# ms: see msc # ms(1)1 to 16: male sterile (1) A series of ethyl-methanesulfonate-induced mutations at the base of the X chromosome (Geer, Bowman, and Tyl, 1979, J. Exp. Zool 209: 387-93). cytological excluded locus location included in from comments _____________________________________________________________ ms(1)1 19F1-20B y+Ymal126 y+Ymal107 ms(1)3 19E8-20A1 y+Ymal108 y+Ymal126 ms(1)4 18F-19E1 y+Ymal+2 y+Ymal102 ms(1)7 19E6-F1 y+Ymal113 y+Ymal108 ms(1)10 19E6-F1 y+Ymal113 y+Ymal108 possible allele of ms(1)7 ms(1)12 19F1-20B y+Ymal126 y+Ymal107 possible allele of ms(1)1 ms(1)14 19E8-20A1 y+Ymal108 y+Ymal126 possible allele of ms(1)3 ms(1)16 20B-F BSY # ms(1)1 phenotype: Few motile sperm; none transferred; morphology nor- mal until coiling stage; however, some axoneme degeneration evident; some failure of individualization. Axoneme stability defective (Dybas, Tyl, and Geer, 1981, J. Exp. Zool. 216: 299-310). cytology: Placed in 19F1-20B based on its being covered by y+Ymal126 (19F1-20A2 to the base) but not by y+Ymal107 (20A1-B to the base) (Geer, Bowman, and Tyl, 1979, J. Exp. Zool. 209: 387-94). other information: Possibly allelic to ms(1)20A. ms(1)12 maps to same region; some males have motile sperm, but no transmis- sion to female; may be allelic. # ms(1)4 phenotype: No sperm motility. Few cysts reach coiling stage; paracrystalline material of major mitochondrial derivative diffuse and differentiation of the derivative irregular; cry- stallization initiated late and within the matrix of the mito- chondrion rather than at a point of contact with the endo- plasmic reticulum (Dybas, Tyl, and Geer, 1981, J. Exp. Zool. 216: 299-310). cytology: Placed in 18F-19E1; covered by Ymal+2 (18F to 20F) but not y+Ymal102 (19C3-E1 to 20F) (Geer, Bowman, and Tyl, 1979, J. Exp. Zool. 209: 387-94). other information: Possibly allelic to ms(1)19E. # ms(1)6S location: 1-. origin: Induced by ethyl methanesulfonate. discoverer: Shadholt. references: Habliston, Stanley, and Bowman, 1977, J. Ultras- truct. Res. 60: 221-34 (fig.). phenotype: Anatomy of the reproductive system of ms(1)6S males normal; however few or no motile sperm. Spermiogenesis defec- tive; some centrioles fail to form basal bodies, reducing the numbers of axonemes formed; basal body fails to make normal attachment to nucleus; mitochondria fuse irregularly but do elongate and elaborate paracrystalline material; large cyto- plasmic units with multiple mitochondrial derivatives but few if any axonemes seen in cross sections; isolated cytoplasmic elements with or without single axonemes also observed, defec- tive acrosome formation; chromatin condensation, nuclear elon- gation, and formation of microtubules around elongating nucleus abnormal. # ms(1)7 phenotype: Males viable but sterile; motile sperm produced and transmitted to females in normal numbers. Sperm fertilize eggs, but development fails. Spermiogenesis ultrastructurally normal (Dybas, Tyl, and Geer, 1981, J. Exp. Zool. 216: 299- 310). cytology: Placed in 19E6-F1 based on its being covered by y+Ymal113, which extends from the base of the X to 19E6-8 but not by y+Ymal108, which extends to 19E8-F1 (Geer, Bowman, and Tyl, 1979, J. Exp. Zool. 209: 387-94). other information: Possibly allelic to ms(1)19Fa. ms(1)10, mapped to same region, also had motile sperm transferred to female; possibly allelic. # ms(1)10A location: 1-33.44. phenotype: Spermiogenesis blocked at or before coiling stage. Abnormal associations of major mitochrondrial derivatives with endoplasmic reticulum give rise to multiple foci of paracrystalline-material formation (Dybas, Harden, Machnicki, and Geer, 1983, J. Zool. 226: 293-302). alleles: allele origin synonym ref ( comments ______________________________________________ ms(1)10A1 EMS ms(1)BP6 2 ms(1)10A2 EMS ms(1)v3 1 ms(1)10A3 EMS ms(1)v6 1 ms(1)10A4 EMS ms(1)v13 1 ms(1)10A5 EMS ms(1)v16 1 ms(1)10A6 EMS ms(1)v101 1 on y+Yv+ ms(1)10A7 EMS ms(1)v102 1 on y+Yv+ ms(1)10A8 EMS ms(1)v105 1 on y+Yv+ ms(1)10A9 EMS ms(1)v111 1 on y+Yv+ ms(1)10A10 EMS ms(1)F3 3, 4 ms(1)10A11 EMS ms(1)F5 3, 4 ( 1 = Geer, Lischwe, and Murphy, 1983, J. Exp. Zool. 225: 107-18; 2 = Zhimulev, Belyaeva, Pokholkova, Kochneva, Fomina, Bgatov, Khudyakov, Patzevich, Semeshin, Baricheva, Aizenzon, Kramers, and Eeken, 1982, DIS 58: 210-14. 3 = Zhimulev, Pokholkova, Bgatov, Umbetova, Solovjeva, and Belyaeva, 1987, Biol. Zentralbl. 106: 699-720. 4 = 1987, DIS 66: 194-97. cytology: Placed in 10A1-5 based on its inclusion in Df(1)v-L1 = Df(1)9F13;10A4-5 but not in Df(1)v-L2 = Df(1)9F13;10A1 (Zhimulev et al.). # ms(1)14 phenotype: Spermiogenesis appears normal, but late degeneration seen. Some sperm enter seminal vesicles and are transferred to females. cytology: Placed in 19E8-20A2; covered by y+Ymal108 (19E8-F1 to 20F) but not by y+Ymal107 (20A1-B to the base) (Geer, Bowman, and Tyl, 1979, J. Exp. Zool. 209: 387-94). other information: Possibly allelic to l(1)19F6; ms(1)3 maps to same region, has few motile sperm which are transferred to females; may be allelic. # ms(1)16 phenotype: Few spermiogenic cysts reach coiling stage; multiple associations of mitochondrial derivative with endoplasmic reticulum producing multiple foci of paracrystalline material elaboration; improper elongation of major mitochondrial derivative or failure of paracrystalline-body formation. Individualization of sperm defective; cellular degeneration obvious; axonemes defective with gaps in the circular arrays of outer microtubular doublets. Cysts with half or twice the normal number of spermatids observed (Dybas, Tyl, and Geer, 1981, J. Exp. Zool. 216: 299-310). cytology: Placed in 20B-F based on its inclusion in BSY (Geer, Bowman, and Tyl, 1979, J. Exp. Zool. 209: 387-94). other information: Possibly allelic to ms(1)20B. # ms(1)19 and 20 origin: Induced by ethyl methanesulfonate. references: Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84. cytological locus location included in excluded from synonym _________________________________________________________________ ms(1)19E 19E1-5 Df(1)B57 Df(1)A118 ms(1)E ms(1)19Fa 19F Df(1)su(f)7085 Df(1)su(f)9122 ms(1)D ms(1)19Fb 19F Df(1)su(f)7085 Df(1)su(f)9122 ms(1)C ms(1)19Fc ( 19F Df(1)su(f)7085 Df(1)su(f)9122 ms(1)19Fd ( 19F Df(1)su(f)7085 Df(1)su(f)9122 ms(1)20A 20A Df(1)su(f)795 Df(1)su(f)7009 ms(1)B ms(1)20B 20A Df(1)su(f)724 Df(1)su(f)733 ms(1)A ( all alleles included on Y mal+. alleles: allele synonym ___________________________ ms(1)19E1 ms(1)E ms(1)19E2 ms(1)496 ms(1)19Fa1 ms(1)D ms(1)19Fa2 ms(1)424 ms(1)19Fa3 ms(1)515 ms(1)19Fa4 ms(1)RA4 ms(1)19Fa5 ms(1)RA10 ms(1)19Fb1 ms(1)C ms(1)19Fb2 ms(1)RB47 ms(1)19Fc1 ms(1)DD19 ms(1)19Fc2 ms(1)DD23 ms(1)19Fc3 ms(1)S5 ms(1)19Fc4 ms(1)S27 ms(1)19Fd1 ms(1)DD5 ms(1)19Fd2 ms(1)DD16 ms(1)19Fd3 ms(1)DD17 ms(1)19Fd4 ms(1)S35 # ms(1)202 origin: Induced by ethyl methanesulfonate. references: Lifschytz and Meyer, 1977, Chromosoma 64: 371-92 (fig.). phenotype: Meiosis I proceeds to metaphase and rarely anaphase; undivided co-oriented bivalents move irregularly toward the poles; more than 32 nuclei per cyst, frequent micronuclei; many cysts do not undergo meiosis. First division spindles tetrapolar, resemble two parallel bipolar spindles. # ms(1)244 origin: Induced by ethyl methanesulfonate. references: Lifschytz and Meyer, 1977, Chromosoma 64: 371-92 (fig.). phenotype: Shape of primary-spermatocyte nuclei highly irregu- lar, with evaginated pockets, which sometimes contain chromo- somes. Multipolar spindles observed; entire bivalents rather than dyads pass to pole at first meiotic anaphase; second division generally arrested, but some cysts with more than 32 nuclei observed. Nuclear size highly variable; micronuclei present. Mutant males exhibit shaking upon etherization. # ms(1)401 location: 1-58. origin: Induced by ethyl methanesulfonate. references: Lifschytz and Hareven, 1977, Dev. Biol. 276: 276- 94 (fig.). phenotype: Primary spermatocytes appear to accumulate; nuclei appear creased; nucleoli fragmented. Some elongating sperma- tids produced, but development arrested early. In XO males primary spermatocytes do not attain full size, and the intermediate-sized nucleolated spermatocytes accumulate; nuclear creases fail to form. cytology: Claimed to be fertile in combinaton with y2Y67g (probably 67g19.1, which carries 20A3-20F). # ms(1)413 location: 1-25. origin: Induced by ethyl methanesulfonate. references: Lifschytz and Hareven, 1977, Dev. Biol. 276: 276- 94 (fig.). Brick, Lifschytz, and Friedlander, 1979, J. Ultrastruct. Res. 66: 151-63 (fig.). phenotype: Males carrying the mutation are sterile; exhibit shaking behavior with intermittent proboscis extension. Meiosis appears to be arrested, but the cellular changes asso- ciated with spermiogenesis continue, including mitochondrial aggregation, nuclear condensation and elongation, cellular elongation, and coiling. Spermatocytes do not divide, but develop directly into spermatids with one nucleus and four axonemes; mitochondria cluster prematurely in the primary spermatocyte but do not form a nebenkern in the spermatid. No chromosome condensation or spindle formation in the spermato- cytes. Irregular distribution of nuclear-envelope annuli, condensed chromatin, and perinuclear microtubules in the sper- matids, basal