#*me: focal melanosis location: 1-29.0. origin: X ray induced. discoverer: Gowen, 1928. references: 1934, Arch. Pathol. 17: 638-47 (fig.). 1934, Cold Spring Harbor Symp. Quant. Biol. 2: 128-36 (fig.). phenotype: Melanotic degeneration occurs at junction of tibia and femur. Lethal at end of pupal stage or shortly after eclosion. RK2. # Me: Moire location: 3-19.2 (to the left of jv; based on location of Me65d). synonym: Mo. phenotype: Eye has watered-silk, shimmering, iridescent pattern owing to a ring of six flecks around normal fleck. Eye color brownish and translucent; 79% normal red pigment and 85% nor- mal brown pigment (Nolte, 1955, J. Genet. 53: 1-10). Larval Malpighian tubes considerably lighter in color than normal but mutant classifiable with difficulty (Brehme and Demerec, 1942, Growth 6: 351-56). Contains a modifier of dominance of dp such that dp/+; Me/+ has truncated wings. Classifiable in single dose in triploids (Schultz, 1934, DIS 1: 55). Homozy- gous lethal. Me/In(3L)P is viable. RK1A. allele: allele origin discoverer ref ( comments _______________________________________________________________ Me1 X ray Muller, 1929 3, 4, 5 *Me2 X ray Moore, 1929 3 T(2;3)Me Me65d EMS E.H. Grell 65d 2 light bristle tips *MeSo Sytko 1 T(2;3)MeSo ( 1 = Agol, 1936, DIS 5: 7; 2 = CP627; 3 = Glass, 1933, J. Genet. 28: 69-112; 4 = Glass, 1934, Am. Nat. 68: 107-14; 5 = Muller, 1930, J. Genet. 22: 299-334 (fig.). cytology: Placed in region 64C12-65E1 on the basis of its inclusion in Df(3L)Vn = Df(3L)64C12-D1;65D2-E1 (Mohr, 1938, Avh. Nor. Vidensk.-Akad. Oslo, Mat. Naturvidensk. Kl. No. 4: 1-7). Associated with In(3L)P = In(3L)63C;72E1-2 (Morgan, Bridges, and Schultz, 1937, Year Book - Carnegie Inst. Wash- ington 36: 301). #*meg: megaoculus location: 1-61.9. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 71. phenotype: Eyes large, abnormally shaped, and rough. Wings abnormally shaped and sometimes extremely small. Wing surface irregularly curved. Inner margin removed to various degrees and venation abnormal. Viability good; both sexes infertile. RK2. other information: One allele induced by CB. 3025. # mei-1: meiotic mutant 1 (J. Valentin) location: 3-45-55. references: Valentin, 1973, Hereditas 75: 5-22. Baker, Carpenter, Esposito, Esposito, and Sandler, 1976, Ann. Rev. Genet. 10: 53-134. phenotype: Reduces exchange on the X chromosome in females by approximately 50% but has little or no effect on autosomal recombination. Recombination is decreased most severely in the central region of the X with more normal frequencies occurring proximally and distally. X chromosome nondisjunc- tion is increased only slightly in mei-1 females, while the fourth chromosomes disjoin quite regularly. # mei-9 (R.S. Hawley) location: 1-6.5. references: Baker and Carpenter, 1972, Genetics 71: 255-86. Carpenter and Sandler, 1974, Genetics 76: 453-75. Boyd, Golino, and Setlow, 1976, Genetics 84: 527-44. Smith, 1976, Mol. Gen. Genet. 149: 73-85. Nguyen and Boyd, 1977, Mol. Gen. Genet. 158: 141-47. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. Baker and Smith, 1979, Genetics 92: 833-47. Carpenter, 1979, Chromosoma 75: 259-92. Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81. Graf, Vogel, Biber, and Wurgler, 1979, Mut. Res. 59: 129-33. Lutken and Baker, 1979, Mut. Res. 61: 221-27. Baker, Gatti, Carpenter, Pimpinelli, and Smith, 1980. DNA Repair in Eukaryotes (Generoso, Shelby, and deSerres, eds.). Plenum Press, New York, London, pp. 189-208. Lawlor, 1980, DIS 55: 81. Smith, Snyder, and Dusenberry, 1980. DNA Repair in Eukaryotes (Generoso, Shelby, and deSerres eds.). Plenum Press, New York, London, pp. 175-88. Carpenter, 1982, Proc. Nat. Acad. Sci. USA 79: 5961-65. phenotype: mei-9 alleles confer sensitivity to mutagens as a consequence of a defect in excision repair (Boyd et al., 1976; Nguyen and Boyd, 1977). This defect in DNA repair is also manifested by a high frequency of mitotic chromosome breakage and instability (Baker et al., 1978; Gatti, 1979). For exam- ple, larval neuroblasts of mei-9/Y males display a high fre- quency of spontaneous chromosome breaks in both the eu- and heterochromatin (Gatti, 1979). Females homozygous for mei-9 show greatly reduced levels of meiotic exchange. However, the residual exchanges are distributed as in wild-type and chiasma interference is maintained. mei-9 is thus considered to be defective in the exchange process itself, rather than in the establishment of the preconditions for exchange (Carpenter and Sandler, 1974). mei-9a and mei-9b have also been assayed with respect to their effects on gene conversion at the rosy locus (Carpenter, 1982). Although neither allele reduces the fre- quency of gene conversion events, both produce post-meiotic segregation events (i.e., mosaic progeny) at high frequency. Thus, the