viability 50% wild type. RK3. other information: One allele each induced by CB. 1540 and CB. 3034. # misformed: see msf # misheld wings: see mwi # misp: misstep (T. Schupbach) location: 2-59. origin: Induced by ethyl methanesulfonate. synonym: mispRQ. references: Schupbach and Wieschaus. phenotype: Maternal-effect lethal, female sterile. Embryos from homozygous mothers do not hatch. In cuticle preparations they show irregular segmentation and variable segment fusions. # misproportioned: see mis # missing: see msg # misstep: see misp # mit: mitotic loss inducer location: 1-57 (between f and Bx). origin: Spontaneous. references: Gelbart, 1974, Genetics 76: 51-63. phenotype: Mosaics produced by loss of maternal or paternal chromosomes in F1 of homozygous mit females; progenies of mit males normal. Chromosome loss (X or 4) usually occurs at third or fourth mitotic division of the zygote, producing mosaic patches of intermediate size. Rod-X chromosomes lost as frequently as rings, but neither XY, nor Y chromosomes eliminated frequently by mit. Relative frequencies of observed loss of maternal and paternal X chromosomes depend on the markers carried rather than the parental origin of the X's. Double mosaic gynandromorphs indicative of independent loss of homologous chromosomes in different lineages. No increase in meiotic nondisjunction or chromosome loss observed. mit stocks show good viability and fertility, though modifiers reducing frequency of mosaics tend to accumu- late. mit-induced gynandromorphs useful in constructing mor- phogenetic fate maps. cytology: Placed in 16A6-F8 since mit is proximal to f (in 15F) and not included in Df(1)B263-20 = Df(1)15F9-16A1;16A6-7 or in Dp(1;1)Bxr = Dp(1;1)17A;17E-F. # mit(1): mitotic (1) A group of fourteen loci identified as temperature-sensitive lethal mutations (Baker) that exhibit, at semirestrictive tem- peratures, elevated frequencies of clones of homozygous mwh cells in the wings of surviving mit(1);mwh/+ males and of y clones and y//mwh twin spots in the abdomens of y mit(1);Dp(1;3)scJ4, y+ mwh/+ males. The presence of large clones is consistant with origin via mitotic exchange, mitotic nondisjunction of both homologues, or mutation; twin spots are not expected to result from somatic mutation; only mitotic nondisjunction produces y Sb+ clones in Dp(1;3)scJ4, y+ Sb/+. Preponderance of small clones suggests origin via chromosome breakage. Mitotic chromosome morphology examined in larval ganglion cells of mit(1) males. inter se allelism tests have not been performed. genetic locus location phenotype ________________________________________________________________________ mit(1)2 1-15.3 small clones; few twin spots; 1.16% chromatid breaks mit(1)3 1-46.1 small clones; twin spots; 1.63% chromatid and isochromatid breaks mit(1)4 1-28.0 large clones; twin spots; chromosomes undercondensed mit(1)5 large clones; twin spots; 2.46% chromatid and isochromatid breaks mit(1)6 1-34.9 small clones; few twin spots; chromosomes normal mit(1)7 1-15.7 large clones; few twin spots; 1.47% chromatid, isochromatid breaks, and exchanges mit(1)8 large clones; few twin spots; 1.72% chromatid and isochromatid breaks mit(1)9 small clones; few twin spots; 1.13% chromatid, isochromatid breaks, and exchanges mit(1)10 1-1.4 large clones; few twin spots; chromosomes normal mit(1)11 1-21.4 small clones; few twin spots; 0.9% chromatid and isochromatid breaks mit(1)12 large clones; few twin spots; 0.99% chromatid and isochromatid breaks mit(1)13 1-36.0 large clones; y Sb+ clones; 1.68% chromatid and isochromatid breaks mit(1)14 1-49.0 small clones; y Sb+ clones; 7.20% chromatid and isochromatid breaks mit(1)15 1-1.2 large clones; y Sb+ clones; mitotic nondisjunction # mit(1)15 synonym: abe; l(1)zw10. phenotype: Semilethal as males or homozygous females; surviving flies have reduced roughened eyes, bristles on the head and thorax sometimes missing, abnormal wings with thin texture and thickened veins; both sexes sterile. Up to 100 fold increase in the incidence of mwh clones per wing in mit15;mwh/+ flies raised at sub-restrictive temperature. Half of all metaphases in larval ganglion cells are hyperploid for one or more chro- mosomes; hyperploidy for nearly all combinations of sex chro- mosomes and autosomes are observed. Chromosome breakage seen in less than 2% of cells. Cytological observations in mit(1)1515, mit(1)153 and mit(1)154 at either restrictive or permissive temperature. alleles: allele origin ( discoverer synonym ref | comments ____________________________________________________________________ mit(1)151 NNG Reichert l(1)zw101c 1 mit(1)152 EMS Kaufman l(1)zw10g2 1 mit(1)153 X ray + EI Alexander l(1)zw10h10 1, 6 temperature sensitive mit(1)154 EI Alexander l(1)zw10i20 1, 6 temperature sensitive mit(1)155 X ray + EI Alexander l(1)zw10l21 1 mit(1)156 EMS l(1)zw10e36 4 mit(1)157 EMS l(1)zw10e87 4 mit(1)158 EMS l(1)zw10e90 4 mit(1)159 TEM l(1)zw1024 4 mit(1)1510 TEM l(1)zw10116 4 mit(1)1511 MMS l(1)zw10m16 5 mit(1)1512 MMS l(1)zw10m29 5 mit(1)1513 MMS l(1)zw10m87 5 mit(1)1514 EMS Lefevre l(1)VE630 3 mit(1)1515 EMS Baker l(1)zw10ts 6 temperature sensitive mit(1)1516 spont Schalet l(1)6-99 l(1)zw10S1 mit(1)1517 mei9 / Schalet l(1)zw10S2M mit(1)1518 HMS l(1)HM468 2 ( EI = ethylenimine, HMS = hycanthon methanesulfonate, NNG = N'-nitro-N-nitrosoguanidine. | 1 = Judd, Shen, and Kaufman, l972, Genetics 71: 139-56; 2 = Kramers, Schalet, Paradi, and Huiser-Hoogtyeyling, 1983, Mutation Res. 107: 187-201; 3 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 4 = Lim and Snyder, 1974, Genet. Res. 24: 1-10; 5 = Liu and Lim, 1975, Genetics 79: 601-11; 6 = Smith, Baker, and Gatti, 1985, Genetics 110: 647-70. / Spontaneous in the paternal X chromosome of a cross between wild-type males and mei9 females, such that the F1 females were mit(1)15/mei9. cytology: Located at 3A8 by Judd, Shen, and Kaufman; included in Dp(1;2)w+70h31 = Dp(1;2)3A6-8;3C2-3 but not in Df(1)64j4 = Df(1)3A8-9;3B1-2. # mitotic: see mit # mk: murky location: 1-0.8. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1950. references: 1958, DIS 32: 71-72. phenotype: Small fly with dull red eyes and extra body pigmen- tation; trident pattern especially marked. Delayed eclosion. Male fertile and viability 50% wild type; mk/+ daughters, but not mk sons of mk mothers survive (Mohler, 1977, Genetics 85: 259-72). RK3. alleles: allele origin discoverer synonym ref ( comments ________________________________________________________ mk1 CB1246 Fahmy, 1950 1 mk2 CB1414 Fahmy, 1950 1 mk3 CB1506 Fahmy, 1950 1 mk4 CB1540 Fahmy, 1950 1 mk5 CB3007 Fahmy, 1950 1 mk6 CB3025 Fahmy, 1950 1 mk7 CB3025 Fahmy, 1950 1 mk8 CB3034 Fahmy, 1950 1 mkMI EMS Mohler fs(1)M7 2, 3 temperature sensitive ( 1 = Fahmy, 1959, DIS 32: 71-72; 2 = Mohler, 1977, Genetics 85: 259-72; 3 = Mohler and Carroll, 1984, DIS 60: 236-41. #*ml: minutelike location: 3-46. discoverer: Mohr, 24c3. synonym: sb: short-bristle. references: 1924, Br. J. Exp. Biol. 2: 189-98 (fig.). phenotype: Bristles small, as in Minute. Late hatching and poorly fertile. RK3. alleles: *ml2 (Nichols-Skog, 36c); spontaneous; allelism inferred from phenotype and location on third chromosome. # Mlc1: Myosin light chain location: 3- {95}. references: Falkenthal, Parker, Mattox, and Davidson, 1984, Mol. Cell. Biol. 4: 956-65. Falkenthal, Parker, and Davidson, 1985, Proc. Nat. Acad. Sci. USA 82: 449-53. phenotype: Encodes the myosin alkali light chain (MLC-ALK), so called because it dissociates from MHC only at high pH. Expressed during periods of myogenesis: late embryo, larvae, late pupae, and adults; not expressed in early embryos or in early pupae during histolysis of larval muscle. cytology: Placed in 98B on basis of in situ hybridization. molecular biology: Genomic clones isolated by screening genomic library with cDNA from stages of active myogenesis. Sequence analysis of genomic and cDNA clones indicates the presence of six exons separated by introns varying in length from 59 to 986 nucleotides; five polyadenylation signals detected within and downstream from the sixth exon; postulated to account for the variation in transcript size. Differential splicing pro- duces one transcript with all six exons, which has a stop codon in exon 5 and one that lacks exon 5 and has the stop codon in exon 6; these generate polypeptides that differ in fourteen C-terminal amino acids; the former is found in both larvae and pupae, whereas the second is found only in pupae. Open reading frames imply a polypeptide of 155 amino acids; the inferred amino-acid sequence reveals a region of espe- cially high homology with one of the three Ca2+ binding domains of chicken MLC-ALK. # Mlc2 location: 3- {102}. synonym: Ifm(3)99Eb. references: Parker, Falkenthal, and Davidson, 1985, Mol. Cell. Biol. 5: 3058-68. Warmke, Krevz, and Falkenthal, 1989, Genetics 122: 139-51. phenotype: Encodes a myosin light chain homologous to chicken MLC2. Expression abundant in late embryo, first and third larval instars, late pupae and adults; no expression in early embryos or early pupae. Phosphorylation of the polypeptide determined to be necessary for filament assembly (Hayashi and Hotta, 1982, Dev. Growth Differ. 