bodies do not associate with nucleus. alleles: Three mutations with similar location 4-5 units to the right of ct and shared somatic and germinal phenotypes presumed to be allelic: ms(1)4131, ms(1)4132 [synonym = ms(1)682], and ms(1)4133 [synonym = ms(1)RD11]. # ms(1)516 location: 1-38. origin: Induced by ethyl methanesulfonate. references: Lifschytz and Hareven, 1977, Dev. Biol. 276: 276- 94 (fig.). Lifschytz and Meyer, 1977, Chromosoma 64: 371-92 (fig.) phenotype: First meiotic divisions normal in both cell morphol- ogy and bivalent structure; second meiotic divisions appear monastral but bipolar; both centrioles pass to the same pole at the second meiotic division producing one daughter nucleus with two basal bodies associated and one with none. Dyads move to the poles as highly condensed bodies with sister cen- tromeres remaining associated; spermatids display numerous micronuclei and nebenkerne of nonuniform size. Occasional apparently normal cysts encountered. Spermiogenesis proceeds albeit abnormally. cytology: Claimed to be fertile in combination with Dp(1;3)sn12a1, which does not include the region to which the mutant maps. # ms(1)RA40 origin: Induced by ethyl methanesulfonate. references: Lifschytz and Meyer, 1977, Chromosoma 64: 371-92 (fig.) phenotype: 90% of cysts in division in early anaphase I; apparently pause there as anaphase proceeds normally producing 32 diploid spermatids with nuclei and nebenkerne of uniform size and developing to a normal onion stage. In rare anaphase II divisions chromosomes appear to pass to the poles at ran- dom. Diploid spermatids have two centriolar bodies, usually both attached to the nuclear membrane; detached centriolar bodies also seen; centriolar bodies, whether attached or detached, undergo same morphological transformations as in normal males. # ms(1)RD7 origin: Induced by ethyl methanesulfonate. references: Lifschytz and Hareven, 1977, Dev. Biol. 276-94 (fig.) Lifschytz and Meyer, 1977, Chromosoma 64: 371-92 (fig.) phenotype: Meiotic figures rare; those that are observed display abnormal chromosome behavior in both meiotic divi- sions. Bivalent rather than dyads pass to first anaphase poles. First meiotic divisions mostly abnormal with monas- tral, deformed diastral and multipolar spindles; second- division chromosome constitutions but not second-division spindles observed. Spermatid cysts contain fewer than 64 but more than 32 cells; two types of spermatic nuclei observed: some with 0-4 detached centrioles in cytoplasm of early sper- matids in which centriolar bodies plus axonemes held together in vicinity of nucleus; others exhibit one centriole of a pair attached to nucleus and the other detached but close by. # ms(1)RD15 origin: Induced by ethyl methanesulfonate. references: Lifschytz and Hareven, 1977, Dev. Biol. 276-94 (fig.) phenotype: Meiosis appears to be held up at prometaphase of the first division; few metaphases or first anaphases encountered; twice as many cysts in division as normal with 90% in first prometaphase; tri- and sometimes tetrapolar spindles observed in M1. Second divisions not observed; cysts contain a maximum of 32 cells. Spermatid differentiation proceeds to an extent similar to that of XO males. # ms(1)RD33 location: origin: Induced by ethyl methanesulfonate. references: Lifschytz and Hareven, 1977, Dev. Biol. 276-94 (fig.). phenotype: Spermatid development arrested at a stage slightly earlier than that observed in XO males; in ms(1)RD33/0 males, however, development arrested before completion of primary- spermatocyte growth. # ms(Y) Male-sterile mutations on the Y chromosome that have been mapped are designated according to the Y-fertility gene affected: kl-1, kl-2, kl-3, or kl-5 on YL and ks-1 or ks-2 on YS. # ms(Y)hd: male sterile (Y) hybrid disgenesis Thirteen sterile Y chromosomes recovered from hybrid dys- genic crosses; Southern blots probed with P sequences reveal male specific bands not seen in the original P strain; comple- mentation tests not carried out to determine locus affected (Schafer and Nahmias, 1985, Mol. Gen. Genet. 200: 182-84). # ms(2)1: male sterile (2) 1 location: 2-65.5. origin: Ultraviolet induced. discoverer: Meyer, 48c. references: Meyer, Edmondson, Byers, and Erickson, 1950, DIS 24: 60. phenotype: Male sterile; female fertile. Sperm present but not motile. RK3. # ms(2)2 location: 2-44.0 (Meyer). origin: Spontaneous. discoverer: Muller, 1951. synonym: ms. references: Meyer, 1959, DIS 33: 97. phenotype: Homozygous male completely sterile; female fairly fertile. RK3. # ms(2)3R location: 2-51. origin: Induced by ethyl methanesulfonate. references: Romrell, Stanley, and Bowman, 1972, J. Ultrastruct. Res. 38: 563-77. Laughran, Stanley, and Bowman, 1976, J. Ultrastruct. Res. 56: 21-30 (fig.). phenotype: Meiosis in homozygous mutant males characterized by apparent failure of the normally occurring incomplete cytok- inesis so that all four meiotic products are seen in one spherical cell. Incomplete cytokinesis and ring-canal forma- tion occur normally during meiosis; however, furrow membranes subsequently fuse and disintegrate; double-membrane fragments and ring canals found freely floating in spermatid cytoplasm. All the mitochondria coalesce into a single nebenkern, which subsequently divides into two and may subdivide into as many as eight mitochondrial derivatives. Elongation appears to take place in separate cytoplasmic units of four spermatids each in which mitochondrial derivatives vary in size and may associate with the endoplasmic reticulum or more than one axoneme, forming like numbers of foci of crystallization. Later stages show massive degeneration. # ms(2)10R location: 2-84. origin: Induced by ethyl methanesulfonate. references: Romrell, Stanley, and Bowman, 1972, J. Ultrastruct. Res. 38: 578-90. phenotype: Spermatid elongation limited; the endoplasmic sheath surrounding the axoneme opens out producing linear rather than circular arrays of microtubular doublets in cross sections of elongating spermatids. Mitochondrial derivatives may be large and irregular in shape with multiple contact points with endo- plasmic reticulum and correspondingly multiple foci of cry- stallization. # ms(2)73d location: 2- (between b and Sd). origin: Spontaneous in In(2L)Cy; separable. references: Hartl, 1980, Genetics 96: 685-96. phenotype: Homozygous males have immature, unelongated sperma- tid bundles. # ms(2)E A series of complementing male-sterile mutations induced by ultraviolet light (Edmonson, 1951, DIS 26: 61). genetic locus location synonym ___________________________________ ms(2)E3 2-28 ms2.3 ms(2)E4 2-47.9 ms2.4 ms(2)E5 2-54.8 ms2.5 ms(2)E6 2-54.8 ms2.6 ms(2)E7 2-54.8 ms2.7 ms(2)E8 2-55.6 ms2.8 ms(2)E9 2-57 ms2.9 ms(2)E10 2-66.5 ms2.10 ms(2)E11 2-68 ms2.11 ms(2)E12 2-68.2 ms2.12 # Ms(2)M: Male sterile (2) of Meyer location: 2- (just to the right of cn). origin: X ray induced. references: Meyer, 1966, DIS 41: 167. phenotype: Heterozygous males sterile; heterozygous females fertile. # ms(3)10R location: 3-. origin: Induced by ethyl methanesulfonate. references: Wilkinson, Stanley, and Bowman, 1974, J. Ultras- truct. Res. 48: 242-58. phenotype: Spermiogenesis of homozygous mutant males defective; nuclear elongation variable owing to variably reduced numbers of perinuclear microtubules; absence of perinuclear microtu- bules associated with irregular condensation of chromatin beneath the nuclear envelope. Evidence for folding in axonemes leading to more than 64 profiles in transferse sec- tions of spermatid bundles. Cross sections of elongating spermatid bundles revealed deranged axonemes with linear rather than circular arrays of the nine pairs of microtubules, with the doublets either still associated with the endoplasmic reticulum or free; mitochondrial derivatives multiply associ- ated with endoplasmic reticulum with up to four foci of depo- sition of paracrystalline material instead of the normal one. # ms(3)HO5A: male sterile (3) of Hardy and Orevi location: 3-45.9. origin: Induced by ethyl methanesulfonate simultaneously with fs(3)H05A, fs(3)HO5B, and ms(3)HO5B. synonym: ms(3)ml5A. references: Nishida, 1980, Jpn. J. Genet. 55: 427-39 (fig.). phenotype: Testes rudimentary; germ-cell development arrested in immature primary-spermatocyte stage; few cysts escape to produce spermatids. A more advanced stage of development attained, including production of motile sperm, in the pres- ence of a recessive suppressor on chromosome 2. other information: Possibly fs(3)HO5A and ms(3)HO5A are the same mutant and should be designated ms(3)HO5A. # ms(3)HO5B location: 3-. origin: Induced by ethyl methanesulfonate simultaneously with fs(3)HO5A, fs(3)HO5B, and ms(3)HO5A. synonym: ms(3)ms25A. references: Nishida, 1980, Jpn. J. Genet. 55: 427-39 (fig.). phenotype: Spermatogenesis proceeds to coiling stage, but no motile sperm produced. # ms(3)K81 location: 3-91.3. origin: Spontaneous. synonym: ph: paternal haploid. references: Fuyama, 1984, Jpn. J. Genet. 59: 91-96. 1986, Genetics 112: 237-48. 