recombinational phenotype of mei-9 involves two com- ponents, namely a decrease in the frequency of heteroduplex repair and a decrease in the frequency of reciprocal exchange. At the ultrastructural level, both synaptonemal complex mor- phology and the number and distribution of recombination nodules are normal in mei-9 females (Carpenter, 1979); but see Boyd et al. (1976). As a consequence of the decreased fre- quency of reciprocal exchange, mei-9 females display greatly elevated frequencies of meiotic nondisjunction and chromosome loss (Baker and Carpenter, 1972). Meiotic chromosome behavior in males is not affected. Nor is there any effect of mei-9 on spontaneous recombination in males (Lutken and Baker, 1979). Neither hypermutable to alkylation nor deficient in excision repair (Smith and Dusenberry, 1988, Mechanisms and Conse- quences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). alleles: Baker and Smith (1979) demonstrated that the mus- 110AT1, mus-110AT2, and mus-110AT3 mutations (Smith 1976) are alleles of mei-9. These mutations have been renamed as mei- 9A1, mei-9A2, and mei-9A3, respectively. mei-9L1, also known as mut159, was identified by Graf et al. (1979). mutagen reduces mitotic allele reference sensitive exchange instability2, 4, 6 _____________________________________________________________ mei-9a 1, 5 + + + mei-9b 1 + + + mei-9A1 | 4, 9 + + + mei-9A2 9 + + mei-9A3 9 + + mei-9D1 8 + + mei-9D2 3, 8 + + mei-9D3 3, 8 + + mei-9D4 3, 8 + + mei-9L1 7 + + ( 1 = Baker and Carpenter, 1972, Genetics 71: 255-86; 2 = Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531- 78; 3 = Baker, Gatti, Carpenter, Pimpinelli, and Smith, 1980, DNA Repair in Eukaryotes (Generoso, Shelby, and deSerres, eds.). Plenum Press, New York, London, pp. 189- 208; 4 = Baker and Smith, 1979, Genetics 92: 833-47; 5 = Boyd, Golino, and Setlow, 1976, Genetics 84: 527-44; 6 = Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81; 7 = Graf, Vogel, Biber, and Wurgler, 1979, Mut. Res. 59: 129-33; 8 = Mason, Green, Shaw, and Boyd, 1981, Mut. Res. 81: 329-43; 9 = Smith, 1976, Mol. Gen. Genet. 149: 73-85. | Synonym: mus110A1. cytology: Placed in 4B3-C1 based on its inclusion in Df(1)bi-D1 = Df(1)4B3-4;4D1-2 but not in Df(1)rb41 = Df(1)4B6-C1;4C7-8 (Banga, Bloomquist, Brodberg, Pye, Larrivee, Mason, Boyd, and Pak, 1986, Chromosoma 93: 341-46). # mei-41 (R.S. Hawley) location: 1-54.2. references: Baker and Carpenter, 1972, Genetics 71: 255-86. Carpenter and Sandler, 1974, Genetics 76: 453-75. Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 352-434. Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506. Boyd and Setlow, 1976, Genetics 84: 507-26. Smith, 1976, Mol. Gen. Genet. 149: 73-85. Mohler, 1977, Genetics 85: 259-72. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. Baker and Smith, 1979, Genetics 92: 833-47. Carpenter, 1979, Chromosoma 75: 259-92. Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81. Nguyen, Boyd, and Green, 1979, Mut. Res. 63: 67-77. Mason, Green, Shaw, and Boyd, 1981, Mut. Res. 81: 329-43. Boyd and Shaw, 1982, Mol. Gen. Genet. 186: 289-94. Hawley and Tartof, 1983, Genetics 104: 63-80. Hawley, Marcus, Cameron, Schwartz, and Zitron, 1985, Proc. Nat. Acad. Sci. USA 82: 8095-99. Banga, Bloomquist, Brodberg, Pye, Larrivee, Mason, Boyd, and Pak, 1986, Chromosoma 93: 341-46. Mason, Scobie, and Yamamoto, 1989, Mol. Gen. Genet. 215: 190-99. phenotype: mei-41 alleles confer sensitivity to mutagens as a consequence of a defect in a caffeine-sensitive post- replication repair pathway (Boyd and Setlow, 1976; Boyd et al., 1976; Boyd and Shaw, 1982). This defect in DNA repair is also manifested by a high frequency of mitotic chromosome breakage and instability (Baker et al., 1978; Gatti, 1979). mei-411 not hypermutable to alkylation nor defective in exci- sion repair; yet mei-41D12 displays hypermutability to alkyla- tion and defective alkylation excision repair (Smith and Dusenberry, 1988, Mechanisms and Consequences of DNA Damage Processing, Alan R. Liss, Inc., pp. 251-55). Allelism based on lack of complementation (Mason, Scobie, and Yamamoto, 1989, Mol. Gen. Genet. 