24: 417). alleles: One allele recovered as a dominant flightless mutant in combination with a closely linked recessive lethal, l(3)99Df1 by Merriam (Warmke et al.). Heterozygous deficiency for the locus also flightless. cytology: Placed in 99E1-3 by in situ hybridization. molecular biology: Genomic clone independently isolated by screening genomic libraries with cDNA from stages of active myogenesis by Parker et al. and by Toffenetti, Mischke, and Pardue (1987, J. Cell Biol. 104: 19-28) and by screening with blastoderm cDNA by Roark, Mahony, Graham, and Lengyel (1985, Dev. Biol. 109: 476-88). Sequence determination from genomic and overlapping cDNA clones reveals alternative transcription start sites 67 and 55 nucleotides upstream from the first codon as well as two termination sites 109 and 259 nucleotides 3' to the stop codon; also there is no TATA box. Two introns, one of 699 nucleotides between amino-acid residues 1 and 2 and the other of 169 nucleotides between residues 82 and 83; these intron positions are conserved in rat MLC2. Northern blots reveal two abundant mRNA's of 1.1 and 1.4 kb plus a minor transcript of 2.7 kb; in vitro translation of hybrid-selected mRNA yields polypeptides of 17 and 26 kilodaltons; amino-acid sequence inferred from the nucleotide sequence suggests high Ca2+ binding affinity; also the serine that is phosphorylated in mammalian MLC2 is conserved in the Drosophila polypeptide, but is not known to be the site of phosphorylation. As in several vertebrate muscle proteins, Drosophila MLC2 has an acylated amino terminus (Toffenetti et al.). other information: A series of alleles recovered on the basis of semilethality in combination with a deficiency for 99D3-E3 and behaving as dominant flightless mutations turn out to map to the same complementation group at 3-54.2 in region 88; the locus is designated l(3)nc99Eb by Warmke et al. # Mlc-c: Myosin alkali light chain cytoplasmic (D.P. Kiehart) location: 1-{14}. references: Chang, Edwards, and Kiehart, in preparation. phenotype: The structural gene for the alkali light chain of non-muscle myosin (whose other subunits are encoded by Mhc-c and sqh). cytology: Localized to 5A6 by in situ hybridization of genomic clones. molecular biology: Cloned using oligonucleotides corresponding to partial peptide sequence of purified non-muscle myosin light chain. A cDNA detects a 1.3 kb transcript at all developmental stages and encodes a 16 kd protein with 60-70% identity to vertebrate smooth-muscle-myosin alkali light chain. # mle: maleless location: 2-55.2 (just distal to ap based on deficiency map- ping). references: Fukunaga, Tanaka, and Oishi, 1975, Genetics: 81: 135-41. Tanaka, Fukunaga, and Oishi, 1978, Genetics 84: 257-66. phenotype: Homozygous males die, but homozygous females sur- vive. Males produced by homozygous females die during the third larval instar, whereas those produced by heterozygous females are late pupal lethals. Females transformed into phenotypic males (tra) or intersexes (dsx) unaffected by mle, i.e. mle acts only upon single-X-bearing flies. No interac- tion with msl-1 or msl-2 (Belote, 1983, Genetics 96: 165-86). mle4 males surviving at 18 are sterile, small, and slow developing. Concluded to be defective in dosage compensation in males based on decreased levels of X-linked-enzyme activi- ties (G6PD, 6GPD, FUM, |-HAD) but not autosomally encoded enzymes (ADH, AO, GPDH, IDH) in homozygous mle4 male larvae and escaping adults, e.g. |-HAD. The incorporation of labeled uridine by the polytene X chromosome relative to that of 2R is lower than normal in mle4 males (Belote and Lucchesi, 1980, Nature 285: 573-75); steady-rate level of Sgs4 mRNA incom- pletely compensated in mle4 and mle4/mle6 male larvae (Breen and Lucchesi, 1986, Genetics 112: 483-91). Polytene X chro- mosome of mle males appears narrower and more densely stained than that of control males. Few homozygous mle gynandromorphs survive; XO patches small, with small bristles, and mostly confined to abdomen (Uenoyama, Uchida, Fukunaga, and Oishi, 1982, Genetics 102: 223-31). mle pole cell transplanted into wild-type hosts incapable of undergoing normal spermatogenesis (Bachiller and Sanchez, 1986, Dev. Biol. 118: 379-84). Homozygous (and to a lesser extent heterozygous) mle females that are heterozygous for SxlF1 (Uenoyama, Fukunaga, and Oishi, 1982, Genetics 