# ma: maroon location: 3-49.7. origin: Spontaneous. discoverer: Bridges, 12c13. references: 1918, Proc. Nat. Acad. Sci. USA 4: 316-18. Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 53 (fig.). phenotype: Eye color dull ruby, approaching wild type with age; classification slow. Larval Malpighian tubes pale yellow (Beadle, 1937, Genetics 22: 587-611). Eye color autonomous in transplant into wild-type host (Beadle and Ephrussi, 1936, Genetics 21: 230). Wild-type levels of aldehyde oxidase and xanthine dehydrogenase activity (Hickey and Singh, 1982, DIS 58: 74.) alleles: ma49, spontaneous (Oftedal, 1951, DIS 25: 69). RK2. #*Ma: Ma dominigene location: 1- (not located). origin: Spontaneous. discoverer: Goldschmidt, 1935. references: Gardner, 1942, Univ. Calif. (Berkeley) Publ. Zool. 49: 95. phenotype: In combination with Ma, vg/+ is strongly scalloped. RK3. # mab: malformed abdomen location: 3- {47}. phenotype: Tergites and sternites show defects in cuticle. Homozygous viable at 18 (wild-type) and 25 (mutant); lethal at 28 (Lewis, Kaufman, Denell, and Tallerico, 1980, Genetics 95: 367-81). allele origin discoverer synonym ref ( ______________________________________________ mab1 EMS R. Lewis Ebmab1 1, 2 mab2 EMS R. Lewis Ecmab2 1, 2 ( 1 = Cavener, Otteson, and Kaufman, 1986, Genetics 114: 111-23; 2 = Lewis, Kaufman, Denell, and Tallerico, 1980, Genetics 95: 367-81. cytology: Placed in 84B based on its inclusion in Df(3R)Scr2 = Df(3R)84A4-5;84C1-4 but not Df(3R)Win3 = Df(3R)84A4-5;84B1-2. # macrofine: see mf # mad: many abnormal discs (A. Shearn) location: 3-78.6. references: Shearn, Rice, Garen, and Gehring, 1971, Proc. Nat. Acad. Sci. USA 68: 2594-98. Shearn, 1974, Genetics 77: 115-25. phenotype: Homozygous lethal; labial and wing discs appear nor- mal; eye-antenna, prothoracic, haltere, leg, and genital discs homeotically transformed. Disc and cell autonomous. allele synonym _______________________ mad1 mad703 mad2 mad1803 mad3 madRO631 mad4 madSE420 mad5 madSH536 mad6 madVC5 mad7 madVD46 mad8 madVF284 mad9 madVF298 mad10 madVJ176 mad11 madVK96 mad12 madVR9 mad13 madVU144 mad14 madVX8 mad15 madVZ410 mad16 madVZ415 # mah: mahogany location: 3-88. discoverer: Beadle, 36b26. references: Beadle and Ephrussi, 1937, Am. Nat. 71: 91-95. phenotype: Eye color translucent brown in young flies, changing toward wild type and becoming dark brown with age. Eyes con- tain 77% normal red pigment and 102% normal brown pigment (Nolte, 1955, J. Genet. 53: 1-10). Larval Malpighian tubes wild type in color (Beadle, 1937, Genetics 22: 587-611). RK3. # mal: maroonlike location: 1-64.8 (Schalet, l963, DIS 38: 82). references: Chovnick, Finnerty, Schalet, and Duck, 1969, Genet- ics 62: 145-60. Finnerty, Duck, and Chovnick, 1970, Proc. Nat. Acad. Sci. USA. 65: 939-46. phenotype: Brownish eye color resulting from reduction in the red (drosopterin) pigments. Larval Malpighian tubes short, bloated, irregularly formed, and contain yellow to orange pteridine globules (Schwinck, 1960, DIS 34: 105). mal is nonautonomous for eye color in mosaics with wild-type tissue (Glassman, 1957, DIS 31: 121-22) and in transplants of mal eyes into wild-type hosts (Ursprung, 1961, Z. Vererbungsl. 93: 119-25). Activities of three molybdo-enzymes reduced or absent: aldehyde oxidase = AO (Courtright, 1967, Genetics 57: 25-39), pyridoxal oxidase = PO (Forrest, Hanley, and Lagowski, 1961, Genetics 46: 1455-63), and xanthine dehydro- genase = XDH (Forrest, Glassman, and Mitchell, 1956, Science 124: 725-26; Glassman and Mitchell, 1959, Genetics 44: 153- 62). Measurements of cross reacting material (e.g., Browder, Wilkes, and Tucker, 1982, Biochem. Genet. 20: 111-24, 125-32) show 75% and 50% normal levels of AO CRM in larval hemolymph and adult extracts respectively and 105% normal level of XDH CRM (see also Warner, Watts, and Finnerty, 1980, Mol. Gen. Genet. 180: 449-53). Activity of a fourth molybdo-enzyme, sulfite oxidase, is unaffected by mal (Bogart and Bernini, 1981, Biochem. Genet. 19: 929-46). Furthermore, unlike mutants in genes thought to be involved with the function of molybdenum cofactor, e.g. cin and lxd, the effects of mal not alleviated by administration of molybdenum; XDH cross reacting material (CRM) isolated from mal flies contains molybdenum (Andres, 1976, Eur. J. Biochem. 62: 591); mal flies contain high levels of molybdenum cofactor by Neurospora nitrate reductase activation assay (Warner and Finnerty, 1981, Mol. Gen. Genet, 184: 72-96). Accumulation of enzyme substrates (Forrest, Glassman, and Mitchell, 1956; Glassman and Mitchell, 1959; Glassman and McLean, 1962, Proc. Nat. Acad. Sci. USA 48: 1712-18) may account for the reported increase in uricase activity (Friedman, 1970, Genetics 68: s22). The absence of XDH activity renders mal flies sensitive to exogenously sup- plied purine (Glassman, 1965, Fed. Proc. 24: 1243), which has been used in selective schemes (Finnerty et al., 1970); the cell autonomy of mal with respect to AO activity provides the basis of a staining procedure for differentiating mal from mal+ tissue in mosaics (Janning, 1972, Naturwissenschaften 59: 516-17). mal offspring of mal+ mothers appear normal in both eye color and Malpighian-tube morphology (Glassman and Mitchell, 1959; Schwinck, 1960); mal+ activity observed in germ line as AO activity (Marsh and Wieschaus, 1977, Dev. Biol. 60: 396-403) and maternally inherited XDH activity in mal offspring detectable until second day of pupal stage (Browder and Williamson, 1976, Dev. Biol. 53: 241-49). Maternal effect suppressed if offspring are also homozygous for lxd (Courtright, 1975, Mol. Gen. Genet. 