1986, Genetics 114: 495-509. phenotype: Homozygous males produce motile sperm capable of fertilizing eggs, but defective in pronuclear function. Development of fertilized eggs initiated; arrested after several nuclear divisions in three-fourths of the embryos, the remainder developing beyond blastoderm and proving to be haploid upon cytological examination. Nuclear division cycle protracted compared to wild type, and the syncytial blastoderm nuclei undergo an extra division to produce twice the normal density prior to cellularization (Edgar, Kiehle, and Schu- berger, 1986, Cell 44: 365-72). A small fraction of the eggs diploidize and yield viable daughters, mostly by fusion of products of the first meiotic division (85%); fusion of pro- ducts of second meiotic divison rare or nonexistent. Incidence of gynogenetic diploids becomes appreciable in crosses to a stock designated G9 by Fuyama (1986, Genetics 114: 495-509). cytology: Placed in 97D2-6 on the basis of the sterility of ms(3)K81/Df(3R)ro-XB3 males [=Df(3R)97D2-3;97D5-6]. # ms(3)KKD: see |Tub85D # ms(3)m1 location: 3-45.9. origin: Induced by ethyl methanesulfonate. references: Nishida, 1980, Jpn. J. Genet. 55: 427-39. phenotype: Homozygous males have rudimentary testes exhibiting degenerating cysts of spermatocytes and cysts arrested early in development. Homozygous females also have rudimentary gonads, but Nishida attributes this to an independent but closely linked mutation; only the male sterility is suppressed by su(msm1). # ms(3)m2 location: 3- (near centromere). origin: Induced by ethyl methanesulfonate. references: Nishida, 1980, Jpn. J. Genet. 55: 427-39. phenotype: Homozygous males sterile; small coiled testes with elongated spermatid cysts. # ms(3)nc2: see hay # ms(3)nc3 location: 3-47.0. origin: Induced by ethyl methanesulfonate. synonym: nc3. references: Fuller, 1986, Proc. Soc. Dev. Biol. 74: 19-41. phenotype: Fails to complement certain |Tub mutant alleles for male fertility although mapping to another site. Male fertil- ity of homozygotes not determined. ms(3)nc3/+ males fertile. cytology: Located at 77E-F. # ms(3)nc4: see wrl # ms(3)nc32 location: 3-82.9. origin: Induced by ethyl methanesulfonate. synonym: nc32. references: Fuller, 1986, Proc. Soc. Dev. Biol. 74: 19-41. phenotype: Fails to complement certain | Tub85D mutant alleles for male fertility although mapping to another site; | Tub85D synthesis, meiosis, and spermatid differentiation are normal in these sterile trans-heterozygotes. ms(3)nc32/ms(3)nc32 males fail to enter meiosis and show no spermatid differentia- tion. Testes from these males contain gonial cells, primary spermatocyte cysts, and cysts with abnormal cells. Adult male homozygotes show no | Tub85D synthesis. ms(3)nc32/+ males fertile. cytology: Located in 95F-96A. # ms(3)nc33: see ( Tub84D # ms(3)neol: see fwd # ms(3)sa: male sterile (3) spermatocyte arrest location: 3-44 (Kemphues). origin: Spontaneous. synonym: ms(3)VO45. phenotype: Primary spermatocytes arrested premeiotically but apparently after attaining full size; testes become filled with mature primary spermatocytes. cytology: Located at 78A3;79E1-2 (Fuller). # ms2: see ms(2)E #*msc: melanoscutellum location: 1-52.6. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. synonym: ms (preoccupied). references: 1958, DIS 32: 72. phenotype: Extra pigmentation confined to scutellum. One or more thoracic bristles duplicated. Eyes slightly more oval than normal. Wings slightly abnormal in shape and position. Characters not always penetrant. Viability and fertility good in both sexes. RK3. other information: One allele each induced by CB. 1506 and CB. 3025; two induced by CB. 3007. # Msc: see ScrMsc under ANTC # msd(gl): modifier of sexual dimorphism of glass location: 1-0.96. origin: Spontaneous. references: Birchler, 1984, Genet. Res. 44: 125-32. phenotype: Two alleles; homozygous gl males carrying the allele that we designate msd(gl)d (dimorphic) have brick-red eyes, whereas msd(gl)d; gl females' eyes are lemon yellow. In the presence of msd(gl)m (monomorphic), however, both gl males and females have the lighter eye color. Thus allelic differences are discernable only in males; females, either normal or homozygous for tra do not respond to msd(gl) genotype. Males carrying duplications for the msd(gl) locus show that msd(gl)d is dominant to msd(gl)m and that the eye colors of males with one or two doses of the dimorphic allele are indistinguish- able. In gl+ flies, the msd(gl) constitution is without phenotypic consequence. Not an allele of zeste. cytology: Located in 3A8-C2 based on the presence of msd(gl)d in Dp(1;2)w+70h = Dp(1;2)3A7-8;3C2-3. # msf: misformed location: 2-55.2 (originally located at 55.6 but arbitrarily placed at 55.2 to be consistent with cytological indication that it is to the left of pk). discoverer: Bridges, 30b8. references: Curry, 1939, DIS 12: 46. phenotype: Eyes misshapen. Wings short and crumpled; legs shortened. Characteristics variable and overlap wild type. RK3. cytology: Placed between 41A and 42A3 on the basis of its inclusion in Df(2R)bwVDe2LCyR = Df(2R)41A-B;42A2-3 (Schultz). Certainly included in Df(2R)M41A-vg11 = Df(2R)40F-41A1;42A19- B1 (Morgan, Schultz, Bridges, and Curry, 1939, Carnegie Inst. Wash. Year Book 38: 275). #*msg: missing location: 2- (not located). origin: Spontaneous. discoverer: Mossige, 50b4. references: 1951, DIS 25: 69. phenotype: Bristles greatly reduced or missing. In extreme cases, almost like sv. Female sterile; male sparingly fer- tile. RK2. # msl-1: male-specific lethal location: 2-53.3. references: Belote and Lucchesi, 1980, Genetics 96: 165-86. phenotype: Homozygous male embryos hatch but die as much as twelve days later in larval or prepupal stages; females and heterozygous males survive; phenotype slightly more severe in sons of homozygous than of heterozygous mothers. Viability of two-X individuals that develop as phenotypic males (tra2) or intersexes (dsx) is unaffected by msl-1, indicating that the one-X condition is required for msl-1 lethality. No interac- tion with mle or msl-2 (Belote, 1983, Genetics 105: 881-96). Females heterozygous for Sxlf1 and homozygous for msl-1 show signs of intersexual development [Skripsky and Lucchesi, 1982, Dev. Biol. 94: 153-64 (fig.)]. Pole cells from msl-1 male embryos capable of undergoing normal spermatogenesis when transplanted into wild-type hosts (Bachiller and Sanchez, 1986, Dev. Biol. 118: 379-84). Concluded to be defective in dosage compensation in males based on decreased levels of X- linked-enzyme activities (G6PD, 6GPD, FUM) but not autosomally encoded enzymes (ADH, AO, GPDH, IDH) in homozygous msl-11 and msl-12 male larvae when compared with non-msl-1 controls (Belote and Lucchesi, 1980, Nature 285: 573-75). alleles: allele origin discoverer synonym ref ( comments ______________________________________________________________ msl-11 EMS Belote 1, 2 amorph msl-12 EMS Belote msl-1b 1, 2 less severe allele ( 1 = Belote and Lucchesi, 1980, Genetics 96: 165-86. 2 = Uenoyama, Uchida, Fukunaga, and Oishi, 1982, Genetics 102: 223-31. cytology: Placed in 36F7-37B8 based on its inclusion in Df(2L)TW3 = Df(2L)36F7-37A1;37B2-8. # msl-2 location: 2-9.0. references: Belote and Lucchesi, 1980, Genetics 96: 165-86. phenotype: Homozygous male embryos hatch but die as much as fourteen days later in larval or prepupal stages; females and heterozygous males survive; no maternal effect. Viability of two-X individuals that develop as phenotypic males (tra2) or intersexes (dsx) is unaffected by msl-1, indicating that the one-X condition is required for msl-1 lethality. No interac- tion with mle or msl-1 (Belote, 1983, Genetics 105: 881-96). Few homozygous msl-22 gynandromorphs survive; XO patches small, with small bristles, and mostly confined to abdomen (Uenoyama, Uchida, Fukunaga, and Oishi, 1982, Genetics 102: 223-31). Pole cells from msl-2 male embryos capable of undergoing normal spermatogenesis when transplanted into wild-type hosts (Bachiller and Sanchez, 1986, Dev. Biol. 118: 379-84). Females heterozygous for Sxlf1 and homozygous (and to a lesser extent heterozygous) for msl-2 show signs of intersexual development; effects greater when mother homozy- gous for msl-2 [Uenoyama, Fukunaga, and Oishi, 1982, Genetics 102: 233-43 (fig.); Skripsky and Lucchesi, 1982, Dev. Biol. 94: 153-64 (fig.)]