102: 233-43; Skripsky and Lucchesi, 1982, Dev. Biol. 94: 153-64) or are the surviving progeny raised at 17 of homozygous da mothers (Cline, 1982, Genetics 100: 641-63) develop as intersexes. alleles: allele origin discoverer synonym ref ( comments _____________________________________________________________________ mle1 spont Oshima, 1971 4, 10, 11 male lethal when homozygous mle1a spont Watanabe, 1978 mle79K 11 independent isolate of mle1 ? mle1b spont Watanabe, 1979 mleK25 11 independent isolate of mle1 ? mle2 mleMAK | 5 male lethal when homozygous mle3 EMS mle13 11 male lethal when homozygous mle4 EMS Belote, 1977 mlets 1, 2, 3 male lethal 11 when homozygous; heat sensitive lethality; 18 survivors sterile, small and slow to develop mle5 spont mll, 7 mleRoma / mle6 EMS mle185 3, 10 mle7 / ray mlepml2 8 mle8 / ray mlepml8 8 mle9 / ray mle/ 38 9 male lethal when homozygous mle10 / ray mle/ 203 9 male lethal when homozygous mle11 / ray mle/ 22 9 male lethal when homozygous mle12 / ray mle/ 235 9 male lethal when homozygous mle13 / ray mle/ 28 9 male lethal when homozygous mle14 / ray mle/ 293 9 male lethal when homozygous mle15 EMS mleRK 6 male lethal when homozygous ( 1 = Belote and Lucchesi, 1980, Genetics 96: 165-86; 2 = Belote and Lucchesi, 1980, Nature 285: 573-75; 3 = Breen and Lucchesi, 1986, Genetics 112: 483-91; 4 = Fukunaga, Tanaka, and Oishi, 1975, Genetics 81: 135-41; 5 = Golubov- sky and Ivanov, 1972, DIS 49: 117; 6 = Kernan, unpublished; 7 = Loverre and Cicchetti, 1980, DIS 55: 88; 8 = Schupbach, unpublished; 9 = Scott and Lucchesi, unpublished; 10 = Tanaka, Fukunaga, and Oishi, 1978, Genetics 84: 257-66; 11 = Uenoyama, Uchida, Fukunaga, and Oishi, 1982, Genetics 102: 223-31. | Allelism confirmed by Ashburner. / Allelism inferred from map position at 2-55.2. cytology: Placed in 42A2-8 as it is uncovered by Df(2R)nap9 = Df(2R)42A (?) (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: mle alleles fail to complement the paralysis caused by nap alleles, indicating that nap and mle are allelic (Kernan and Ganetzky). # mle3 location: 3-25.8. references: Uchida, Uenoyama, and Oishi, 1981, Jpn. J. Genet. 56: 523-27. phenotype: Homozygous males exhibit delayed development; sur- vive as larvae for ten days. Ten-day-old male larvae have small undeveloped imaginal discs, which, however, when tran- splanted into wild type larvae are capable of undergoing nearly complete (wing, leg) or partial (eye-antenna) differen- tiation; few homozygous mle gynandromorphs survive; XO patches small, with small bristles, and mostly confined to abdomen [Uenoyama, Uchida, Fukunaga, and Oishi, 1982, Genetics 102: 223-31(fig.)]. No interaction with mle. Females transformed into phenotypic males (tra, tra2) or intersexes (dsx) unaffected by mle3, i.e. mle3 acts only upon single-X- bearing flies. Females heterozygous for SxlF1 and homozygous (and to a lesser extent heterozygous) for mle3 show signs of intersexual development; effect less severe when mothers homozygous for mle3 [Uenoyama, Fukunaga, and Oishi, 1982, Genetics 102: 233-43 (fig.)]. Staining of polytene X chro- mosome of mle3 males similar to that of mle males (Lucchesi, Skripsky, and Tax, 1982, Genetics 100: s42; Okuno, Satou, and Oishi, 1984, Jpn. J. Genet. 59: 237-47). alleles: allele origin synonym ref ( _________________________________ mle31 spont mle(3)132 3, 4 mle32 EMS msl-3 2 mle33 | EMS msl-3b 1, 2 ( 1 = Bachiller and Sanchez, 1989, Roux's Arch. Dev. Biol. 198: 34-38; 2 = Lucchesi, Skripsky, and Tax, 1982, Genetics 100: s42; 3 = Okuno, Satou, and Oishi, 1984, Jpn. J. Genet. 59: 237-47; 4 = Uchida, Uenoyama, and Oishi, 1981, Jpn. J. Genet. 56: 523-27. | Cell autonomous; clones homozygous for mutant are deleteri- ous (Bachiller and Sanchez, 1989). # mll: see mle # mmy: mummy location: 2-16. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. (fig.). phenotype: Embryonic lethal; mouth parts and denticles poorly differentiated. alleles: Five including one temperature-sensitive and one weak allele. mmy1 and mmy2 (isolated as IK and IL) retained. # mMdh: see Mdh2 # mn: manikin location: 1-38.4. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine. discoverer: Fahmy, 1954. synonym: dwxmn. references: 1959, DIS 33: 88. phenotype: Fly small with narrow abdomen. Reduction in size may be bilaterally asymmetrical and may affect abdomen and thorax independently. Male viability reduced; flies rarely survive more than 48 hr. Sterile, probably owing to reduced vigor. RK3. alleles: One X-ray-induced allele. # mnb: minibrain (J.C. Hall) location: 1-58.2 (apparently part of "Sh complex"). origin: Induced by ethyl methanesulfonate or from hybrid dys- genesis. discoverer: M. Heisenberg (from a mutagenized X provided by J. Merriam). synonym: min. references: Fischbach and Heisenberg, 1984, J. Exp. Biol. 112: 65-93. Heisenberg and Wolf, 1984, Vision in Drosophila: Genetics of Microbehavior, Springer-Verlag, Berlin, pp. 207, 209, 227. Heisenberg, Borst, Wagner, and Byers, 1985, J. Neurogenet. 2: 1-30. Helfrich, 1986, J. Neurogenet. 3: 321-43. phenotype: Brain mass approximately half normal, including smaller than normal optic lobes and reduction in cell number (Fischbach and Heisenberg, 1984; Heisenberg and Wolf, 1984); exceptions: neuropile of the lamina optic ganglion appears normal in size and general morphology, and peduncle of mush- room body has apparently normal number of fibers; mnb flies take abnormally long to eclose (i.e., emergence per se from the pupal case is a slow process); behaviorally, mnb leads to relatively subtle behavioral defects, such as mild leg shaking under ether (see "other information"), absence of learning in tests using olfactory stimuli (Heisenberg et al., 1985), and aberrant visual fixation. In tests of locomotor activity rhythms (Helfrich, 1986), singly mutant mnb adults are basi- cally normal, but a high proportion of mnb so double mutants show complex rhymicities (dual circadian periodicities) with about 20% being arrhythmic (3 times greater than wild type). Other behaviors, such as basic optomotor responses (M. Heisen- berg, unpublished) and male courtship song (Kulkarni and Hall, 1987, Genetics 115: 461-475), are normal; physiologically, mnb--when linked to reduced optic lobes and small optic lobes mutations--has been tested for effects on electroretinogram, which have diminished amplitudes of light-on and light-off transient spikes in the triple mutant (Coombe, 1986, J. Comp. Physiol. 159: 655-665). alleles: Two alleles: mnb1 (Heisenberg) induced by ethyl methanesulfonate and mnb2 originally designated mnbUB913, produced by hybrid dysgenesis and has a P-element insertion in 16EF. cytology: Located in 16E3-F3 based on coverage of mnb1 by prox- imal X duplication in Dp(1;3)JC153 = Dp(1;3)16E3-4;17AB;99D, but failure to be covered by duplication segregating from T(1;Y)B55 = T(1;Y)16F2-3 or T(1;Y)W32 = T(1;Y)16F3-4; females carrying the deletion segregating from Tp(1;3)JC153 plus the XPYD element of T(1;Y)W32, with mnb1 being on the homologous X, have the mutation's effects uncovered. other information: Seems to be allelic to Sh, given map posi- tion and mnb-associated leg shaking (A. Ferrus and M. Heisen- berg, unpublished); yet, Sh mutations do not lead to any grossly aberrant brain morphology, and Sh5 plus Sh14 comple- ment mnb1 with regard to anatomical defects caused by the latter (M. Heisenberg, unpublished); mnb1 also complements lethal alleles of 3 genes mapping just distally to Sh alleles (see Tanouye, Lam, and Iverson, 1986, Ann. Rev. Neurosci. 9: 255-76), i.e., l(1)16Fa, l(1)16Fb and l(1)16Fc; an X- linked enhancer of mnb has been identified, which causes lethality when expressed along with the latter (M. Heisenberg, unpublished); the former maps near cv and (when in combination with mnb1) leads to death late in pupation (mutants can be "rescued" by opening the pupal case). # mo: micro-oculus location: 1-6.7. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 72. phenotype: Eyes small. Wings narrow and frequently pleated longitudinally with irregular hairs, giving slight opacity. Body size slightly reduced. Not easily classified. Viability and fertility good in both sexes. RK3. other information: Two alleles each induced by CB. 3007 and CB. 3026; four induced by CB. 1528; one each induced by CB. 1506, CB. 1540, CB. 1592, and CB. 3025. # mo: see moo # Mo: see Me # MoK: see Mot-K # mod: see e(gs) # mod: see rsd # modifier of Bar: see Su(B) # modifier of garnet: see e(g) # modifier of sexual dimorphism of glass: see msd(gl) # moira: see mor # Moire: see Me # Monoplane: see Mpl #*moo: moorish location: 3-48.3. origin: X ray induced. discoverer: Thompson. synonym: mo (preoccupied). references: 1959, DIS 33: 99. phenotype: Body color black. Homozygous lethal in male; female viability about 10% normal. RK3. # Moonrat: see Mrt # moorish: see moo # mor: moira (J.A. Kennison) location: 3-58.1 (based on 18 recombinants between jvl and sbd2). origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1983. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Isolated as a dominant suppressor of the antenna- to-leg transformation in a Pc2 AntpNs double heterozygote. Strongly suppresses the antennal transformation in an AntpNs heterozygote, but does not suppress the antennal transforma- tion in a strain containing a heat-shock driven Antennapedia cDNA. Also behaves as a dominant suppressor of Pc and Pcl mutations. All alleles associated with a common recessive embryonic lethality. Mitotic clones induced during larval growth lead to transformation of haltere tissue to wing tis- sue. Ubx130/mor has low frequency of haltere to wing transformation. alleles: alleles origin _____________________ mor1 EMS mor2 EMS mor3 EMS mor4 EMS mor5 / ray mor6 / ray cytology: Placed in 89A11-B4 based on its inclusion in Df(3R)sbd105 = Df(3R)88F9-89A1;89B9-10 but not in Df(3R)Po4 = Df(3R)88F7-89A1;89A11-13 nor Df(3R)sbd45 = Df(3R)89B4;89B10 (Hughes, Nelson, Yanuk, and Szauter). # morula: see mr # Mos location: 3-. origin: Spontaneous. references: Golubowsky and Zakharov, 1979, Genetika 15: 1798- 1808. phenotype: Dominant factor on third chromosome that reduces dorsocentral, scutellar, and occasionally other thoracic bris- tles; penetrance 30-50%, higher in the presence of unstable sn+ alleles. Causes increased rates of mutation of unstable sn+ in both germ line and soma. other information: Probably a manifestation of hybrid dys- genesis. #*mot-28: mottled location: 3-46.0. origin: Found among progeny of males given supersonic treat- ment. discoverer: Hersh, 28i19. references: Hersh, Karrer, and Loomis, 1930, Am. Nat. 64: 552-59. Hersh, 1934, DIS 1: 30. Surrarrer, 1935, Genetics 20: 357-62 (fig.). 1938, Genetics 23: 631-46 (fig.). 1940, DIS 13: 51. phenotype: Eyes mottled with patches of dark brown or black on wild-type background. Sensitive to temperature. Always mot- tled at 18, almost never above 25. Temperature-effective period is 25-35 hr after beginning of pupation. Mottling more easily seen in presence of v, also manifested in w homozygotes (Schultz). RK1 at 18; RK3 above 25. #*mot-32l location: 1- (not located). origin: X ray induced. discoverer: Oliver, 32l28. references: 1937, DIS 7: 19. phenotype: Eye color mottled in female only. RK3. #*mot-36e location: 3- [left arm, with In(3L)P]. discoverer: Bridges, 36e11. references: 1937, DIS 7: 12. phenotype: Eyes mottled with translucent spots and roughness. Bristles twisted and stubby; hairs irregular. Wing venation plexoid around posterior crossvein. Female sterile. Enhances somatic crossing over in first, second, and third chromosomes. RK3. # Mot-K: Mottled of Krivshenko location: 2- or 3- (rearrangement). origin: X ray induced. discoverer: Krivshenko, 54c25. synonym: MoK. references: 1954, DIS 28: 75. 1955, DIS 29: 76. phenotype: Eyes liberally mottled with dark color on wild-type background; character barely noticeable in young flies but striking in older ones; number and size of spots variable. Homozygous lethal. Viability and fertility of heterozygotes good. RK2A. cytology: Associated with T(2;3)Mot-K = T(2;3)41;60D;80-81. # mottled: see mot # mottler of white: see mw # mp: microptera location: 3-0.0. discoverer: Serebrovsky, 40g8. references: 1941, DIS 15: 19. phenotype: Wings small and spoonlike; veins irregular. Tarsi four jointed (rarely 3 or 5); joints 3 and 4 usually fused. Antennae shortened. Ecloses somewhat late. Viability and fertility low. RK2. # Mp20: Muscle protein 20 kd location: 3-{68}. references: Ayme-Southgate, Lasko, French, and Pardue, 1989, J. Cell Biol. 108: 521-31. phenotype: Encodes a 20-kd protein, that is not detected in the asynchronous oscillatory flight muscles, but is found in most, if not all, other muscles (the synchronous muscles). cytology: Placed in 49F9-13 based on in situ hybridization and deficiency mapping. molecular biology: Identified in a cDNA library produced from pulsating cultured myotubes and prehybridized with mRNA from Schneider cells. The cDNA clones identify two myotube- specific transcripts of 0.9 and 1.0 kb, the difference resid- ing in the 3 untranslated region. Southern blots indicate that the gene is not a member of a multigene family. The cod- ing sequence contains two introns, one of 140 nucleotides between codons 10 and 11, and the other of 67 nucleotides between codons 121 and 122. The open reading frame encodes a polypeptide of 184 amino acids with a molecular mass of 20,166 daltons. Two stretches of twelve amino acids match the pro- posed consensus sequence for the calcium binding site