142: 231-38). Interallelic complementation in females of constitution mal1/malF1; eye color and Malpighian-tube morphology appear normal, but XDH activity about 10% normal (Glassman and Mitchell, 1959; Schwinck, 1960); complementation not seen in flies raised at 29 and reduced in flies that are also homozy- gous for lxd (Courtright, 1975, Mol. Gen. Genet. 142: 231- 38); physical properties of XDH and AO altered in different heteroallelic combinations (Finnerty, McCarron, and Johnson, 1979, Mol. Gen. Genet. 172: 37-43; Finnerty and Johnson, 1979, Genetics 91: 696-722). mal1, malF1, and malF3 comple- ment for eye color in all pairwise combinations; however, malF1 malF3/mal1 is mutant. mal and ry extracts complement to produce XDH activity (Glassman, 1962, Proc. Nat. Acad. Sci. USA 48: 1491-97); they do not complement intercellularly in vivo, however, since reciprocal eye-disk or Malpighian-tube transplants reported to behave autonomously with respect to drosopterin formation (Schwinck, 1960; 1963, DIS 38: 87). alleles: allele origin discoverer synonym ref ( comments | ______________________________________________________________________ mal1 X ray Oliver, 30l1 2, 3, 9 IV mal2 X ray Schalet, 1961 2, 10 II mal14 TEM 2, 12 I mal20 TEM 2, 12 I mal21 EMS 2, 12 II mal23 EMS 2, 12 I mal24 TEM 2, 12 II mal25 TEM 2, 12 I mal26 TEM 2, 12 II mal27 TEM 2, 12 II mal28 TEM 2, 12 I mal29 TEM 2, 12 mal30 EMS 2, 12 II mal60 DNA Fahmy, 60j malbz60j 4 mal106 X ray 2, 12 y+Ymal106, I mal116 X ray 2, 12 y+Ymal116, III malC1 EMS 1 malC2 EMS 1 malC3 EMS 1 malC4 EMS 1 normal eye color, no XDH activity malC5 spont 1 leaky allele, I malF1 / N mustard Fahmy, 1954 bz, malbz 2, 6, 7 III malF2 MMS Fahmy mal bz56k 2, 5 I malF3 ENU Fahmy mal65c 2, 5 V malF4 ENU Fahmy bz65c 2, 5 III malF5 CB3007 ` Fahmy 6 malF6 CB3025 ` Fahmy 6 malF7 CB3051 ` Fahmy 6 malQ 8 I malS spont Schalet 11 ( 1 = Bentley and Williamson, 1982, Can. J. Genet. Cytol. 24: 11-17; 2 = Chovnick, Finnerty, Schalet, and Duck, 1969, Genetics 62: 145-60; 3 = CP552; 4 = CP627; 5 = Fahmy and Fahmy; 6 = Fahmy and Fahmy, 1958, DIS 32: 68; 7 = Fahmy and Fahmy, 1958, Nature 184: 1927-29; 8 = Finnerty, McCarron, and Johnson, 1979, Mol. Gen. Genet. 172: 37-43; 9 = Oliver, 1935, DIS 3: 28; 10 = Schalet, 1961, DIS 38: 82; 11 = Schalet, 1986, Mutat. Res. 163: 115-44; 12 = Schalet and Finnerty, 1968, DIS 43: 65-66. | Complementation groups for eye color. / malF1 does not complement mal1 when kept at 29-30 throughout development; complementation occurs provided development proceeds at 25 during either of the two critical periods: the third quarter of the third larval instar or the middle of the pupal stage (Schalet, 1971, Mol. Gen. Genet. 110: 82-85). ` CB3007 = DL-p-N,N-di-(2-chloroethyl)aminophenylalanine. CB3025 = L-p-N,N-di-(2-chloroethyl)aminophenylalanine. CB3051 = ? cytology: Placed in 19D2-3 based on its inclusion in the region of overlap of Df(1)16-2-19 = Df(1)19A5;19D3 and Df(1)16-3-35 = Df(1)19D2-3;19E34. other information: The alleles of mal have been mapped both by complementation for eye color and by recombination. Five com- plementation units have been defined (Chovnick, Finnerty, Schalet, and Duck, 1969, Genetics 62: 145-60), and malC2 said to define a sixth (Bentley and Williamson, 1982, Can. J. Genet. Cytol. 24: 11-17). There is but a single lethal com- plementation group in heteroallelic combinations raised on purine-enriched medium. Recombinational mapping utilized purine sensitivity to select for mal+ recombinants (Finnerty et al., 1970). Maps co-linear. Complementation map of mal alleles (groups I to V above) com- pared to genetic map; relative positions of mutants in each complementation group with respect to genetic map indicated (modified from Duck and Chovnick, 1974, Genetics 79: 459-66). Program by D. Conner. # Mal: Malformed location: 2-44-50 (between stw and cn; Bridges inferred two loci, one near right end of 2R and one on chromosome 4). origin: Spontaneous. discoverer: Steinberg, 36k13. references: 1937, DIS 7: 15, 20. Baker and Tsai, 1977, Dev. Biol. 57: 221-25 (fig.). phenotype: Heterozygote has either malformed pit in middle of eye or, more often, nick at front edge of eye and has bristle- or antenna-like outgrowth; outgrowth determined to be mirror image duplication of part of the orbital region includ- ing the orbital and fronto-orbital bristles; several sequen- tial duplications