215: 190-99). Most alleles of mei-41 also reduce female fertility and in some cases are female-sterile as homozygotes. Females homozygous for the more fertile alleles of mei-41 exhibit reduced levels of meiotic exchange. The observed reductions in exchange are not uniform, but rather are most extreme in distal regions. Chiasma interfer- ence is also diminished (Carpenter and Sandler, 1974; Baker and Hall, 1976). These reduced levels of exchange allow for high frequencies of meiotic loss and nondisjunction (see Baker and Hall, 1976). Ultrastructural analysis of pachytene in mei-41 and mei-412 females demonstrates a reduced number of late recombination nodules which are distributed in a fashion that parallels residual exchange events (Carpenter, 1979). Over half of those nodules which are observed are morphologi- cally abnormal and are associated with unusual regions of relatively uncondensed chromatin. Stocks in which mei-41 is carried in the male are frequently observed to carry or acquire a bb mutation on the mei-41-bearing X chromosome (Haw- ley and Tartof, 1983). Several alleles of mei-41 have also been shown to inhibit rDNA magnification in the male germline (Hawley and Tartof, 1983; Hawley et al., 1985). Moreover, mei-41 males undergoing magnification also produce a high fre- quency of X-Y exchanges which result from one break within the X-chromosome rDNA cluster and the other at any of a large number of sites on the Y chromosome (Hawley and Tartof, 1983). alleles: More than fifty alleles of this locus have been recovered. This includes the mus-103 and mus-104 mutations which were shown by Mason et al. (1989) to be allelic to mei- 41. The most commonly used alleles are listed in the table below. A fine structure map of the locus is presented in Mason et al. (1989). reduces female mitotic allele synonym ref ( exchange fertility instability | ______________________________________________________________ mei-41 1 ++ reduced + mei-412 mei-41195 1 ++ reduced + mei-41D1 2 sterile mei-41D2 2 + reduced mei-41D3 2 sterile mei-41D4 2 sterile mei-41D5 2-4 + reduced mei-41D6 3 + reduced mei-41D7 3 + reduced mei-41D8 3 + reduced mei-41D9 3 - fertile mei-41D10 3 - reduced mei-41D11 3 sterile mei-41D12 mus103D1 1a, 4 - fertile + mei-41D13 mus103D2 1a, 4 - + mei-41D14 mus104D1 2, 4 - fertile + mei-41D15 mus104D2 3, 4 mei-41D16 mus104D3 2, 4 mei-41D17 mei-41A1-A17 7 reduced mei-41D18 mei-4112-1007 3, 4 sterile mei-41D19 mei-41AM 3, 6 sterile ( 1 = Baker and Carpenter, 1972, Genetics 71: 255-86; 1a = Boyd, Golino, Nguyen, and Green, 1976, Genetics 84: 485-506; 2 = Boyd, Golino, and Setlow, 1976, Genetics 84: 527-44; 3 = Mason, Green, Shaw, and Boyd, 1981, Mut. Res. 81: 329-43; 4 = Mason, Scobie, and Yamamoto, 1989, Mol. Gen. Genet. 215: 190-99; 5 = Mohler, 1977, Genetics 85: 259-72; 6 = Nguyen, Boyd, and Green, 1979, Mut. Res. 63: 67-77; 7 = Smith, 1976, Mol. Gen. Genet. 149: 73-85. | Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81. cytology: Placed in 14C4-6 by deficiency analysis (Banga and Boyd). # mei-218 (R.S. Hawley) location: 1-56.2 (Whyte and Hawley, unpublished data). references: Baker and Carpenter, 1972, Genetics 71: 255-86. Carpenter and Sandler, 1974, Genetics 76: 453-75. Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 352-434. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. Sandler and Szauter, 1978, Genetics 90: 699-712. Carpenter, 1979, Chromosoma 75: 259-92. Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81. Lutken and Baker, 1979, Mut. Res. 61: 221-27. Carpenter, 1982, Proc. Nat. Acad. Sci. USA 79: 5961-65. Carpenter and Baker, 1982, Genetics 101: 81-89. Carpenter, 1984, Cold Spring Harbor Symp. Quant. Biol. 49: 23-29. Carpenter, 1989, Genome 31: 74-80. phenotype: Females homozygous for mei-218 exhibit reduced lev- els of meiotic exchange. The residual exchanges are distri- buted such that the probability of euchromatic exchange becomes more nearly proportional to the polytene-chromosome length (Baker and Carpenter, 1972; Carpenter and Sandler, 1974; Baker and Hall, 1976). This relaxation of the normal constraints on the distribution of euchromatic exchange is clearly demonstrated by the ability of mei-218 females to allow exchange between the normally achiasmate fourth chromo- somes (Sandler and Szauter, 1978). mei-218 does not, however, permit exchanges to occur in heterochromatic intervals (Car- penter and Baker, 1982). Ultrastructural analysis of pachy- tene in mei-218 and mei-2186-7 females demonstrates a reduced number of late recombination nodules (to about 8% of normal), which are distributed in a fashion that parallels the residual exchange events (Carpenter, 1979, 1989). Many of the nodules which are observed are morphologically abnormal. There is also some evidence that early recombination nodules may be either fewer in number or more ephemeral in mei-218 females (Carpenter, 1989). Although mei-218 alleles reduce the fre- quency of reciprocal meiotic exchange, the absolute frequency of gene conversion at the rosy locus is two-fold elevated relative to wild-type controls (Carpenter, 1982, 1984). More- over, co-conversion distances are shorter than those recovered from controls or from mei-9 females (Carpenter, 1984). Thus the function of this locus is required for the generation of reciprocal exchanges and not for gene conversion (Carpenter, 1984). The reduced levels of reciprocal exchange which are characteristic of mei-218 females allow