of calcium-binding proteins are found between residues 20-31 and 93-104. No other significant sequence homologies were found in the protein data base. # Mpl: Monoplane location: 3-{50}. origin: X ray induced. discoverer: Shelton. references: Hughes and Shelton, 1980, DIS 55: 204. phenotype: Wings held out at 90 from body axis; tibial-tarsal joint of metathoracic legs swollen. Homozygotes exhibit reduced viability and sterility; heterozygous viability also reduced. Partially suppresses expression of ey. cytology: Associated with 3R breakpoint of T(2;3)Mpl = T(2;3)35B2-3;86C1-2 (Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91). mr: morula # mr: morula location: 2-106.7. discoverer: Bridges, 13c8. references: Bridges and Morgan, 1919, Carnegie Inst. Wash. Publ. No. 278: 230 (fig.). Bridges, 1937, Cytologia (Tokyo), Fujii Jub., Vol. 2: 745-55. phenotype: Eyes rough. Bristles irregularly reduced in size and number. Abdominal sclerites often smaller. Developmental study by Lees and Waddington [1942, Proc. Roy. Soc. (London), Ser. B 131: 87-100] shows that effect on bristles results from general slowing of bristle growth. Female entirely sterile, has underdeveloped ovaries. At 19, bristles nearly normal and eyes nearly wild type. RK2 at 25 and above. cytology: Placed in salivary chromosome region between 59E2 and 60B10 based on its being to the right of In(2R)bwVDel = In(2R)41B2-C1;59E2-4 and to the left of Df(2R)Px = Df(2R)60B8-10;60D1-2 (Bridges, 1937). # mr2 origin: Spontaneous. discoverer: Bridges, 25k24. phenotype: Less extreme than mr. Nearly wild type at 19. Female entirely sterile. Oogenesis normal through stage 4; then compound nurse cell chromosomes fall apart and degen- erate. Karyosome of oocyte also disappears. Oogenesis does not proceed beyond sixth stage (King, 1964, Royal Entomol. Soc. London Symposium 2, Insect Reproduction, pp. 13-25). RK2 at 25 or above. # MR: Male Recombination location: 2-54 [(between Tft and pr; 2/10 Tft-pr crossovers between Tft and MR (Slatko and Green, 1980, Biol. Zentralbl. 99: 149-55)]. origin: Spontaneous. synonym: Mister; MRF. phenotype: A series of second chromosomes isolated from natural populations in diverse regions of the globe that, in crosses of MR-bearing males to laboratory-strain females, but not in the reciprocal crosses, produce dysgenic progeny. Such pro- geny transmit the MR chromosome at reduced levels compared with the homologous second chromosome; abnormalities in sper- miogenesis including failure of individualization observed in dysgenic males account for 70% of the deficiency in recovery of MR (Matthews, 1981, Genetics 97: 95-111). Increased lev- els of gonial recombination observed in both sons (Hiraizumi, 1971, Proc. Nat. Acad. Sci. USA 68: 268-700) and daughters [demonstrated in c3G females by Sinclair and Green (Mol. Gen. Genet. 170: 219-24)]; mitotic crossing over in wing disks unaffected (Thompson and Woodruff, 1980, Genetica 49: 77-80). Both sons and daughters exhibit increased rates of spontaneous mutations, both lethal (Slatko and Hiraizumi, 1973, Genetics 75: 643-49) and at some but not all specific loci (e.g., Green, 1977, Proc. Nat. Acad. Sci. USA 74: 3490-93); the latter types of mutants usually unstable, undergoing further mutation either to more extreme alleles or back to wild type; increased mutation rates observed when combined with mei9 and mei41 (1981, Mutat. Res. 83: 191-200). All classes of chro- mosome rearrangements produced by dysgenic progeny, but with preferential points of breakage (Yannopoulos, Stamatis, Zacharopoulou, and Pelecanos, 1983, Mutat. Res. 108: 185- 202); also shown in some cases to promote gonadal aplasia, especially at higher temperatures (Stamatis, Yannopoulos, and Pelecanos, 1981, Genet. Res. 38: 125-35); metaphase I of meiosis normal, but bridges and fragments observed in anaphase I and anaphase II in dysgenic males (Henderson, Woodruff and Thompson, 1973, Genetics 88: 93-107; Yannopoulos, 1978, Genet. Res. 239-47). Gross deletion of X-chromosome material induced by MR shown to involve an array of breakpoints, which, by in situ hybridization, are free of P-element sequences; postulated to arise through illegimate mitotic exchange (Green, Yamamoto, and Miklos, 1987, Proc. Nat. Acad. Sci. USA 84: 4533-37). The majority of the activity in several of the isolates maps to a site between Tft and pr on the left arm of chromosome two, but when that site removed residual activity remains in the genome. Mappability of the major effect to the same site in