sometimes observed. Penetrance low in heterozygote; supposedly enhanced by addition of extra brewer's yeast to medium. Homozygote shows larger nick and antennal outgrowth with up to 100% expression in pr Mal stock. RK3. # Malate dehydrogenase: see Mdh # male diplolethal: see mdl # Male Recombination: see MR # male-female-sterile: see mfs # male-specific lethal: see msl # male-sterile: see ms # Male-specific transcript: see Mst # maleless: see mle # Malformed: see Mal # malformed abdomen: see mab # Malic enzyme: see Men # mam: master mind (J.C. Hall) location: 2-70.3. synonym: N-2G. references: Lehmann, Dietrich, Jimenez, and Campos-Ortega, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 226-29. Lehmann, Jimenez, Dietrich, and Campos-Ortega, 1983, Roux's Arch. Dev. Biol. 192: 62-74. Campos-Ortega, 1985, Trends Neurosci. 8: 245-50. Smoller, Friedel, Schmid, Bettler, Lam and Yedvobnick, 1990, Genes Dev. 4: 1688-1700. phenotype: Homozygous embryonic lethal; embryos display neural hyperplasia with compensatory epidermal hypoplasia; caused by failure of most ventral ectodermal cells to differentiate as epidermal cells rather than neuroblasts, as seen in N, amx, bib, neu, Dl, and E(spl); mam tends to have less extreme neural hyperplasia than mutants at the other neurogenic loci. A similar diversion of cells from epidermigenic into neuro- genic pathways seen to generate supernumerary peripheral nerve cells (Hartenstein and Campos-Ortega, 1986, Roux's Arch. Dev. Biol. 195: 210-21 (fig.)]. When mam expressed in female germ cells and the ensuing embryos, neural hyperplasia is enhanced, but mam+ embryos from oocytes are normal [Jimenez and Campos Ortega, 1982, Roux's Arch. Dev. Biol. 191: 1901-201 (fig.)]. Homozygous clones in the eye display irregular ommatidial pat- tern characterized by lack of interommatidial bristles, enlarged facets with supernumerary retinular cells and reduced numbers of pigment cells; in the cuticle, clones homozygous for mam2 are devoid of bristles [Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32 (fig.)]. mam1 (formerly N-2G) heterozygotes occasionally exhibit apical wing nicking; not recorded for other alleles. Phenotype of homozygotes for null allele reduced by duplications for normal alleles of other neurogenic loci, N, neu, Dl, E(spl), and H, but not amx or bib (de la Concha, Dietrich, Weigel, and Campos-Ortega, 1988, Genetics 118: 499-508). alleles: allele origin discoverer synonym ref ( comments | _________________________________________________________________________________ mam1 spont Ives. 41l17 N-2G 3, 4 nicks; In(2R)50C20;54B1; breakpoint near -27 kb mam2 EMS mamIB99 1, 5, 6, 7 stronger allele mam3 EMS mamIF33 7 mam4 EMS mamIIH57 7 mam5 EMS mamIIJ14 7 mam6 EMS mamIIL61 7 mam7 EMS mamIIV06 7 mam8 EMS mamIJ113 6, 7 stronger allele mam9 EMS mamIL42 7 mam10 EMS mamIL115 7 mam11 EMS Wetter mamQ19 intermediate allele, deltas mam12 EMS Wetter mamQ78 weak allele, deltas, nicks mam13 EMS Wetter mamu12 intermediate allele, deltas mam14 EMS Wetter mamu97 weak allele, deltas, nicks mam15 EMS Wetter mamu112 intermediate allele, deltas, nicks mam16 EMS Wetter mamu127 intermediate allele, deltas mam17 EMS Wetter mamu129 weak allele, deltas mam18 EMS Wetter mamu168 intermediate allele, deltas mam19 EMS Wetter mamu196 intermediate allele, deltas, nicks mam20 EMS Wetter mamu199 2 weak allele mam21 EMS Wetter mamz3 extreme allele, deltas mam22 EMS Wetter mamz9 weak allele, deltas mam23 EMS Wetter mamz14 strong allele mam24 EMS Wetter mamz33 intermediate allele, deltas, nicks mam25 EMS Wetter mamz36 weak allele, deltas, nicks mam26 EMS Wetter mamz47 weak allele, deltas mam27 EMS Wetter mamz48 weak allele, deltas mam28 EMS Wetter mamz62 strong allele, deltas, nicks mam29 X ray Lehmann mam2l11 mam30 X ray Dietrich mam217-4 mam31 X ray Dietrich mam223-4 mam32 X ray Dietrich mam315-5 mam33 X ray Dietrich mam466-1 mam34 X ray Shrons maml3-25 mam35 X ray Shrons maml21-10 T(2;3)50C20-23;67 mam36 X ray Lehmann mamc2-4 2 mam37 X ray Lehmann mamc7-9 stronger allele mam38 X ray Lehmann mamcll4-3 stronger allele mam39 X ray Lehmann mamFX4 stronger allele mam40 P Weigel mamKP1 P element at 50C20-23 mam41 HD / HD2/3 8, 9 11.5 to 23.5 kb (including exons 5-7) deleted mam42 HD HD3/1 8, 9 In(2R)42C-D;50C-D; breakpoint near 0 ` mam43 HD HD6/4 8, 9 complex rearrangement; mam44 HD HD10/6 8, 9 P insert near -50 kb; at nucleotide 23 of exon 1 mam45 HD HD11/2 8, 9 In(2R)50C-D;57B; breakpoint at 0 mam46 HD HD13/6 8, 9 In(2R)42C-D;50C-D; breakpoint near 0 mam47 HD HD15/2 8, 9 unstable allele, P excised mam48 HD HD17/7 8, 9 strong allele, P excised 146 bp deletion near -2.0 kb in exon 4 - mam49 P-lacw Jan mam1E7 8 P-lacw insert near -48 kb mam50 P-lacw Jan mam10E1 8 P-lacw insert near -48 kb mam51 P-lacw Jan mam2B11 8 P-lacw insert near -15 kb ( 1 = Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32; 2 = Hartenstein and Campos-Ortega, 1986, Roux's Arch. Dev. Biol. 195: 210-21; 3 = Ives, 1943, DIS 17: 50; 4 = Ives, 1957, DIS 31: 83; 5 = Jimenez and Campos-Ortega, 1982, Roux's Arch. Dev. Biol. 191: 191-201; 6 = Lehmann, Jimenez, Dietrich, and Campos-Ortega, 1983, Roux's Arch. Dev. Biol. 192: 162-74; 7 = Nusslein-Volhard, Wieschaus, and Kluding, 1984, Roux's Arch. Dev. Biol. 193: 267-82; 8 = Smoller, Friedel, Schmid, Bettler, Lam and Yedvobnick, 1990, Genes Dev. 4: 1688-1700; 9 = Yedvobnick, Smoller, Young, and Mills, 1988, Genetics 118: 483-97 (fig.). | "deltas" refers to the presence of delta-like widenings of the veins 2, 3, and 4 at the margins of the wings of hetero- zygotes. "nicks" refers to terminal notching of the wing margins of heterozygotes; penetrance 100% for mam1, about 25% for other alleles. / Eight alleles induced by hybrid dysgenesis in Harwich second chromosomes, which has P-elements at 42C-D, 50C-D, and 57B. ` 0 coordinate = the insertion point of the defective P- element at 50C-D in the Harwich strain; positive values to the right. - Frameshift -> product with first 377 residues normal fol- lowed by 69 amino acids from frameshifted sequence before termination after residue 446. cytology: Maps at 50C20-23, by virtue of P-element insertion at this site, in mam40; consistent with this is the fact that mam1 is associated with In(2R)G = In(2R)50C19;54B1; and that mam35 = T(2;3)mam35 = T(2;3)50C20-23;67 (Campos-Ortega). molecular biology: Gene isolated by chromosome walking, physi- cal mapping of breakpoints, and transposon tagging (Weigel, Knust, and Campos-Ortega, 1987, Mol. Gen. Genet. 207: 374-84; Yedvobnick, Smoller, Young, and Mills, 1988, Genetics 118: 483-97). Locus delimited to ca. 70 kb, within which mam-mutant lesions mapped over a 45 kb interval (cf. Weigel et al.; 1987 Smoller et al., 1990). This region is rich in opa repeats (first noted by Weigel et al., 1987), and regions encoding them are portions of mam exons; these are all con- tained within a 6.3 kb cDNA, cloned from an 8-12 hour library (Smoller et al., 1990) probed with "unique-ORF"-containing (non-opa) genomic probes. Genomic sequence comprises seven exons (312, 127, 1010, 2073, 286, 1090, and 1435 bp) spanning 67 kb; transcription from left to right. Northern blots and in situ hybridizations (Smoller et al., 1990) reveal complex pat- terns of mam mRNA expression: a maternal transcript; four embryonic ones (6.5-8.5 kb), two of which appear earlier than the other two, with all four waning by L1; transcripts return in late L3/early pupation; ubiquitous spatial expression in embryos seen during germ-band elongation, with neural- restricted signals observed later. Sequencing of the 6.3 kb cDNA revealed a 4788 bp ORF and predicts an 1596-amino-acid protein; there are 21 poly-Gln runs within the ORF, four poly-Gly, three poly-Asn, and one poly-Ala run; there are also 47 Gly-Gly doublets and three Gly-Val runs; the predicted pro- tein contains relatively few charged residues. Antibodies generated using mam -fusion proteins detect a polypeptide of predicted size on Western blots and a nuclear signal in Schneider S2 cells and in whole mounts of early embryos (Smoller et al., 1990). other information: N-2G considered an allele based on its failure to complement other mam alleles and on the embryonic phenotype of such non-complementing trans heterozygotes. Interacts with dx, in that the great majority of dxENU/Y; mam10/+ zygotes die as pupae (Xu and Artavanis-Tsakonas, 1990, Genetics 126: 665-77). # man: mandarin location: 3-50.5. origin: Spontaneous. references: Aparisi and Najera, 1987, DIS 66: 13-14. 1988, DIS 67: 4-5, 5-6. phenotype: Eye color bright orange. # manikin: see mn # many abdominal discs: see mad # map: midgut amylase pattern (W.W. Doane) Two closely linked genes that determine the pattern of alpha-amylase activity in three contiguous segments of the anterior portion of the adult midgut (gene mapA) and two seg- ments of the posterior portion of the adult midgut (gene mapP). The short non-digestive middle midgut is without amylase activity in any genotype. mapP has three known alleles and mapA appears to have five since all 15 possible haplotypes have been reported (Doane, 1980, DIS 55: 36-39). In most cases, the pattern observed in the larval midgut is different from that seen in the adult of the same genotype. A pattern in which all three anterior segments and both poste- rior segments exhibit enzyme activity is designated 123-12 and one with no activity 000-00. The pattern observed is affected both by nutrition and adult age; for example, in some strains a 123-00 pattern may change to a 123-12 pattern at approxi- mately 14 days of age in adults; in other strains, this change does not occur (Doane, Treat-Clemons, Gemmill, Levy, Hawley, Buchberg, and Paigen, 1983, Isozymes: Current Topics in Bio- logical and Medical Research 9: 63-90). [Additional, as yet unnamed, genetic factors control amylase patterns in the ante- rior midgut and posterior midgut of larvae (Treat-Clemons and Doane, 1983, Isozyme Bull. 16: 66; Klarenberg, Visser, Wil- lemse, and Scharloo, 1986, Genetics 