for high frequencies of meiotic loss and nondisjunction (see Baker and Hall, 1976). Nondisjunction occurs at the first meiotic division and only nonexchange chromosomes nondisjoin (Carpenter and Sandler, 1974). All assays for an effect of mei-218 on mitotic chromo- some behavior in males or on somatic chromosome behavior are negative (Baker and Carpenter, 1972; Baker et al., 1978; Lutken and Baker, 1979; Gatti, 1979). alleles: There are two well characterized alleles of this locus: mei-218 (Baker and Carpenter, 1972) and mei-2186-7 (Baker et al., 1978). # mei-195: see mei-41 # mei-251 (R.S. Hawley) location: 1- unlocated. references: Baker and Carpenter, 1972, Genetics 71: 255-86. Baker, Carpenter, Esposito, Esposito, and Sandler, 1976 Annu. Rev. Genet. 10: 53-134. Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 352-434. Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81. Carpenter and Baker, 1982, Genetics 101: 81-89. phenotype: Females homozygous for mei-251 exhibit reduced lev- els of meiotic exchange (to approximately 80% of control lev- els). The residual exchanges are distributed such that the probability of euchromatic exchange becomes more nearly pro- portional to polytene-chromosome length (Baker and Carpenter, 1972; Carpenter and Sandler, 1974; Baker and Hall, 1976). Both X and fourth chromosomal nondisjunction are slightly elevated, presumably as a consequence of decreased recombina- tion. Cytological analysis of larval-neuroblast metaphases reveals no increase in spontaneous mitotic chromosome breakage in the presence of mei-251 (Gatti, 1979). # mei-254: see noda # mei-352 (R.S. Hawley) location: 1- unmapped. origin: Induced by ethyl methanesulfonate. references: Baker and Carpenter, 1972, Genetics 71: 255-86. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 352-434. Carpenter and Baker, 1982, Genetics 101: 81-89. Gatti, 1979, Proc. Nat. Acad. Sci. USA 76: 1377-81. Sandler and Szauter, 1978, Genetics 90: 699-712. phenotype: mei-352 females exhibit near normal levels of mei- otic exchange but the distribution of crossover events is abnormal (i.e., exchanges are more uniformly distributed per unit length than they are in wild-type). This relaxation of the normal constraints on the distribution of euchromatic exchange is clearly demonstrated by the ability of mei-352 females to allow exchange between the normally achiasmate fourth chromosomes (Sandler and Szauter, 1978). mei-352 does not, however, permit exchanges to occur in heterochromatic intervals (Carpenter and Baker, 1982). It remains to be demonstrated that the reduced fertility and the exchange phenotype are the consequence of the same mutational lesion. Although no increase in spontaneous chromosome aberrations was observed upon direct cytological examination of larval neurob- lasts (Gatti, 1979), the mei-352 mutation was shown to increase mitotic chromosome instability approximately three- fold when assayed genetically (Baker et al., 1978). This sug- gests that the mei-352+ gene product is required both during meiosis and mitosis. #*mei-1029 (R.S. Hawley) location: 3- unlocated. references: Szauter, 1984, Genetics 106: 45-71. phenotype: Females homozygous for mei-1029 show reduced levels of meiotic recombination and an abnormal distribution of resi- dual recombination events. X and fourth chromosomal nondis- junction are elevated and occur at the first meiotic division. The observed X chromosome nondisjunction primarily results from the nondisjunction of nonexchange chromosomes. #*mei-1946 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-1966 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-2185 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-2199 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-2220 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-2245 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-2439 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-2593 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-2696 (R.S. Hawley) Entry identical to that of mei-1029. #*mei-B (R.S. Hawley) location: Unlocated, probably 2. references: Bridges, 1915, J. Exp. Zool. 19: 1-21. Bridges, 1929, Carnegie Inst. Wash. Publ. 399: 63-83. Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 352-434. phenotype: Females homozygous for mei-B exhibit reduced levels of meiotic exchange (to approximately 33% of control levels). The reduction in exchange is most severe in distal intervals (Baker and Hall, 1976). The effects of this mutation on dis- junction were not examined. However its low fertility sug- gests that nondisjunction may be frequent. # mei-G17 location: 2- (distal third of 2R). origin: Induced with ethyl methanesulfonate. references: Gethmann, 1974, Genetics 78: 1127-42. phenotype: A male-specific and chromosome specific meiotic mutant. Homozygous males, but not females, exhibit elevated frequencies of nondisjunction of second and sex but not third or fourth chromosomes. The incidence of X-Y nondisjunction varies from 4-6%, with nullo-sex-chromosome offspring greatly outnumbering X-Y bearing offspring; nondisjunction seems to occur in the first meiotic division. Among regular progeny, X-bearing genotypes are recovered in excess of Y-bearing geno- types. The frequency of second-chromosome exceptions varies, depending on the Y chromosome present, from 0.25 (BSY) to 1.0 (normal Y) exceptions per parental male; this difference is attributable to variable recoveries of nullo-2 but not diplo-2 offspring. Generally the products of nullo-2 sperm are recovered more frequently than those of diplo-2 sperm. Sex- chromosome exceptions are more frequent in products of second-chromosome nondisjunction than in progeny that are reg- ular for chromosome 2; furthermore, XX;0 and 0;22 products are recovered much more frequently than XX; 22 and 0;0 products. # mei-G87 location: 3- (approximately half way between al and b). origin: Induced with ethyl methanesulfonate. references: Gethmann, 1974, Genetics 78: 1127-42. 1984, Genetics 107: 65-77. phenotype: A chromosome-specific but not sex-specific meiotic mutant; causes both reductional and equational nondisjunction of chromosome 2 in both males and females. In females, equa- tional nondisjunction is independent of exchange, but reduc- tional exceptions are primarily derived from non-exchange tetrads. In crosses of mei-G87 males to C(2)EN females, in which half the exceptions are recoverable, 6-10 exceptions per thousand eggs were recovered; in the reciprocal cross, in which all the diplo-2 exceptions are theoretically recover- able, there were 1-2 exceptions per thousand eggs. In primary spermatocytes, a low incidence of cases in which the chroma- tids of one pair of autosomes have separated are observed. # mei-I1 location: 3-1.8 (1/15 the distance between ru and h). origin: Induced with ethyl methanesulfonate. references: Ivy, 1981, PhD thesis, University of California, San Diego. phenotype: Homozygous males produce 43-49% gametes exceptional for sex chromosomes and 39-44% exceptional for chromosome 4. Sex and fourth chromosomes misassort independently. Con- sistently produce an excess of nullo-X-nullo-Y over XY-bearing gametes, but nullo-4 and diplo-4 gametes equally frequent. Nondisjunction confined to first meiotic division. Chromo- somes 2 and 3 also give high frequencies of nondisjunction; appear to disjoin randomly based on chromosome analysis of secondary spermatocytes. Primary spermatocytes show mostly univalents; MII appears normal except for the non-haploid com- plements resulting from MI chromosome misbehavior. Spermatids often contain micronuclei, and nullo exceptions are more fre- quent than diplo exceptions, both indicative of chromosome loss. cytology: Placed in 61A-62B1 based on the ability of YP3D of T(Y:3)D8 = T(Y;3)60A10-B1 but not YP3D of T(Y;3)A114 = T(Y;3)61A to cover both the genetic and cytological effects of mei-I1. # mei-I3 location: 3- (unmapped). origin: Induced with ethyl methanesulfonate. references: Ivy, 1981, PhD thesis, University of California, San Diego. phenotype: In males homozygous for this mutation, all chromo- somes nondisjoin at meiosis I and reciprocal meiotic products are recovered with unequal frequencies. Furthermore, the X chromosomes nondisjoin at meiosis II. The meiotic behaviors of the sex and fourth chromosomes are positively correlated, i.e., more double exceptions were recovered than expected; among double exceptions, however, nonhomologues behave independently. Homozygous females virtually sterile owing either to mei-I3 or to a closely linked independent mutation. #*mei-O81 location: 3- (unmapped). origin: Natural population. references: Sandler, Lindsley, Nicoletti, and Trippa, 1968, Genetics 60: 525-58. phenotype: Male-specific recessive meiotic mutant. Apparently causes nondisjunction of all chromosomes; 5.0% for sex chromo- somes, 7.8% for fourth chromosomes, and 0.78% double nondis- junction. Failure of homologous pairing seen in primary sper- matocytes. cytology: Polytene chromosomes normal. #*mei-S8 location: 2-79.7. origin: Natural population. references: Sandler, Lindsley, Nicoletti, and Trippa, 1968, Genetics 60: 525-58. phenotype: Male-specific recessive meiotic mutant. Causes high nondisjunction of chromosome 4, but has no effect on the sex chromosomes. Nullo-4 exceed diplo-4 gametes. Cytological examination of primary spermatocytes reveals nondisjunction of chromosome 4 in the first meiotic division. cytology: Polytene chromosomes normal. # mei-S51 (R.S. Hawley) location: Synthetic with at least one component on each large autosome. references: Robbins, 1971, Mol. Gen. Genet. 