. Concluded to be defective in dosage com- pensation in males based on decreased levels of X-linked- enzyme activities (G6PD, 6GPD, FUM) but not autosomally encoded enzymes (ADH, AO, GPDH, IDH) in homozygous msl-21 male larvae when compared with non-msl controls (Belote and Luc- chesi, 1980, Nature 285: 573-75). alleles: allele origin discoverer synonym ref ( ___________________________________________ msl-21 EMS Belote 1 msl-22 EMS Oishi, 1976 msl-227 2 ( 1 = Belote and Lucchesi, 1980, Genetics 96: 165-86; 2 = Uenoyama, Uchida, Fukunaga, and Oishi, 1982, Genetics 102: 223-31. # msl-3: see mle32 # msl-3b: see mle33 # Msp: Muscle specific proteins location: 3- {50}. references: Bernstein, Glenn, Emerson, and Donady, 1981, Genet- ics 97: s10. cytology: Placed at two sites in 87B by in situ hybridization. molecular biology: Isolated as clones homologous to mRNA's cod- ing for several developmentally regulated, sequence related polypeptides of 22,500 daltons molecular weight. Genes activated at fusion stage of myogenesis. Restriction maps and partial sequencing as yet uninformative. # Mst: Male-specific transcript Refers to cloned sequences isolated from genomic libraries differentially screened with male and female cDNA. Cytologi- cal localizations all determined by in situ hybridization. genetic cytological locus location location ref ( synonym comments | ______________________________________________________________________ Mst25F 2-{17} 25F 2 mst323 germ line Mst26Aa 2-{20} 26A 1, 4 mst355a accessory gland Mst26Ab 2-{20} 26A 1, 4 mst355b accessory gland Mst47A 2-{59} 47A 2 mst325 germ line Mst51F 2-{73} 51F 5 mst(2)ag-35 accessory gland Mst57D 2-{99} 57D 5, 6, 3 mst(2)ag-1 accessory gland Mst66D 3-{26} 66D 2 mst349 germ line Mst75C 3-{45} 75C 5 mst(3)ag-2 accessory gland Mst87F 3-{54} 87F 3, 5 mst(3)gl-9 germ line Mst95E 3-{81} 95E 1, 2 mst316 accessory gland Mst95EF 3-{81) 95E-F 2 mst345 germ line Mst95F 3-{81} 95F 5 mst(3)ag-3 somatic Mst98CE 3-{95} 98C-E 2 mst336 germ line ( 1 = Chapman and Wolfner, 1988, Dev. Biol. 126: 195-202; 2 = DiBenedetto, Lakich, Kruger, Belote, Baker, and Wolfner, 1987, Dev. Biol. 119: 242-51; 3 = Kuhn, Schafer, and Schafer, 1988, EMBO J. 7: 447-54; 4 = Monsma and Wolfner, 1989, Genes Dev. 2: 1063-73; 5 = Schafer, 1986, Mol. Gen. Genet. 202: 219-25; 6 = Schafer, 1986, EMBO J. 5: 3579-82. | Tissue-specific expression. # Mst26Aa phenotype: Expressed in males. but not in females; also expressed in the germ-cell-free sons of tud females as well as in XX individuals that are homozygous for dsx, ix, tra2, or tra. 1986, Presence of tra2+ activity in XX flies during a part of the third larval instar is sufficient to repress expression of Mst26Aa and prevent accessory-gland development; absence of tra2+ activity during that period leads to accessory-gland formation and the production of Mst26Aa tran- script. molecular biology: Transcribed from the same strand as Mst26Ab, the transcription terminating 20 base pairs 5' to the initia- tion of Mst26Ab transcription. 0.9 kilobase transcript has a 56-base-pair intron between the first and second nucleotides of codon 12. Open reading frame encodes a 265-amino-acid polypeptide. Conceptual amino-acid sequence reveals a region in which 11 of 17 amino acids are identical to the egg-laying hormone of the sea hare Aplysia californica. # Mst26Ab phenotype: Expressed in males, but not in females; also expressed in the germ-cell-free sons of tud females as well as in XX individuals that are homozygous for dsx, ix, tra2, or tra. Presence of tra2+ activity in XX flies during a part of the third larval instar is sufficient to repress expression of Mst26Ab and prevent accessory-gland formation and the produc- tion of Mst26Ab transcript. molecular biology: Transcription begins 20 base pairs down- stream from the termination of transcription and on the same strand as Mst26Aa. 0.5 kilobase transcript sequence reveals intron of 61 base pairs between the first and second nucleo- tides of codon 11. Open reading frame encodes a 90-amino-acid polypeptide. # Mst51F phenotype: Expressed in normal and X0 males, as well as in the XX pseudomales or intersexes homozygous for dsx, ix, tra2, or tra and in the germ-cell-free sons of tud females. # Mst87F phenotype: Expressed in normal and X0 males, but not in the XX pseudomales homozygous for dsx, ix, tra2, or tra nor in the germ-cell-free sons of tud females. molecular biology: Sequence analysis shows that the gene comprises two exons of 79 and 338 base pairs separated by a 91-base-pair intron. A 165 base pair open reading frame is in the second and larger exon. Conceptual amino acid sequence reveals repeated motifs of Cys Cys Gly Pro or Cys Gly Pro such that Cys, Gly, and Pro comprise 38, 29, and 20% of the amino acids present. 102 base pairs of upstream sequences suffice to specify the gene's specific expression characteristics, i.e., premeiotic transcription and postmeiotic translation separated by three days of development (Kuhn, Schafer, and Schafer, 1988, EMBO J. 7: 447-54). # Mst95E phenotype: Expressed in males, but not in females; also expressed in the germ-cell-free sons of tud females as well as in XX individuals that are homozygous for dsx, ix, tra2, or tra. Presence of tra2+ activity in XX flies during a part of the third larval instar is sufficient to repress expression of Mst95E and prevent accessory-gland development; absence of tra2+ activity during that period leads to accessory-gland formation and the production of Mst95E transcript. # mtA: see tu-bw # mt: see mu1 #*mtb: matt brown location: 1-3.6. origin: Induced by ethyl methanesulfonate (CB. 1528). discoverer: Fahmy, 1956. references: 1959, DIS 33: 88. phenotype: Eye color flat and browner than normal with greatly reduced reflection spots. Wing position varies from slightly to completely outspread, sometimes upheld. Male sterile; via- bility about 30% wild type. RK2. # mTmI: see Tm2 # mTmII: see Tm1 # Mtn: Metallothionein (G. Maroni) location: 3-48.8. references: Lastowski-Perry, Otto, and Maroni, 1985, J. Biol. Chem. 260: 1527-1530. Maroni, Otto and Lastowski-Perry, 1986, Genetics 112: 493- 504. phenotype: Codes for metallothionein, a metal binding protein. Inducible by ingestion of Cu or Cd (but not Zn) ions. In lar- vae, it is expressed mainly in the midgut. No point mutations are available, but Dp(3;3)Mtn+H22 shows increased tolerance to Cd. cytology: 85E10-15 based on in situ hybridization and its inclusion in Df(3R)by10 but not in Df(3R)/B104 (Maroni et al.). molecular biology: Restriction maps and sequences of genomic and cDNA clones are available. The gene size is 631 bp; this includes 120 bp of coding sequence and a 365 bp intron. It shows similarity to the mammalian metallothioneins both at the amino-acid and nucleotide sequence level. Metal-inducible promoter useful in molecular constructs (Bunch, Grinblat, and Goldstein). #*mu: mussed location: 3-50. origin: Spontaneous. discoverer: Mohr, 37l21. references: Mossige, 1939, DIS 12: 47. phenotype: Wings thin textured. Dorsal surface of thorax arched. RK1. # mu1: mutator location: 3-57. origin: Spontaneous. synonym: mt; mu (preoccupied). references: Green, 1970, Mutat. Res. 10: 353-63. Green and Lefevre, 1973, Mutat. Res. 16: 59-64. Gold and Green, 1974: Mol. Gen. Genet. 135: 245-55. phenotype: Homozygous and hemizygous females exhibit increased rates of sex-linked visible and lethal mutations (e.g., y2 ->y+ = 1/2500; more rarely mutations to intermediate or more extreme alleles; also f3N reversions and wa ->w); heterozygous females display slightly elevated rates of mutation; about half of mutants occur as clusters indicating premeiotic ori- gin. Lethal mutations frequently associated with deficiencies of one to several bands. Mutation rates not elevated in males. y - sn recombination reduced 30% in mu1 homozygous and 25% in mu1/+ heterozyous females; also females but not males display elevated frequencies of nondisjunction. Effects of 100r on the induction of sex-linked lethals significant in mu1 but not + females (Gold and Green, 1975, Genetics 80: s35). The incidence of y and f36 clones is five times control values in mu1/mu1 and ten times control in mu1/Df(3R)sbd105 females (Martensen and Green, 1976, Genetics 83: s47). cytology: Placed in 88F9-89B10 based on its inclusion in Df(3R)sbd105 = Df(3R)88F9-88A1;89B9-10. # mu2 location: 3-{1.5}. origin: Spontaneous. discoverer: Green, 1977. references: Mason, Strobel, and Green, 1984, Proc. Nat. Acad. Sci. USA 81: 6090-94. phenotype: Irradiation of females homozygous for mu2 with low doses of X rays produces substantial numbers of terminal defi- ciencies for all chromosome arms, [see for example Df(1)yT]; irradiation of heterozygous females produces frequencies of deficiencies intermediate between those obtained from homozy- gous mu2 and wild-type females. Extents of deficiencies lim- ited only by the ability to recover them in viable offspring. Incidence of terminal losses linear with dose; such deficien- cies visible cytologically and can be shown by in situ hybrid- ization to lack sequences characteristically present at the termini of chromosome arms. Irradiation of mu2 females does not increase the incidence of either interstitial deficiencies or sex-linked lethal mutations. Irradiation of mu2 males does not increase the frequency of deficiencies. cytology: Placed in polytene section 62, (Biessmann). molecular biology: Newly formed chromosome ends unstable; lose approximately 75 base pairs per generation (Biessmann and Mason, 1988, EMBO J. 7: 1081-86). # Mu(f3N): Mutator forked-3N location: 1-56.7-59.4 (between f and Bx). references: Woodruff, 1975, Genet. Res. 25: 163-77. phenotype: A dominant cis-acting enhancer of the reversion rate of f3N; thought responsible for reported instability of f3N. Ineffective in reverting other alleles and in increasing the rate of sex-linked lethal mutations. #*mu-F: mutability factor from Florida location: 2- (not located). origin: Spontaneous in Florida wild stock. discoverer: Demerec, 1936. references: 1937, Genetics 22: 469-78. phenotype: Homozygote shows increase in lethal and visible mutation rate. Factor acts during development of germ cells in both male and female. Description resembles that of MR. RK3. # mud: mushroom body defect (J.C. Hall) location: 1-50 [(Heisenberg, 1980), but cytology implies 1- {47}]. 