114: 1131-45); one is a cis-regulator of amylase activity in the anterior midgut and is located within 0.1 cM of Amy (Klarenberg et al., 1986)]. # mapA: Anterior midgut amylase pattern location: 2-82 (based on 7 recombinants between Amy and mapA). synonym: map-AMG. references: Doane, 1980, DIS 55: 36-39. phenotype: The anterior adult midgut is divided into three seg- ments which express discreet patterns of amylase activity. alleles: Different mapA alleles exhibit enzyme activity in dif- ferent combinations of the three segments of the anterior midgut. Presence of activity in the three regions is desig- nated, from anterior to posterior, 1, 2, and 3; absence or near absence of activity in any region is designated 0; these notations appear as three-digit superscripts in mapA allelic designations: mapA000, mapA100, mapA103, mapA120, and mapA123. # mapP: Posterior midgut amylase pattern location: 2-79 [based on 433 recombinants between Amy and wt (Klarenberg et al., 1986); mapP also shown to lie to the left of mapA by crossovers between them (Doane, 1980) and to the left of nw (Doane, 1987, DIS 66: 49). synonym: map (Abraham and Doane, 1978); map-PMG (Doane, 1980). references: Abraham and Doane, 1978, Proc. Nat. Acad. Sci. USA 75: 4446-50. Doane, 1980, DIS 55: 36-39. Klarenberg, Visser, Willemse, and Scharloo, 1986, Genetics 114: 1131-45. Doane, Treat-Clemons, Gemmill, Levy, Hawley, Buchberg, and Paigen, 1983, Isozymes: Current Topics in Biological and Med- ical Research 9: 63-90. Treat-Clemons and Doane, 1983, Isozyme Bull. 16: 66. Doane, 1987, DIS 66: 48. Thompson and Doane, 1988, J. Cell Biol. 107: 331a. Doane, Thompson, Norman, and Hawley, 1990, Isozymes: Struc- ture, Function, and Use in Biology and Medicine, Prog. Clin. Biol. Res. 344: 19-48. phenotype: Determines the level of amylase activity, amylase protein and amylase RNA in the posterior midgut. Trans regu- lation of amylase activity observed in adults (Abraham and Doane, 1978; Doane et al., 1983, Klarenberg et al., 1986) and in larvae of some strains (Treat-Clemons and Doane, 1983), but not others (Klarenberg et al., 1986); nutritional control of Amy gene expression by dietary glucose repression, which is strain-specific in its magnitude (Hickey and Benkel, 1982, Biochem. Genet. 20: 1117-29), affects the level of amylase activity systemically in both the posterior midgut and the anterior midgut and can affect amylase activity patterns (Thompson and Doane, 1988; Doane et al., 1990); similarly, dietary maltose, which is digested to glucose, can affect amylase activity patterns (Klarenberg et al., 1986). alleles: Two discrete regions of the larval and adult posterior midgut can express amylase activity on cornmeal-molasses-yeast food or a yeast diet with glucose containing sugars. Presence of activity in the anteriormost region of the posterior midgut is designated 1 in the superscript, and activity in the region just behind the first region is designated 2; absence of activity in either region is designated 0. The following alleles have been recorded by Doane (1980): mapP00, mapP10, and mapP12 [synonyms mapA, mapB, and mapC, respectively (Abra- ham and Doane, 1978)]. Map205: Microtubule-associated protein 205 kd location: 3- {105}. references: Goldstein, Laymon, and McIntosh, 1986, J. Cell. Biol. 102: 2076-87. phenotype: Encodes a 205 kd microtubule-associated protein, which by immunostaining can be localized to cytoplasmic micro- tubules and to the mitotic spindle. cytology: Placed in 100E-F by in situ hybridization. molecular biology: Genomic sequence isolated by screening an expression library with antibody. The genomic sequence hybri- dizes to a 6 kb mRNA on Northern blots. # mar: metaphase arrest location: 3-{84}. origin: X ray induced. references: Gonzalez, Molina, Casal, and Ripoll, 1989, Genetics 123: 371-77. phenotype: Hemizygotes die as third-instar larvae; cells in larval brain have highly condensed X-shaped chromosomes, a mitotic index twice that of wild type, and a thirty-fold reduction in the ratio of anaphases to metaphases. Only about 1% of cells are tetraploid, the remainder remaining diploid. Complements asp, which is just to the left. cytology: Placed in 96B based on its association with T(Y;3)B97 = T(Y;3)h3;96B, as indicated by the mar phenotype of T(Y;3)B197/Df(3R)L16 = Df(3R)96A1-10;96E. # Mar: Margin location: 2-72. origin: Induced by ethyl methanesulfonate. references: Whittle, 1977, DIS 52: 2. phenotype: Heterozygotes exhibit scalloping of wing margins; have gaps in triple row and double row of bristles and margi- nal hairs; wing outline sometimes ragged. Similar to BxG; penetrance incomplete. Homozygous lethal. # marionette: see mrn # maroon: see ma # maroonlike: see mal # Mas: see dsxM # Masculinizer: see dsxM # master mind: see mam # mat(2)cell: maternal lethal (2) cellularization defects (T. Schupbach) A series of ethyl methanesulfonate-induced maternal-effect- lethal female-sterile mutations on the second chromosome, which all result in the same phenotype. Embryos from homozy- gous females show variable defects in cellularization at the blastoderm stage; they form cuticles with holes, variable head defects, and segment fusions. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. genetic cytological locus location location included in _____________________________________________________ mat(2)cellHK35 2-54 mat(2)cellPK42 2-60 mat(2)cellPH65 2-67 mat(2)cellPQ49 2-12 mat(2)cellQA13 2-64 mat(2)cellQC13 2-35 mat(2)cellQE1 2-54 mat(2)cellQL46 2-67 mat(2)cellQQ55 2-68 mat(2)cellRE43 2-57 42C1-43F8 Df(2R)pk78s mat(2)cellRH36 2-31 mat(2)cellRQ41 2-86 # mat(2)dorsal: see dl # mat(2)ea: maternal lethal (2) early arrest (T. Schupbach) A series of EMS induced maternal-effect-lethal, female- sterile mutations on the second chromosome, which all result in the same phenotype: Homozygous females lay eggs which show no signs of development when observed under transmitted light in a stereomicroscope. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. genetic cytological locus location location included in excluded form ____________________________________________________________________ mat(2)eaPB28 2-72 51A1-B4 Df(2R)48 mat(2)eaPGP44 2-60 mat(2)eaQA26 2-61 mat(2)eaQD68 2-78 mat(2)eaQM47 2-40 31B-32A Df(2L)J27 mat(2)eaRL4 2-41 mat(2)eaRS32 2-17 25D7-E1 Df(2L)cl1 Df(2L)cl7 mat(2)eaRU28 2-54 # mat(2)N: maternal lethal (2) Notchlike (T. Schupbach) location: 2- {97}. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal, female sterile. Embryos from homozygous mothers form only a piece of dorsal cuticle, similar to the zygotic lethal Notch (N). alleles: allele origin synonym ___________________________________ mat(2)N1 EMS mat(2)NRA mat(2)N2 EMS mat(2)NQI mat(2)N3 EMS mat(2)NRQ cytology: Placed in either 57B5-14, or in 57D8-58B, since uncovered by Df(2R)D17 = Df(2R)57B5;58B1-2, but not by Df(2R)PL3 = Df(2R)57B20;59D8-9 (cytology according to O'Donnell, Boswell, Reynolds, and MacKay, 1989, Genetics 121: 273-80). other information: All three alleles are semilethal over Df(2R)D17. # mat(2)syn: maternal lethal (2) syncytial blastoderm arrest (T. Schupbach) A series of EMS-induced maternal-effect lethal mutations on the second chromosome, which all result in the same phenotype: Homozygous females lay eggs in which a narrow halo of clear cytoplasm appears around the time when nuclei would be expected to migrate to the egg periphery, but no cellulariza- tion takes place. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. genetic cytologycal locus location location included in _______________________________________________________ mat(2)synHB5 2-49 mat(2)synHi10 2-40 mat(2)synHK21 2-65 mat(2)synPA75 2-59 mat(2)synPJ50 2-{40} 31B-32A Df(2L)J27 mat(2)synPL63 2-72 51E3-52D1 Df(2R)TE51D-18 mat(2)synQF75 2-63 mat(2)synRE48 2-24 mat(2)synSE10 2-41 # mat(3)1 location: 3-54.8. origin: Induced by ethyl methanesulfonate. discoverer: Rice. references: Rice and Garen, 1975, Dev. Biol. 43: 277-86 (fig.). Regenass and Bernard, 1978, Mol. Gen. Genet. 164: 85-91. 1980, Wilhelm Roux's Arch. Dev. Biol. 188: 127-32. phenotype: Maternal-effect lethal; embryos produced by homozy- gous females produce pole cells, but syncytial blastoderm fails to cellularize. Pole cells from defective mat(3)1/+ embryos of mat(3)1 mothers functional when transplanted into normal hosts (Regenass and Bernard). # mat(3)3 location: 3-45.3. origin: Induced by ethyl methanesulfonate. discoverer: Rice. references: Rice and Garen, 1975, Dev. Biol. 43: 277-86 (fig.). phenotype: Maternal-effect lethal; embryos produced by homozy- gous females produce pole cells, but syncytial blastoderm fails to cellularize completely; the posterior-dorsal 30% of the surface fails to form cells and is separated from the remainder of the blastoderm surface by a belt of incompletely cellularized nuclei. Mutant phenotype expressed in females kept at 29; females kept at 25 are fertile and produce normal offspring; temperature-sensitive period during the last 12 hr of oogenesis. # mat(3)6: see spg # maternal haploid: see mh # maternal lethal: see mat # matt brown: see mtb #*mb: minus bar location: 3-43.4. discoverer: Nordenskiold, 33a30. references: 1934, DIS 2: 7. phenotype: Modifies Bar in such a way that B/B resembles B/+, and B/+ appears almost wild type; B male modified to resemble Bi. Homozygous female highly infertile. RK3. # mbd: mushroom body-deranged (J.C. Hall) location: 1-56. origin: Induced by ethyl methanesulfonate. synonym: mbdKS65. references: Heisenberg, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York, pp. 373-90. Technau and Heisenberg, 1982, Nature (London) 295: 405-07. Borst and Heisenberg, 1982, J. Comp. Physiol. 