110: 144-66. Sandler, Lindsley, Nicoletti, and Trippa, 1968, Genetics 60: 525-558. phenotype: Females homozygous for mei-S51 exhibit reduced exchange and high frequencies of nonhomologous disjunction, particularly with respect to the X and fourth chromosomes (XX <-> 44 segregations are frequent). In addition mei-S51 decreases the frequency of secondary nondisjunction in struc- turally normal XXY females and increases the frequency of non- disjunction in X inversion heterozygotes. Robbins (1971) proposed that mei-S51 disrupts a number of aspects of chromo- some pairing and alignment prior to metaphase and therefore both reduces exchanges and prevents proper partner choice within the distributive system. # mei-S282 (R.S. Hawley) location: 3-5. origin: Spontaneous. references: Sandler, Lindsley, Nicolleti, and Trippa, 1968, Genetics 60: 525-58. Parry, 1973, Genetics 73: 465-86. Sandler, Romans, and Figenshow, 1974, Genetics 77: 299-307. Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 352-434. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. phenotype: Females homozygous for mei-S282 exhibit reduced lev- els of meiotic exchange. The residual exchanges are distri- buted such that the probability of euchromatic exchange becomes more proportional to unit length (Parry, 1973; Baker and Hall, 1976). This relaxation of the normal constraints on the distribution of euchromatic exchange is clearly demon- strated by the ability of mei-S282 females to allow exchange on the normally achiasmate fourth chromosome (Sandler and Szauter, 1978). The reduced levels of reciprocal exchange which are characteristic of mei-S282 females allow for high frequencies of meiotic loss and nondisjunction (see Baker and Hall, 1976). Nondisjunction occurs at the first meiotic divi- sion and only nonexchange chronmosomes nondisjoin (Parry, 1973). The mei-S282 mutation also causes mitotic chromosome instability (Baker et al., 1978) when assayed genetically. This suggests that the mei-S282+ gene product is required both during meiosis and mitosis. # mei-S332 (R.S. Hawley) location: 2-95. origin: Spontaneous. references: Sandler, Lindsley, Nicolleti, and Trippa, 1968, Genetics 60: 525-58. Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 352-434. Davis, 1971, Mol. Gen. Genet. 113: 251-72. Sandler, Romans, and Figenshow, 1974, Genetics 77: 299-307. Hardy, 1975, Genetics 79: 231-64. Davis, 1977, DIS 52: 100. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. Goldstein, 1980, Chromosoma 78: 79-111. phenotype: mei-S332 is a semidominant autosomal mutation that increases nondisjunction of all chromosomes to the same extent in both sexes. Although female recombination is normal, mei- S332 causes high frequencies of equational nondisjunction in both sexes as well as chromosome loss (Davis, 1971; Goldstein, 1980). In the male germline sister chromatid associations are generally normal during prophase I and metaphase I. However, by telophase I sister chromatids have frequently undergone precocious separation (Goldstein, 1980). The equational exceptions produced by mei-S332 males and females presumably result from precociously separated sister chromatids going to the same pole at anaphase II. Goldstein (1980) has also sug- gested that "in the case of mei-S332, chromosomes which lag in the second meiotic division are usually lost and most of the genetically observed loss in mei-S332 occurs in the second meiotic division." The hypothesis that lagging chromatids are often lost at anaphase II is consistent with Hardy's observa- tion that mei-S332 has micronuclei present at the early sper- matid stages (Hardy, 1975). Thus mei-S332 presumably defines a function required for sister chromatid cohesion. Sandler et al. (1974) have shown that ring chromosomes are frequently converted into dominant lethals in mei-S332 females, presum- ably resulting from an impaired ability to resolve sister ring chromosomes at anaphase II. Baker et al. (1978) have also shown that mitotic chromosome instability is elevated in the presence of mei-S332. They suggest that the function of the mei-S332+ locus is to delay the separation of sister chroma- tids at all divisions. Because the sole mei-S332 allele is viable, they have further suggested that either this allele is leaky or that there are overlapping or redundant functions that can compensate for this defect. cytology: Placed in 58A-E by Davis (1971, 1977); further con- fined to 58B by deficiency mapping (Kerrebrock and Orr- Weaver). # mei-W5: see pal # mei-W22: see c(3)G # mei-W68 (R.S. Hawley) location: 2-94. references: Baker, Carpenter, Esposito, Esposito, and Sandler, 1976, Ann. Rev. Genet. 