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 295: 405-07. phenotype: Neuropile of mushroom bodies (usually in dorsal brain) is missing (Heisenberg, 1980); penetrance for this ana- tomical phenotype (on which criterion the mutant was isolated) ca. 90%. Calyces that should innervate pedunculi and lobes of mushroom bodies are enlarged, as are antennal lobes in ante- rior brain. At sites of calyces, large numbers of thin axons form distinct lobes outside main neuropile of brain. Viabil- ity of mutant females poor, and they are sterile as well. Development of mushroom bodies apparently normal until pupa- tion, when "reconstruction" of this bilaterally paired brain entity (this process being a normal feature of wild-type metamorphosis) is aberrant (Technau and Heisenberg, 1982). Supernumerary neuroblasts observed in the larval brain, owing to anomalous proliferation of such cells postembryonically. alleles: allele origin discoverer synonym comments _______________________________________________________ mud1 EMS Heisenberg mudKS63 mud2 P Fischbach mudUB686 no P insert mud3 EMS Heisenberg mud4 EMS Heisenberg cytology: maps to 12E9-11 (Fischbach), based on its inclusion in Df(1)KA9 = Df(1)12E2-3;12F5-13A1 but in neither Df(1)g-l = Df(1)12A;12E9-11 nor Df(1)RK5 = Df(1)12E9-11;13A9-B1. # mud: see mudl # Mud: Muddled location: 1- (rearranged). discoverer: E.H. Grell. phenotype: Heterozygote has rough eyes with fused facets; eye color brownish. Hemizygous males have low viability but are fertile. cytology: Associated with In(1)Mud = In(1)3C3-4;5A6-B1. other information: Not allelic to Sc2. # mudl: mudlike location: 3-50.5. origin: Spontaneous. synonym: mud. references: Aparisi and Najera, 1988, DIS 67: 4-5 and 5-6. phenotype: Eye color grayish brown. # mul: multiple location: 1-0.0 (between l(1)Ca and tw). phenotype: Eyes rough and oval. Wings weak and held out. Bristles occasionally missing or disarranged. Body may show abnormal protuberances covered with hairs. Female sterile. After a few generations in stock, mul1 showed only the eye abnormality. RK2. alleles: allele origin ( discoverer synonym ref | comments __________________________________________________________________ mul1 spont Neel, 41c13 4 mul2 X ray Lefevre l(1)JF1 3 mul3 Dysgenesis Eeken l(1)D1 2 P element insert mul4 Dysgenesis Eeken l(1)D52 2 P element insert mul5 ENU Voelker l(1)A89 1 mul6 ENU Voelker l(1)A110 mul7 ENU Voelker l(1)B23 mul8 ENU Voelker l(1)B37 mul9 ENU Voelker l(1)B41 mul10 ENU Voelker l(1)B42 mul11 EMS Voelker l(1)C7 mul12 EMS Voelker l(1)C8 ( 1 = Eberl, Hilliker, and Voelker, 1988, DIS 67: 36; 2 = Eeken, Sobels, Hyland, and Schalet, 1985, Mutat. Res. 150: 261-75; 3 = Lefevre and Watkins, l986, Genetics 113: 869-95; 4 = Neel, 1942, DIS 16: 51. cytology: Located in 1C by deficiency analysis (Voelker). # multimorph: see bcd # multiple: see mul # multiple wing hairs: see mwh # Multiple sex comb: see Msc # mum: see bcd # mummy: see mmy #*mur: murrey location: 1-14.3. origin: Spontaneous as one mosaic male. discoverer: E. H. Grell, 57c. references: 1957, DIS 31: 81. phenotype: At 25, eye color reddish purple, bristles very small, and body size reduced. At 17, eye color and body size normal but bristles rather small. Original mosaic male transmitted only an X containing mur. He was mated to his daughters to produce homozygous mur females. mur/mur female and mur male are sterile. RK3. # murky: see mk # murrey: see mur # mus: see mbm # mus: mutagen sensitive A series of mutants selected on the basis of their enhanced sensitivity to various mutagenic treatments. The nomenclatural conventions employed depart somewhat from those of other mutants that share a particular phenotype. mus followed by a number between 101 and 199 indicates a mutation on the X chro- mosome, 201-299 on the second chromosome, and 301-399 on the third chromosome; thus mus101 [formerly redundantly designated mus(1)101] represents the first locus identified on the X. Some allelic designations begin with an upper-case letter indicating the laboratory in which the allele was selected; D = University of California, Davis, A = Emory University in Atlanta, B = University of British Columbia. # mus101 (J.B. Boyd) location: 1-44.2 [0.2 cM to the left of g (Schalet)]. references: Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506. Boyd and Setlow, 1976, Genetics 84: 507-26. phenotype: Survival of homozygous and hemizygous larvae hyper- sensitive to exposure to methyl methanesulfonate, nitrogen mustard, 2-acetylaminofluorene, and gamma rays. Partially deficient in post-replication repair (Boyd and Setlow, 1976; Brown, and Boyd, 1981, Mol. Gen. Genet. 183: 356-62); nitrogen-mustard mutagenesis abolished; mus101+ implicated in recovery from DNA crosslinking (Graf, Green, and Wurgler, 1979, Mutat. Res. 63: 101-12). Displays hypermutability to alkylating agents; defective in alkylation repair pathway (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Increases X-ray-induced post-meiotic chromosome loss (Cooper and Zimmer- ing, 1981, Mutat. Res. 81: 345-56). Mutants inhibit premei- otic rDNA magnification in males (Hawley, Marcus, Cameron, Schwartz, and Zitron, 1985, Proc. Nat. Acad. Sci. USA 82: 8095-99). mus101 function required for chorion-gene amplification (Snyder, Galanopoulous, and Kafatos, 1986, Proc. Nat. Acad. Sci. USA 83: 3341-45). Homozygotes for female- fertile allele exhibit elevated meiotic nondisjunction (Boyd et al., 1976). Causes mitotic chromosome instability (mus101D1, Baker and Smith, 1979, Genetics 92: 833-47), and defective mitotic condensation of heterochromatin (musts1, Gatti, Smith, and Baker, 1983, Science 221: 83-85). alleles: allele origin discoverer ref ( comments _____________________________________________________ mus101D1 EMS Boyd 1 female fertile mus101D2 EMS Boyd 1 female sterile mus101SM mei-9 | Schalet lethal mus101ts1 EMS Baker 2 ( 1 = Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506; 2 = Gatti, Smith, and Baker, 1983, Science 221: 83-85. | Spontaneous in the paternal X chromosome in a cross of wild-type males to mei-9 females such that the F1 female was mus101SM/mei9. cytology: Located in 12A6-D3 (Mason, Green, Shaw, and Boyd, 1981, Mutat. Res. 81: 329-43). # mus102 (J.B. Boyd) location: 1-0.5 (Smith, 1976). references: Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506. Smith, 1976, Mol. Gen. Genet. 149: 73-85. phenotype: Survival of homozygous and hemizygous larvae hyper- sensitive to exposure to methyl methanesulfonate, formaldehyde (Alexandrov, Alexandrova, and Ankina, 1982, DIS 58: 12-13), and gamma rays. No evidence of hypermutability to alkylation nor defects in excision repair functions (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Homozygous females fertile; exhibit elevated frequencies of nondisjunction. Increases frequency of mwh clones in mwh/+ wings; also increases incidence of isochromatid breaks in the heterochromatin and euchromatin of mitotic cells, with breaks occurring 1.4-1.6 times more frequently in females than males ( Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81). alleles: allele origin discoverer ref ( ___________________________________ mus102A1 EMS Smith 3 mus102A2 EMS Smith 3 mus102A3 EMS Smith 3 mus102A4 EMS Smith 3 mus102A5 EMS Smith 3 mus102A6 EMS Smith 3 mus102A7 EMS Smith 3 mus102A8 EMS Smith 3 mus102D1 EMS Boyd 1 mus102D2 EMS Boyd 1 mus102D3 EMS Mason 2 ( 1 = Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506; 2 = Mason, Green, Shaw, and Boyd, 1981, Mutat. Res. 81: 329-43; 3 = Smith, 1976, Mol. Gen. Genet. 149: 73-85. cytology: Placed between 1B14 and 2B17-18 (Baker and Smith, 1979, Genetics 92: 833-47). # mus103: see mei41 # mus104: see mei41 # mus105 (J.B. Boyd) location: 1- {14}. synonym: l(1)d.deg-1. references: Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506. Smith, 1976, Mol. Gen. Genet. 149: 73-85. phenotype: Strong alleles originally recovered as late larval lethals with degenerate imaginal discs (Stewart, Murphy, and Fristrom, 1972, Dev. Biol. 27: 71-83; Baker, Smith, and Gatti, 1982, Proc. Nat. Acad. Sci. USA 79: 1205-09). Weaker alleles viable and female fertile; hypersensitive to methyl methanesulfonate; interact synergistically with mus109D1; increase the incidence of mwh clones in mwh/+ wings. All alleles tested display increased frequencies of breaks and exchanges in euchromatin of mitotic cells, with breaks occur- ring 1.5 times more frequently in females that males (Baker, Smith, and Gatti, 1982, Proc. Nat. Acad. Sci. USA 79: 1205- 09; Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81). alleles: allele origin discoverer synonym ref ( _________________________________________________ mus105A1 EMS Smith 3 mus105D1 EMS Boyd 2 mus105la EMS l(1)d.deg-1a 1, 4 mus105lb EMS l(1)d.deg-1b 4 mus105lc EMS l(1)d.deg-1c 1, 4 mus105ld EMS l(1)d.deg-1d 1, 4 ( 1 = Baker, Smith, and Gatti, 1982, Proc. Nat. Acad. Sci. USA 79: 1205-09; 2 = Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506; 3 = Smith, 1976, Mol. Gen. Genet. 