147: 479-84. phenotype: Most axons in peduncles of mushroom bodies in dorsal brain absent; no detectable lobes associated with these bodies (cf. alpha, beta, and gamma lobes of wild-type); posterior calyces of mushroom bodies enlarged. During post-larval mush- room body regeneration (on the first day of pupation), axons roll up at periphery of brain; other parts of mutant brains appear normal. Mushroom body abnormalities are variable; most behaviors of mutant adults are normal, including basic ability to discriminate between different odors; in tests using olfac- tory stimuli, learning in third larval instar is normal, but olfactory learning in mutant adults is aberrant (Heisenberg, Borst, Wagner and Byers, 1985, J. Neurogenet. 2: 1-30). Penetrance of the morphological phenotype diminishes rapidly under normal culturing, but does not wane when maintained in heterozygous condition. cytology: Maps within 17A-18A2, based on uncovering by Df(1)N19. # mbm: mushroom-body-miniature (J.C. Hall) location: 2-{0} (inferred from cytology; also, maps to distal 2L meiotically). origin: Induced by ethyl methanesulfonate. discoverer: H. Heisenberg and K. Fishbach (from mutagenized second chromosome provided by C. Nusslein-Volhard). synonym: mus: mushroom-bodies-small, a preempted symbol. references: Heisenberg, Borst, Wagner and Byers, 1985, J. Neu- rogenet. 2: 1-30. phenotype: Abnormally small calyces associated with mushroom bodies in dorsal brain; peduncles and lobes are thin or miss- ing, owing to degeneration of Kenyon cell fibers during third larval instar; these defects are essentially limited to mutant females. Mushroom bodies appear nearly normal in brains of mbm males. Osmotropotaxis (re odor discrimination) is essen- tially normal in females; mutant females (larvae or adults) are defective in learning tests involving odors, electric shock, or sugar, whereas males are normal or less defective. cytology: Maps to 21B8-D1, because mbm is uncovered by Df(2L)al = Df(2L)21B8-C1;21C8-D1. alleles: Three mutant alleles: mbmN337, mbmK1, mbmK7 (see "other information"). other information: All three mbm alleles, when heterozygous with Df(2L)al, lead to stronger mutant phenotypes than mutant homozygotes or heteroallelic combinations; mbmK1/ mbmK7 causes a very weak (i.e., near normal) mushroom body defect. mbmK1 and mbmK7 are from stocks originally termed Df(2L)netK1 and Df(2L)netK7; each of these turns out not to be a deletion, i.e. they appear to be cytologically normal, but the former is mutant for net, mbm and a vital gene, as is the latter, though the lethal here complements that on the K1 chromosome. In both of these stocks, the various abnormalities are separable by recombination. # mbmB: mushroom-body-miniature-B (J.C. Hall) location: 2-31. origin: Induced by ethyl methanesulfonate. synonym: rem: reduced-mushroom-bodies; mbmBN806. references: Heisenberg, Borst, Wagner and Byers, 1985, J. Neu- rogenet. 2: 1-20. phenotype: Phenotype similar to that of mbm, but less extreme, and mushroom body defect occurs in both males and females; learning is weak in tests using olfactory stimuli. # mbmC: mushroom-body-miniature-C (J.C. Hall) location: 2-35. origin: Induced by ethyl methanesulfonate. synonym: opa: olfactory pathway, a preempted symbol; mbmCN28. references: Heisenberg, Borst, Wagner and Byers, 1985, J. Neu- rogenet. 2: 1-30. phenotype: Phenotype similar to that of mbm; also, the pair of antennal lobes differ in volume in most mbmC adults (i.e. left smaller than right, or vice versa); learning very poor in tests of females, using olfactory stimuli. #*mbs: miniature blistered location: 2-56. origin: Spontaneous. discoverer: Neel, 41c13. references: 1942, DIS 16: 51. phenotype: Wings small, curled, blistered, and plexate. Bris- tle positions irregular and bristles often bent and twisted. Viability and fertility poor. RK3. mc: microchaete Edith M. Wallace, unpublished. # mc: microchaete location: 1-54.0. origin: X ray induced. discoverer: Demerec, 28f20. synonym: tb-53. references: 1935, DIS 3: 13. phenotype: Hairs on thorax fewer than wild type, more irregu- lar, and frequently doubled. Bristles smaller, more sparse on scutellum, and occasionally on head. Eyes rough. Wings ovoid and short; marginal bristles disarranged. Abdominal sclerites ridged. RK1. #*mc2 origin: Induced by D-p-N,N-di-(2-chloroethyl)amino-pheny- lalanine (CB. 3026). discoverer: Fahmy, 1955. synonym: mc-like. references: 1958, DIS 32: 71. phenotype: Thoracic hairs irregularly distributed, occasionally reduced in number. Bristles small, sparse on scutellum. Eyes small and rough. Wings ovoid and short. Tergites in female sometimes disarranged. Viability and fertility good in both sexes. mc2/mch is wild type. RK2. other information: Allelism inferred from location of mc2 at 52.1 and from phenotype. # Mc: Microcephalus location: 3-59.0 (about 0.2 unit to the right of bx). origin: Spontaneous. references: Bateman, 1944, DIS 18: 40. 