10: 53-134. Baker, Carpenter, and Ripoll, 1978, Genetics 90: 531-78. phenotype: Females homozygous for mei-w68 show a complete absence of meiotic recombination (Baker, unpublished data). Ultrastructural studies of pachytene reveal an absence of chromosome condensation and little synaptonemal complex (Car- penter, cited in Baker et al., 1976). A less severe allele (mei-w68L1-Lindsley) reduces exchange to approximately 60% of control levels and also alters the distribution of residual exchanges. Analysis of mitotic chromosome behavior (Baker et al., 1978) suggests that the mei-w68+ gene product is also required in mitotic cells. # meiotic-: see mei- # mel: melanized location: 1-64.1. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1953. references: 1958, DIS 32: 71. phenotype: Body color darker than normal, especially in thorax; trident pronounced. Eye color dull red. Wing tips frequently curve upward. Classification rather difficult, best in young flies. Viability and fertility good in both sexes. RK3. cytology: Placed in 19C2-3 by Schalet and Lefevre [1976, Genet- ics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1B, pp. 847-902)]. other information: One allele induced by L-p-N,N-di-(2- chloroethyl)amino-phenylalanine (CB. 3025). # mel: see mat # mel(1)R1: see pcx # mel(3)5: see ndl # mel(3)9: see Tl8r # melanized: see mel # melanizedlike: see mell # melanoscutellum: see msc # melanotic lesions: see md # melanotic tumor-A: see tu-bw # mell: melanizedlike location: 1-{64}. references: Schalet and Lefevre, 1976, Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, and San Francisco, Vol. 1B, pp. 847-902. phenotype: Abdominal tergites have slight transverse wrinkles; perhaps thorax darker than normal; flies somewhat smaller with slightly broader wings; eyes of males slightly rough, wings of females variably wrinkled or curled. cytology: Placed in 19D2-E1 based on mell phenotype of hetero- zygotes between Df(1)16-3-35 = Df(1)19D2-3;19E6-7 and Df(1)mel8 = Df(1)18F4-5;19E1. # Men: Malic enzyme location: 3-51.73 [based on 91 recombinants between kar (3- 51.7) and ry (3-52.0)]. synonym: Mdh-NADP. references: Franklin and Rumball, 1971, DIS 47: 37. Voelker, Ohnishi, Langley, Gausz, and Gyrukovics, 1981, Biochem. Genet. 19: 525-34. phenotype: Structural gene for malic enzyme = (S)-Malate: NADP+ oxidoreductase [MEN (EC 1.1.1.40)], a tetramer with subunit molecular weight of 58,000 (Lee, Langley, and Burkhart, 1978, Anal. Biochem. 86: 697-296) or 67,250 (Geer, Krochko, Oliver, Walker, and Williamson, 1980, Comp. Biochem. Physiol. 65B: 25-34). Biochemical characterization by Geer, et al., (1980). Enzyme known to provide NADP for lipogenesis; levels in larvae increased by dietary carbohydrate and decreased by dietary lipid. Levels normally high in early third-instar larvae, reducing to half in late third instar, rising again in ageing adults. Highest specific activity found in larval fat body and, among cellular fractions, in the cytosol (Geer, Kro- chko, and Williamson, 1979, Biochem. Genet. 17: 867-79). Histochemical staining of larval imaginal discs reveals enzyme activity localized to nervous elements, including ommatidial precursors, the morphogenetic furrow, and the optic nerve in the eye antennal disc; and the chordotonal organ and the nerve traversing the leg discs; wing, haltere, labial, and genital discs unstained; however genital disc derivatives, the ejacu- latory duct and paragonia in males and oviducts of females are stained in adults (Finkbohner, Cunningham, and Kuhn, 1985, Wilhelm Roux's Arch. Dev. Biol. 194: 217-23). Staining of morphogenetic groove absent in D. simulans and in simulans- melanogaster hybrids except when such hybrids contain two copies of 3R from D. melanogaster and none from D. simulans (Kuhn and Sprey, 1987, Genetics 115: 277-81). All null alleles tested survive and are fertile in combination with Df(3R)ry3l, which lacks Men+ (Voelker et al.). The NADPH/NADP ratio in such null genotypes is one-seventh that of wild type (Geer et al., 1979). Presence of an extra dose of the region from 8D10-12 to 9A1-2 results in an approximately 25% increase in MEN activity (Williamson and Bentley, 1983, Genetics 103: 649-58). alleles: allele origin synonym ref ( comments | _______________________________________________________________ Men2 spont Men0.90 2, 5 slow migration Men4 spont Men1.0 2, 5 common allele, p = 0.95 intermediate migration Men6 spont Men1.1 2, 5 fast migration MennNC1 spont 1, 4, 6 3-5% normal activity /; dimer - MennNC2 spont 1, 4 no activity; dimer - MennNC3 spont 1, 4 no activity; dimer - MennNC4 spont 1, 4 no activity; dimer - MennNC5 spont 1, 4 residual activity; dimer - MennNC6 spont 1, 4 residual activity; dimer - MennNC311 spont 3 CRM - MennNC506 spont 3 CRM - MennGB1 spont 1 no activity; dimer - ( 1 = Burkhart, Montgomery, Langley, and Voelker, 1984, Genet- ics 107: 295-306; 2 = Franklin and Rumball, 1971, DIS 47: 37; 3 = Lee and Bronson, 1979, J. Biochem. 