149: 73-85; 4 = Stewart, Murphy, and Fristrom, 1972, Dev. Biol. 27: 71-83. cytology: Placed in 5A8-C3 on the basis of its inclusion in Df(1)C149 = Df(1)5A8-9;5C5-6, but not in Df(1)N73 = Df(1)5C2- 3;5D5-6 (Baker and Smith, 1979, Genetics 92: 833-47). # mus106 location: 1- {m - g [Smith et al., 1980, DNA Repair and Mutagenesis in Eukaryotes (Generoso, Shelby, and de Serres, eds.). Plenum, New York, pp. 175-88]}. references: Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506. phenotype: Survival of homozygous and hemizygous larvae hyper- sensitive to exposure to methyl methanesulfonate and gamma rays. Hypermutable to alkylating agents; defective in alkyla- tion repair pathway (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Homozygous females sterile. alleles: A single ethyl-methanesulfonate-induced allele, mus106D1. # mus107D1: see mus109D1 # mus108 location: 1-11. references: Smith, Snyder, and Dusenbery, 1980, DNA Repair and Mutagenesis in Eukaryotes (Generoso, Shelby and de Serres, eds.). Plenum Press, New York, pp. 175-88. phenotype: Survival of homozygous and hemizygous larvae hyper- sensitive to exposure to methyl methanesulfonate (Smith et al.) and gamma rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31). Moderately deficient in post-replication repair (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94). Both premeiotic and meiotic magnification of rRNA sequences inhibited in males (Hawley, Marcus, Cameron, Schwartz, and Zitron, 1985, Proc. Nat. Acad. Sci. USA 82: 8095-99). # mus109 location: 1-30.2. references: Smith, 1976, Mol. Gen. Genet. 149: 73-85. Mason, Green, Shaw, and Boyd, 1981, Mutat. Res. 81: 329-43. phenotype: Strong alleles are recessive lethal; for weaker alleles, survival of homozygous and hemizygous larvae hyper- sensitive to exposure to methyl methanesulfonate (Mason et al.; Smith et al.) and gamma rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31). Exhibits synergistic interac- tion with mus105D1 (Baker, Smith, and Gatti, 1982, Proc. Nat. Acad. Sci. USA 79: 1205-09). Females homozygous for viable alleles are sterile. Causes increased incidence of mwh clones in mwh/+ wings (Baker and Smith, 1979, Genetics 92: 833-47) and chromosome breakage at euchromatic-heterochromatic junc- tions in larval ganglion cells (Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81; Baker, Smith, and Gatti, 1982, Proc. Nat. Acad. Sci. USA 79: 1205-09). alleles: allele origin discoverer synonym ref ( _____________________________________________ mus109A1 EMS Smith 4 mus109D1 EMS Boyd mus107D1 3 mus109D2 EMS Mason 2 mus109lS spont Schalet 1 ( 1 = Baker, Smith, and Gatti, 1982, Proc. Nat. Acad. Sci. USA 79: 1205-09; 2 = Mason, Green, Shaw, and Boyd, 1981, Mutat. Res. 81: 329-43; 3 = Nguyen, Green, and Boyd, 1978, Mutat. Res. 49: 139-43; 4 = Smith, 1976, Mol. Gen. Genet. 149: 73-85. cytology: Placed in 8E-9B2 based on the female sterility of mus109 alleles in combination with Df(1)C52 = Df(1)8E;9C-D but not Df(1)v-L15 = Df(1)9B1-2;10A1-2 (Baker and Smith, 1979, Genetics 92: 833-47). Restricted to 8F3-9A2 by Mason based on refined cytology of the above deficiencies. # mus110A1: see mei-9A1 # mus111 (J.B. Boyd) location: 1-27. origin: Induced by ethyl methanesulfonate. references: Mason, Green, Shaw, and Boyd, 1981, Mutat. Res. 81: 329-43. phenotype: Survival of homozygous and hemizygous larvae hyper- sensitive to exposure to methyl methanesulfonate, nitrogen mustard, gamma rays and X rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31). Homozygous females sterile. # mus201 location: 2-23 (based on 14 recombinants between dp and b). references: Boyd, Snyder, Harris, Presley, Boyd, and Smith, 1982, Genetics 100: 239-57. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, nitrogen mustard, and ultraviolet light; weakly hypersensitive to X rays. Female fertility unimpaired, and meiotic disjunction regular. Homozygotes devoid of detectable excision repair (Boyd et al.; Dusenbery, McCormick, and Smith, 1983, Mutat. Res. 112: 215-30); postreplication repair and repair of single-strand breaks induced by X rays normal. Hypermutable to alkylating agents (Smith and Dusen- berg, 1988, Mechanisms and Consequences of DNA Damage Process- ing, Alan R. Liss, Inc., pp. 251-55). Mutant defect rescued by transformation with the endonuclease V gene (denV) of bac- teriophage T4 (Banga, Boyd, Valerie, Harris, Kurz, and de Riel, 1989, Proc. Nat. Acad. Sci. USA 86: 3227-31). alleles: Two alleles: mus201A1, recovered by Smith among chro- mosomes treated with ethyl-methanesulfonate by Hardy and Orevi; and mus201D1 (Boyd, Golino, Shaw, Osgood and Green, 1981, Genetics 97: 607-23). # mus202 location: 2- (not located). origin: Induced by ethyl methanesulfonate. references: Snyder and Smith, 1982, Mol. Gen. Genet. 188: 249-55. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, nitrogen mustard, formaldehyde, ultraviolet light, and X rays. Fecundity of homozygous females reduced, although partial rescue effected by fertilization with sperm carrying mus202+. X-chromosome disjunction regular; slight increase in the number of fourth-chromosome exceptions noted. alleles: One allele, mus202A1. # mus203 location: 2- (not located). origin: Induced by ethyl methanesulfonate. references: Snyder and Smith, 1982, Mol. Gen. Genet. 188: 249-55. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, nitrogen mustard, formaldehyde, ultraviolet light, and X rays. Fecundity of homozygous females reduced, although partial rescue effected by fertilization with sperm carrying mus203+. Small but significant increase in X- and fourth-chromosome nondisjunction in the first but not the second meiotic division; X-chromosome recombination reduced to 80% normal levels. alleles: One allele, mus203A1. # mus204 location: 2- (not located). origin: Induced by ethyl methanesulfonate. references: Snyder and Smith, 1982, Mol. Gen. Genet. 188: 249-55. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, formaldehyde, and ultraviolet light, weakly sensitive to nitrogen mustard, but insensitive to X rays. Hypermutability to alkylating agents; defective both in alky- lation and UV excision repair pathways (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Fecundity of homozygous females reduced, although partial rescue effected by fertili- zation with sperm carrying mus204+. Small but significant increase in X- and fourth-chromosome nondisjunction in the first but not the second meiotic division; X-chromosome recom- bination reduced to 80% normal levels. alleles: One allele, mus204A1. # mus205 location: 2-54.9 origin: Induced by ethyl methanesulfonate. references: Snyder and Smith, 1982, Mol. Gen. Genet. 188: 249-55. Henderson, Bailey, Sinclair, and Grigliatti, 1987, Mutat. Res. 177: 83-93. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate and ultraviolet light, moderately sensitive to benzo[a]pyrene, but not to formaldehyde, nitrogen mustard or ionizing radiation. Partially deficient in excision repair (Boyd and Harris, 1981, Chromosoma 97: 607-23) and postrepli- cation repair (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94; Brown, and Boyd, 1981, Mol. Gen. Genet. 183: 356-62). Displays hypermutability to alkylating agents; defective both in alkylation and UV excision repair pathways (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Fecundity of homozygous females reduced, although partial rescue effected by fertilization with sperm carrying mus205+. X- chromosome disjunction regular; slight increase in the number of fourth-chromosome exceptions noted. alleles: Two alleles, mus205A1 and mus205B1 (Henderson et al.). # mus206 location: 2- (not located). origin: Induced by ethyl methanesulfonate. references: Snyder and Smith, 1982, Mol. Gen. Genet. 188: 249-55. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, nitrogen mustard, and ultraviolet light, but not to formaldehyde or X rays. Partially deficient in postre- plication repair (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94). Hypermutability to alkylating agents; defec- tive in alkylation repair pathway (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Fecundity of homozygous females nor- mal. alleles: One allele, mus206A1. # mus207 location: 2- (not located). origin: Induced by ethyl methanesulfonate. references: Snyder and Smith, 1982, Mol. Gen. Genet. 188: 249-55. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, nitrogen mustard, and ultraviolet light; weakly sensitive to formaldehyde and X rays. Hypermutability to alkylating agents; defective in alkylation repair pathway (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Fecundity of homozygous females normal. alleles: One allele, mus207A1. # mus208 location: 2-89. origin: Induced by ethyl methanesulfonate. references: Henderson, Bailey, Sinclair, and Grigliatti, 1987, Mutat. Res. 177: 83-93. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, N-acetyl-2-aminofluorene (mus208B2 only weakly sensitive), and benzo[a]pyrene; slight allele-specific sensitivity to nitrogen mustard, and gamma rays. alleles: Two alleles, mus208B1 and mus208B2. # mus209 location: 2-92.8. origin: Induced by ethyl methanesulfonate. references: Henderson, Bailey, Sinclair, and Grigliatti, 1987, Mutat. Res. 177: 83-93. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate and gamma rays, but not to N-acetyl-2- aminofluorene, benzo[a]pyrene, or nitrogen mustard. alleles: One allele, mus209B1. # mus210 location: 2-69.1. origin: Induced by ethyl methanesulfonate. synonym: mus(2)201GI (mus201 preoccupied); mus212. references: Khromykh and Zakharov, 1981, Genetika (Moscow) 17: 658-66. Luchkina, Khromykh, and Sharigin, 1982, Genetika (Moscow) 18: 625-33. Levina and Sharigin, 1984, Genetika (Moscow) 20: 416-24. Henderson, Bailey, Sinclair, and Grigliatti, 1987, Mutat. Res. 177: 83-93. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, N-acetyl-2-aminofluorene, and benzo[a]- pyrene, moderately sensitive to nitrogen mustard, and insensi- tive to gamma rays. Excision of pyrimidine dimers impaired; 4-5 fold decrease in activity of ultra-violet-specific endonu- clease observed in primary cell cultures. alleles: Two alleles, mus210B1 and mus210G1. # mus211 location: 2-47 (alleles mapped to 50.4 and 44.7). origin: Induced by ethyl methanesulfonate. references: Henderson, Bailey, Sinclair, and Grigliatti, 1987, Mutat. Res. 177: 83-93. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate, nitrogen mustard, and gamma rays; insensi- tive to N-acetyl-2-aminofluorene and benzo[a]pyrene. alleles: Two alleles, mus211B1 and mus211B2. # mus212: see mus210 # mus301 (J.B. Boyd) location: 3-23 (between ru and h). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to X rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31), methyl methanesulfonate, and nitrogen mustard. When fertile, homozygous females exhibit elevated frequencies of nondisjunc- tion. alleles: allele origin discoverer comments ____________________________________________ mus301D1 EMS Boyd fertile mus301D2 EMS Boyd male sterile mus301D3 EMS Boyd male sterile mus301D4 EMS Boyd female sterile mus301D5 EMS Boyd fertile # mus302 (J.B. Boyd) location: 3-45 (between st and cu). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to X rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31), methyl methanesulfonate, and nitrogen mustard. Postreplication repair deficient (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94); partially excision deficient (Boyd and Harris, 1981, Chromosoma 97: 607-23). Homozygotes exhibit increased X-ray-induced chromosome loss in postmeiotic cells (Cooper and Zimmering, 1981, Mutat. Res. 81: 345-56), increased sex- chromosome loss following treatment of males with procarbazine and diethylnitrosamine (Zimmering, 1982, Mutat. Res. 103: 141-44), and decreased incorporation of DNA precursors following ultra-violet irradiation (Brown, and Boyd, 1981, Mol. Gen. Genet. 183: 356-62). alleles: allele origin discoverer comments ________________________________________________ mus302D1 EMS Boyd mus302D2 EMS Boyd homozygous sterile mus302D3 EMS Boyd mus302D4 EMS Boyd mus302D5 EMS Boyd mus302D6 EMS Boyd # mus304 (J.B. Boyd) location: 3-46 (between st and cu). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate and nitrogen mustard. Neither hypermutable to alkylating agents nor defective in alkylation repair path- way; however, defective in UV-damage repair pathway (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). When fertile, homozygous females exhibit uniformly decreased recombination along the X chromosome (Green, 1982, Biol. Zentralbl. 101: 223-26). Partially deficient in post-replication repair (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94) and exci- sion (Boyd and Harris, 1981, Chromosoma 97: 607-23); DNA syn- thesis modified (Boyd and Shaw). alleles: allele origin discoverer comments _______________________________________________ mus304D1 EMS Boyd female fertile mus304D2 EMS Boyd female sterile mus304D3 EMS Boyd female fertile; sensitive only to MMS # mus305 (J.B. Boyd) location: 3-44 (between st and cu). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to X rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31), methyl methanesulfonate, and nitrogen mustard. Homozygous females display elevated rates of nondisjunction. alleles: allele origin discoverer comments __________________________________________ mus305D1 EMS Boyd mus305D2 EMS Boyd male sterile mus305D3 EMS Boyd # mus306 (J.B. Boyd) location: 3-56 (between cu and sr). origin: Induced by ethyl methanesulfonate. references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival sensitive to exposure to methyl methanesulfonate. Displays hypermutability to alkylating agents; defective both in alkylation and UV excision repair pathways (Smith and Dusenberg, 1988, Mechanisms and Conse- quences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Homozygotes fertile. Partially excision deficient (Boyd and Harris, 1981, Chromosoma 97: 607-23). alleles: One allele, mus306D1. # mus307 (J.B. Boyd) location: 3-59 (between cu and sr). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to X rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31), methyl methanesulfonate, and nitrogen mustard. Homozygotes fertile. Modified DNA synthesis (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94). alleles: One allele, mus307D1. # mus308 (J.B. Boyd) location: 3-55 (between cu and sr). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to X rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31), and nitrogen mustard. Partially deficient in post-replication repair (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94) and excision (Boyd and Harris, 1981, Chromosoma 97: 607-23); DNA synthesis modified (Boyd and Shaw). Displays hypermuta- bility to alkylating agents; defective both in alkylation and UV excision repair pathways (Smith and Dusenberg, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Defective in levels of nuclease 3, which is apparently active in the repair of DNA cross links (Boyd, Sakaguchi, and Harris, 1990, Genetics 125: 813-19). alleles: allele origin discoverer comments __________________________________________ mus308D1 EMS Boyd homozygous fertile mus308D2 EMS Boyd mus308D3 EMS Boyd male sterile mus308D4 EMS Boyd male sterile mus308D5 EMS Boyd male sterile mus308D6 EMS Boyd male sterile # mus309 (J.B. Boyd) references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate and nitrogen mustard. alleles: allele origin discoverer comments ____________________________________________ mus309D1 EMS Boyd homozygous sterile mus309D2 EMS Boyd female sterile mus309D3 EMS Boyd # mus310 (J.B. Boyd) location: 3-47 (between st and cu). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate. Post-replication repair deficient with modified DNA synthesis (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94); reduced incorporation of DNA precursors follow- ing ultra-violet treatment (Brown, and Boyd, 1981, Mol. Gen. Genet. 183: 356-62). Displays hypermutability to alkylating agents; defective both in alkylation and UV excision repair pathways (Smith and Dusenberg, 1988, Mechanisms and Conse- quences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). alleles: One allele, mus310D1. # mus311 (J.B. Boyd) location: 3-47 (between st and cu). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to methyl methanesulfonate. Post-replication repair deficient with modified DNA synthesis (Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94). When fertile, females produce elevated rates of nondisjunction. alleles: allele origin discoverer comments ____________________________________________ mus311D1 EMS Boyd female sterile mus311D2 EMS Boyd female fertile mus311D3 EMS Boyd female fertile # mus312 (J.B. Boyd) location: 3-18 (between ru and h). references: Boyd, Golino, Shaw, Osgood and Green, 1981, Genet- ics 97: 607-23. phenotype: Larval survival hypersensitive to exposure to X rays (Oliveri, Harris, and Boyd, 1990, Mutat. Res. 235: 25-31), methyl methanesulfonate, and nitrogen mustard. Reduces meiotic recombination (Green, 1981, Chromosoma 82: 259-66). alleles: allele origin discoverer comments ________________________________________________ mus312D1 EMS Boyd homozygous fertile mus312D2 EMS Boyd male sterile # Muscle myosin heavy chain: see Mhc # Muscle protein: see Mp # Muscle specific proteins: see Msp # mushroom-body-defect: see mud # mushroom-body-deranged: see mbd # mushroom-body-miniature: see mbm # mussed: see mu # mutability factor from Florida: see mu-F # mutagen sensitive: see mus # mutator: see mu # mw: mottler of white location: 1-30.9. references: 1946, DIS 20: 88-89. Gelbart, 1971, Genetics 68: s22. Birchler, 1986, Genetics 113: s47. Birchler, Hiebert, and Rabinow, 1989, Genes Dev. 3: 73-84. phenotype: Normal by itself. A specific dilutor of wa and other intermediate alleles at the w locus. Eyes assume a lighter mottled appearance. Affects wa and seven other inter- mediate alleles (Gelbart), including wa4, wbf, wh wsp55, and z wzm (Birchler); without effect on other intermediate alleles. Sensitive alleles are insertion alleles as determined by Zachar and Bingham (1982, Cell 30: 529-41); at least six dif- ferent transposable elements involved. Insensitive w alleles are not insertion mutants. Expression not affected by dosage of Y chromosome (Oster, 1957, DIS 31: 150). RK1. alleles: allele origin discoverer ref ( __________________________________________ mw1 spont Muller, 1946 4 mw2 spont Gelbart 3 mw2a | dysgenesis Birchler 2 mw3P dysgenesis Birchler 1 ( 1 = Birchler, 1986, Genetics 113: s47; 2 = Birchler, Hiebert, and Rabinow, 1989, Gene Dev. 3: 73-84; 3 = Gel- bart, 1972, Genetics 68: s22; 4 = Muller, 1946, DIS 20: 88-89. | wa mw2a/Y males not mottled like other wa mw/Y males (Birchler et al., 1989). cytology: Located between 9A2 and 9B1 on the basis of being covered by Dp(1;2)v+75d = Dp(1;2)9A2; 10C2; 40-41 and not being deleted by Df(1)v-L15 = Df(1)9B1;10A1. (Birchler et al., 1989). # mwg: microwing location: 2- (left arm). origin: Spontaneous. references: Moran and Neeley, 1971, DIS 46: 43. phenotype: Wings reduced in size, extending slightly beyond scutellum; only proximal regions of veins obvious; wings usu- ally curled or curved at posterior margins, often filled with fluid. Halteres slightly shorter than normal. Homozygous females fully fertile. mwh: multiple wing hairs Wing hairs. Left: wild type. Right: mwh. A. Di Pasquale, unpublished. # mwh: multiple wing hairs location: 3-0.3 [between fap and ru (Robertson and Riviera, 1972, DIS 48: 21; Roberts and Evans-Roberts, 1979, Genetics 93: 663-79). See also Strommer and Falk (1980, DIS 56: 196)]. origin: Spontaneous. discoverer: di Pasquale, 50l. references: 1951, DIS 25: 70. 