1945, DIS 19: 47. phenotype: Eyes of heterozygote small or absent. Scutellars curve upward. Viability and fertility good. Homozygote usu- ally more extreme than heterozygote but not reliably distin- guishable. ale Mc homozygotes completely eyeless; fertile except when crossed to each other (Golubovsky and Zakarov, 1972, DIS 49: 112). Viability of homozygote varies from 100 down to 40%. RK1A. cytology: Associated with a minute tandem repeat of one or more bands in 89E7-11; partially restores fertility to Df(3R)P9 heterozygotes [Lewis, 1978, Nature (London) 276: 565-70]. Duplication appears to include at least a portion of the AbdB segment of BXC (Struhl and White, 1985, Cell 43: 507-19). # mc-like: see mc2 #*mch: minute chaetae location: 1-52.0. origin: Induced by methyl methanesulfonate (CB. 1540). discoverer: Fahmy, 1956. references: 1959, DIS 33: 87. phenotype: Extremely short, fine bristles. Hairs and body also small; delayed eclosion. Male viable and fertile. mch/mc2 is wild type. RK2. other information: One allele each induced by CB. 1246, CB. 1356, and CB. 3026. # Mcp: see BXC #*md: melanotic lesions location: 3-38.0. origin: Found in experiments using benzopyrene. discoverer: Gowen, 1933. phenotype: Lesions occur in many places throughout head, thorax, and abdomen. RK3. #*mdg: midgoid location: 1-64.7. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1955. references: 1958, DIS 32: 71. phenotype: Small in all dimensions; frequently underpigmented. Male infertile; viability about 20% wild type. RK3. # Mdh1: Malate dehydrogenase location: 2-37.2. synonym: Mdh2 (Grell, 1969, DIS 44: 47); MdhD (Johnson and Schaeffer, 1973, Biochem. Genet. 10: 149-63); sMdh (Hay and Armstrong, 1976, Insect Biochem. 6: 367-76); cMdh (Voelker, Ohnishi, and Langley, 1979, Biochem. Genet. 17: 947-56). references: Grell, 1969, DIS 44: 47. O'Brien, 1969, DIS 44: 42, 113. 1973, Biochem. Genet. 10: 191-205. Johnson and Schaffer, 1973, Biochem. Genet. 10: 149-63. Voelker, Ohnishi, and Langley, 1979, Biochem. Genet. 17: 947-56. phenotype: The structural gene for the cytoplasmic, NAD- dependent malate dehydrogenase = (S)-Malate: NAD+ oxidoreduc- tase [MDH1 (EC 1.1.1.37)]. Extracts from homozygotes produce two bands of activity plus a lighter, more electronegative band on gels; heterozygotes produce hybrid bands, indicating that the enzyme is a dimeric molecule. Subunit molecular weight estimated at 30,000 Daltons. Not necessary for sur- vival, since Mdh1n1/Df(2L)J is viable. Purification and biochemical characterization carried out by McReynolds and Kitto (1970, Biochim. Biophys. Acta 198: 165-75), Hay and Armstrong (1976, Insect Biochem. 6: 367-76), and Alhiotis (1979, Comp. Biochem. Physiol. 62B: 375-80). alleles: For the electrophoretic variants, the Research Trian- gle Park conventions (1978, DIS 53: 117) are used; super- script 4 designates the most common allele; superscripts <4 migrate more slowly and >4 more rapidly than the most common allele. Null alleles all derivatives of Mdh14. allele origin synonym ref ( comments | ______________________________________________________ Mdh12 spont MdhA 1, 2 rare allele Mdh12a spont 7 derivative of Mdh14 Mdh14 spont Mdh2S 4 common allele; Mdh1A 8 p > 0.90 Mdh1B 2 Mdh16 spont Mdh2V 4 rare allele Mdh1B 8 sMdh2 5 MdhC 2 Mdh1n1 / ray cMdhn-*10069 9 in SM1; CRM-; dimer- Mdh1n2 / ray cMdhn-*10081 9 in SM1; CRM+; dimer- Mdh1nNC1 spont 3, 6 residual activity; dimer- Mdh1nNC2 spont 3, 6 residual activity; dimer- ( 1 = Alhiotis, 1974, DIS 51: 88; 2 = Alhiotis, 1979, Comp. Biochem. Physiol. 62B: 375-80; 3 = Burkhart, Montgomery, Langley, and Voelker, 1984, Genetics 107: 295-306; 4 = Grell, 1969, DIS 44: 47; 5 = Hay and Armstrong, 1976, Insect Biochem. 6: 367-76; 6 = Langley, Voelker, Leigh Brown, Ohnishi, Dickson, and Montgomery, 1981, Genetics 99: 151-56; 7 = Mukai and Cockerham, 1977, Proc. Nat. Acad. Sci. USA 74: 2514-17; 8 = O'Brien, 1969, DIS 44: 42, 113; 9 = Racine, Langley, and Voelker, 1980, Environ. Mutagen. 2: 167-77. | CRM = cross-reacting material; dimer- = no evidence of dimer formation in heterozygotes with Mdh14 or Mdh16. cytology: Placed in 31B-E based on its being deleted by Df(2L)J2 = Df(2L)31B;32A and included in Dp(1;Y)B31 = Dp(1;Y)27D;31E (Voelker, Ohnishi, and Langley). # Mdh2 location: 3-62.6 [based on 21 recombinants between sr (3-62.0) and gl (3-63.1)]. synonym: mMdh. references: Voelker, Ohnishi, and Langley, 1979, Biochem. Genet. 17: 947-56. phenotype: Structural gene for the mitochondrial NAD-dependent malate dehydrogenase = (S)-Malate: NAD+ oxidoreductase [MDH2 (EC 1.1.1.37)]. alleles: Mdh24 is the common allele; Mdh26, which is more elec- tronegative, was encountered only once. cytology: Placed in 90C2-91A3 based on its inclusion in Df(3R)P14 = Df(3R)90C2-D1;91A2-3. # Mdh-NADP: see Men # mdl: male diplolethal location: 1-{6}; between cho and bi. references: Steinmann-Zwicky and Nothiger, 1985, Cell 42: 877-87. Steinmann-Zwicky, 1988, EMBO Journal 7: 3889-98. phenotype: Locus inferred from the rescue of males hyperploid for the distal fourth of the X chromosome, which are normally inviable, by substitution of Df(1)HC244 = Df(1)3E8;4F11-2 for the normal X. Lethality of the duplication observed in Sxl+ males but survival of such males carrying Sxlf1 reported. cytology: Placed in 4A based on inclusion of the inferred gene in Df(1)cho2 = Df(1)3E;4A but not Df(1)cho5 = Df(1)3D;4A.