independent isolates suggests the presence of an element that is able to promote transposition but that itself is unable to transpose. Circumstantial evidence indicates that the element is P and that in addition to a functional P element, MR second chromosomes also carry defective P's. Males inheriting two doses of MR from mei-S332 fathers crossed to C(2)EN/0 females not discernably different from males with one dose; two doses of MR inherited from the mother are inac- tive (Green and Slatko, 1979, Mutat. Res. 62: 529-39). geographical isolate origin ref ( ______________________________________________________ MR-23.5 Patras, Greece 14, 15 MR-31.1 Patras, Greece 14 MR-gb39 Sonoma County, California 3 MR-h12 Haifa, Israel 2, 3, 4, 9 MR-n1 Napa County, California 3, 4, 5 MR-OK1 Oklahoma City, Oklahoma 7, 13 MR-S90 | Northern California 1 MR-T007 Harlingen, Texas 6, 8, 10, 11 MR-WO Ohio? 12 ( 1 = Bencze and Slatko, 1984, Genet. Res. 43: 149-58; 2 = Green, 1977, Proc. Nat. Acad. Sci. USA 74: 3490-94; 3 = Green, 1984, Biol. Zentralbl. 103: 1-8; 4 = Green and Shepherd, 1979, Genetics 92: 823-32; 5 = Green and Slatko, 1979, Mutat. Res. 62: 529-31; 6 = Hiraizumi, 1971, Proc. Nat. Acad. Sci. USA 68: 268-70; 7 = Henderson, Woodruff, and Thompson, 1978, Genetics 88: 93-107; 8 = Hiraizumi, Slatko, Langley, and Nill, 1973, Genetics 73: 439-44; 9 = Sinclair and Green, 1979, Molec. Gen. Genet. 170: 219- 24; 10 = Slatko, 1978, Genetics 90: 105-24; 257-76; 11 = Slatko and Hiraizumi, 1973, Genetics: 75: 643-49; 12 = Waddle and Oster, 1974, J. Genet. 61: 177-83; 13 = Woodruff and Thompson, 1977, Heredity 38: 291-307; 14 = Yannopoulos and Pelecanos, 1977, Genet. Res. 29: 231- 38; 15 = Yannopoulos, Stamatis, Zacharapolou, and Pelecanos, 1983, Mutat. Res. 108: 185-202. | Also carries Sd. # mrn: marionette (Fuller) location: 3-42.6 (between Ly and th). synonym: nc16, l(3)E35. references: Fuller, 1986, Gametogenesis and the Early Embryo, (G.J. Gall, ed.). Proc. Soc. Dev. Biol. 44, pp 19-41. Robertson and Fuller, unpublished. Irick and Cherbas, unpublished. phenotype: Recessive larval lethal. Individuals heterozygous for certain combinations of alleles reach late third instar but do not pupate; they have small discs and small brains. The original allele nc16, is associated with a dominant enhancer of the B2tn -tubulin mutation, suggesting a role for the gene in microtubule function. The dominant enhancer and the lethal mutation associated with nc16 were not separated in 82 recombinants between Ly and th. None of the other alleles are dominant enhancers of B2tnull (Robertson and Fuller, unpublished). alleles: allele synonym origin ref ( phenotype | ___________________________________________________ mrn1 mrnnc16nc16 EMS 1, 2 mrn2 mrnE35 EMS 2 b mrn3 mrnE67 EMS 2 c mrn4 mrnE72 EMS 2 c mrn5 mrnE94 EMS 2 b mrn6 mrnE96 EMS 2 b mrn7 mrn13B EMS 3 c mrn8 mrn10C EMS 3 c ( 1 = Fuller (1986); 2 = Irick and Cherbas, unpublished; 3 = Robertson and Fuller, unpublished; | a = Larval lethal, isolated as dominant enhancer of tubulin mutants. b = Larval lethal, isolated as lethal under Df(3L)BK10. c = Lethal phase not yet established, isolated as lethal under Df(3L)BK10. cytology: Placed in 71D-F, based on its being uncovered by Df(3L)BrdR6 and Df(3L)BK10, but not Df(3L)878.3. # Mrt: Moonrat (J.A. Kennison) location: 3-79.7 (based on 211 recombinants between es and ca). origin: Spontaneous. discoverer: Kennison. phenotype: Heterozygote shows partial transformation of ante- rior wing to posterior (triple row bristles replaced by double row bristles in patches). A network of extra veins appears in the anterior compartment, beginning at the distal edge in the least affected flies, and covering the entire anterior com- partment in the more extreme cases. Wing blade expanded ante- riorly at the distal edge. Wing blade expansion and extra veins resemble phenotypes seen in en1 homozygotes in the pres- ence of Minute mutations. Bubbles often form in the wing blade. More rarely, a mirror-image outgrowth from the ante- rior edge is present. Mirror-image duplications sometimes appear in halteres. Legs sometimes appear deformed (similar to phenotype of enlethal clones induced in the larva). Dom- inant phenotypes strongly temperature-sensitive. Penetrance greater than 99% at 18 (with strong expressivity) but only 30-40% at 29 (with very weak expressivity). Shows paternal effect. Penetrance greater when mutant allele inherited from father than when inherited from mother. Mrt/+/+ indistin- guishable from Mrt/+.