1952, Rend. Ist. Lombardo Sci. Lettere, Ser. B 85: 1-8. Peyer and Hadorn, 1965, Arch. Julius Klaus-Stift. Vererbungs- forsch. Sozialanthropol. Rassenhyg. 40: 19-26 (fig.). phenotype: Affects the trichomes (hairs) of all body regions in the same general way: An increase in the number of elements is correlated with a reduction in length and a disturbance of orientation. Aristae and bracts are included in this pattern; bristles and other sensilla are not. Wing cells contain groups of 2-7 hairs instead of one hair per cell as in wild type; causes supernumerary trichomes over entire integument, but tufts of trichomes only in wing blade (Ouweneel, 1970, Genetica 41: 1-20); may be supernumerary hairs and sensilla on halteres (Ouweneel and van der Meer, 1972, Wilhelm Roux's Arch. Entwicklungsmech. Org. 172: 149-61). Also causes disr- uption of polarity in legs, wings, and halteres; may disrupt orientation of hairs on leg without affecting their numbers (Bryant and Schneiderman, 1969, Dev. Biol. 20: 263-90); tri- chomes on wings tend to diverge from vein L3 rather than parallel it as in wild type (Gubb and Garcia-Bellido, 1982, J. Embryol. Exp. Morphol. 68: 37-57). mwh/+ develop mwh pheno- type following heat shock at or just prior to the time of cell-hair-extrusion (Mitchell and Petersen, 1984, Genetics 107: s74). Transplants of mutant wing disks to wild-type hosts develop autonomously (Ursprung and Hadorn, 1962, Dev. Biol. 4: 40-60). Widely used as a cell marker in the analysis of cuticular clones. The frequency of mwh spots after somatic recombination in mwh/+ flies increases with increase in the temperature at which the larvae and pupae are raised (Graf, 1986, DIS 63: 65). RK1. cytology: Placed in 61E2-62A3 (Roberts and Evans-Roberts). #*mwhsemi: multiple wing hairs-semi origin: Spontaneous derivative of mwh. discoverer: di Pasquale, 51e. phenotype: Like mwh except that the groups of wing hairs are restricted to wing margins. Cells of wing surface between second and fifth longitudinal veins have single hair with only an occasional group. mwhsemi/mwh is like mwhsemi/mwhsemi. RK1. #*mwi: misheld wings location: 1-0.4. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 72. phenotype: Wings diverge upward and outward at various angles. Eye shape oval. Viability and fertility good in male and reduced in female. RK2. # Myb: Myb proto-oncongene sequence location: 1- {50}. origin: Isolated from genomic library using the c-myb sequence as probe. references: Katzen, Kornberg, and Bishop, 1985, Cell 41: 449- 56. phenotype: Considered to be the Drosophila homologue of avian c-myb. Open reading frame identified to date encodes a polypeptide exhibiting 73% homology with chicken c-myb pro- tein. molecular biology: Cloned region of homology (probably < half the total) sequenced; 67% identity (253/375 residue) with chicken c-myb nucleotide sequence. Drosophila C-myb appears to lack two upstream exons present in chicken; the portion cloned comprises a single open reading frame, lacking two introns present in the homologous genomic sequence of the chicken. Homologous transcripts of 3.8 (predominantly) and 3.0 kb found in Drosophila embryos. cytology: Probe hybridizes to the 13E-F boundary. # Myc: Myc proto-oncogene sequence location: 2- {58}. origin: Isolated from a genomic library using N-myc probe from human neuroblastoma. references: Voss, Strand, Anderson, Nystrom, Spiver, and McDonald, 1986, Genetics 113: s37. cytology: Located to 44A by in situ hybridization. molecular biology: Homologous to a major 7 kb transcript as well as six less abundant transcripts ranging in size from 2-5 kb. # Myofibrillar contractile protein: see Mfcp # myofibrillar defective: see mfd # Myosin heavy chain: see Mhc # Myosin heavy chain-cytoplasmic: see Mhc-c # Myosin light chain: see Mlc # mys: myospheroid location: 1-21.7. references: Rizki, 1956, J. Exp. Zool. 131: 203-22 (fig.). Wright, 1958, Proc. Intern. Congr. Genet., 10th., Vol. 2: 323. 1960, J. Exp. Zool. 143: 77-99 (fig.). Leptin, Bogaert, Lehman, and Wilcox, 1989, Cell 56: 401-08. phenotype: Structural gene for the | subunit of position- specific integrins 1 and 2, PS1 and PS2. Twenty-hour embryos (25) show middorsal herniation of brain and midgut, or both; abnormal somatic, visceral, and pharyngeal muscles; and incom- plete morphogenesis of yolk-filled midgut. Development of embryo normal up to 13 hr, even in embryos produced from homozygous germ-line clones (Wieschaus and Noell, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 63-73). Between 13 and 14.5 hr the first muscular contractions occur, while basement membrane is incomplete. This results in dorsal rupture of hypoderm and retraction of myogenic elements of somatic and pharyngeal muscles into spheroidal masses. Continuation of myogenesis produces spheroidal muscles with a cortex of disoriented fibrillae surrounded by a medulla of nucleated sarcoplasm. Homozygous clones of mys11 on either surface of the wing lead to separation of the two surfaces of the mem- brane and the formation of blisters in the vicinity of the clone [Brower and Jaffe, 1989, Nature (London) 342: 285-87]. Western blots with antibodies specific to the | subunit of Drosophila PS integrins detects no | integrin in mys10, mys11, and Df(1)C128; in addition, PS1( is not cleaved properly in these genotypes, nor do ( chains become localized in mutant embryos. PS| expression in wild type is diffuse in early embryos, becoming localized between the mesodermal and ecto- dermal layers at the extended-germ-band stage; also seen at interfaces between epidermal cells and deep in the interseg- mental grooves where intersegmental muscles attach. In late embryos antibody staining is seen at basal surface of entire gut epithelium and is also concentrated at muscle attachment sites. alleles: allele origin discoverer synonym ref ( comments ______________________________________________________________________ mys1 32P Poulson 48j l(1)48j 4, 7, 8 mys2 EMS l(1)40 2 mys3 EMS Lefevre l(1)DA548 3 mys4 EMS Lefevre l(1)DA573 3 mys5 EMS Lefevre l(1)EF484 3 mys6 EMS Lefevre l(1)VA333 3 mys7 EMS Lefevre l(1)VE609 3 mys8 EMS nj42 5 adults survive as nonjumpers mys9 P l(1)L74 1 roo insert at 21.7 to 23.4 kb mys10 EMS l(1)mysxB87 6 mys11 EMS l(1)mysxG43 6 mys12 EMS 6 mys13 EMS 6 mysts1 EMS Wright 9 E, L mysts2 EMS Wright 9 E, L mysts3 EMS Wright 9 E ( 1 = Digan, Haynes, Mozer, Dawid, Forquignon, and Gans, 1986, Dev. Biol. 114: 161-69; 2 = Gans, Audit, and Masson, 1975, Genetics 81: 683-704; 3 = Lefevre and Watkins, 1986, Genet- ics 113: 869-95; 4 = Rizki, 1956, J. Exp. Zool. 131: 203- 22 (fig.); 5 = Thomas, 1982, Neurosci. Abstr. 6: 742; 6 = Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Roux's Arch. Dev. Biol. 193: 296-307; 7 = Wright, 1958, Proc. Int. Congr. Genet., 10th, Vol. 2: 323; 8 = Wright, 1960, J. Exp. Zool. 143: 77-99 (fig.); 9 = Wright, 1968, Proc. Int. Congr. Genet., 12th, Vol. 1: 141. cytology: Placed in 7D1-6 based on its inclusion in Df(1)C128 = Df(1)7D1;7D5-6. molecular biology: Gene localized in an eighty-kilobase walk by virtue of the roo insert associated with mys9; the position of the insert is in a 1.7 kb restriction fragment between 21.7 and 23.4 kb distal to the first Sma1 site proximal to Df(1)C128, which is designated as the 0 coordinate. mys2, mys5 and mys8 have no gross molecular lesion (Digan et al.). Sequences from this region identify a 4.4-kb mRNA on Northern blots; cDNA clones provide a sequence accounting for a message of such length; the conceptual amino-acid sequence contains a 23-amino acid N-terminal signal sequence and a single 23- amino-acid hydrophobic membrane-spanning domain, and specifies an 846-amino-acid polypeptide of 90 kd following removal of the signal sequence; there are six consensus sites for glycosylation of asparagine residues. The molecule contains 56 cystein residues arranged into cystein-rich motifs charac- teristic of the vertebrate family of | integrins. Overall it displays 45% identity with chicken | integrin with substantial segments in both the intracellular and extracellular domains showing up to 95% identity (MacKrell, Blumberg, Haynes, and Fessler, 1988, Proc. Nat. Acad. Sci. USA 85: 2633-37.