254: 6374- 81; 4 = Voelker, Langley, Leigh-Brown, Ohnishi, Dickson, Montgomery, and Smith, 1980, Proc. Nat. Acad. Sci. USA 77: 1091-95; 5 = Foelker, Ohnishi, Langley, Gausz, and Gyrukovics, 1981, Biochem. Genet. 19: 525-34; 6 = William- son, 1982, Can. J. Genet. Cytol. 24: 409-16. | dimer- indicates inability of product to form heterodimer with electrophoretically variant polypeptides; CRM = immuno- logically cross-reacting material; quasi-null alleles derived from Men4. / Enzyme extracted from MennNC1 homozygotes kinetically indis- tinguishable from wild-type enzyme; Williamson accordingly proposes that MennNC1 is a cis-acting regulatory mutant. cytology: Placed in 87C9-D1 based on its exclusion from Df(3R)kar3J = Df(3R)87B15-C1;87C9-D1 on the left and Df(3R)ry27 = Df(3R)87D1-2;87F1-2 on the right. # merry-go-round: see mgr # mes: messy A location: 1-51.9. discoverer: Schalet. references: Schalet, Kernaghan, and Chovnick, 1964, Genetics 50: 1261-68. Hilliker, Clark, Chovnick, and Gelbert, 1980, Genetics 95: 95-110. phenotype: Extra head and thoracic bristles, especially ante- rior scutellars; wings inflated, turned somewhat upward and outward, and shorter and broader than normal; posterior crossvein gapped or missing. Semilethal; male considerably less viable than female; sterile. RK3. allele origin discoverer synonym ref ( __________________________________________________ mesA1 X ray Schalet mes1 1, 4 mesA2 X ray Schalet mes2 1, 4 mesA3 EMS Hilliker, Clark l(3)2-34 2, 3 mesA4 EMS Hilliker, Clark l(3)4-22 2, 3 mesA5 EMS Hilliker, Clark l(3)8-9 2, 3 mesA6 EMS Hilliker, Clark l(3)10-140 2, 3 mesA7 EMS Hilliker, Clark l(3)13-62 2, 3 mesA8 EMS Hilliker, Clark l(3)A12-2 2, 3 mesA9 EMS Hilliker, Clark l(3)A13-1 2, 3 mesA10 EMS Hilliker, Clark l(3)A27-2 2, 3 mesA11 EMS Hilliker, Clark l(3)B26-1 2, 3 mesA12 EMS Gelbart l(3)G2 2, 3 mesA13 EMS Gelbart l(3)G3 2, 3 mesA14 EMS Gelbart l(3)G8 2, 3 mesA15 EMS Gelbart l(3)G19 2, 3 ( 1 = CP627; 2 = Hilliker, Clark, and Chovnick, 1981, DIS 56: 64-72; 3 = Hilliker, Clark, Chovnick, and Gelbart, 1980, Genetics 95: 95-110; 4 = Schalet, Kernaghan, and Chovnick, 1964, Genetics 50: 1261-68. cytology: Placed in 87D4-8 based on its inclusion in Df(3R)ry1608 = Df(3R)87D4-6;87E1-2 but not Df(3R)ry74 = Df(3R)87D8;87D12. other information: All alleles complement mesB. # mesB location: 3-51.9. discoverer: Schalet. references: Schalet, Kernaghan, and Chovnick, 1964, Genetics 50: 121-68. Hilliker, Clark, Chovnick, and Gelbart, 1980, Genetics 95: 95-110. phenotype: Wings outspread at about 45 from mid-line. Trident dark; occasional thoracic bristle duplication. Subtly abnor- mal abdomen. Semilethal. RK3. alleles: Existence of thirteen alleles recorded by Skinner, Cole, and Chovnick. mesB alleles only partially complement alleles of l(3)87De. allele origin discoverer synonym ref ( _________________________________________________ mesB1 X ray Schalet mes3 1, 4 mesB2 X ray Schalet mes4 1, 4 mesB3 X ray Schalet mes5l 1, 4 mesB4 X ray Schalet mes6l 1, 4 mesB5 EMS Hilliker, Clark l(3)34-2 2, 3 mesB6 EMS Hilliker, Clark l(3)B14-1 2, 3 ( 1 = CP627; 2 = Hilliker, Clark, and Chovnick, 1981, DIS 56: 64-72; 3 = Hilliker, Clark, Chovnick, and Gelbart, 1980, Genetics 95: 95-110; 4 = Schalet, Kernaghan, and Chovnick, 1964, Genetics 50: 1261-68. cytology: Placed in 87D8-12 based on its inclusion in the region of overlap of Df(3R)ry74 = Df(3R)87D8;87D12 and Df(3R)kar-lG27 = Df(3R)87B3-5;87D6-12. other information: Interacts in trans with l(3)87De (Skinner, Cole, and Chovnick). # messy: see mes #*Met: Metatarsi irregular location: 2- or 3- (rearrangement). origin: X ray induced. discoverer: Jonsson, 56a10. references: Luning, 1956, DIS 30: 73. phenotype: First and second tarsal joints fused and swollen with extra hairs. Male sex combs enlarged. Fully penetrant when balanced with Cy; however, Met/ss is wild type or nearly so. RK2A. cytology: Associated with T(2;3)Met. # Met: see Rst(1)JH # Metallothionein: see Mtn # metaphase arrest: see mar # Mex156: see Sxl #*mf: macrofine location: 1-5.5. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino-phenylalan- ine (CB. 3025). discoverer: Fahmy, 1955. references: 1958, DIS 32: 71. phenotype: Fly slightly smaller than normal with short, thin, bristles. Male viable and fertile. Female slightly delayed in eclosion and reduced in viability. RK3. # Mfcp: Myofibrillar contractile protein location: 3 {50-51}. references: Bernstein, Glenn, and Emerson, 1981, Genetics 97: s10. phenotype: Structural genes for several contractile polypep- tides of approximately 22,500 daltons molecular weight that initiate expression at the fusion stage of myogenesis (Bern- stein and Donady, 1980, Dev. Biol. 79: 388-98). cytology: Placed in 87B by in situ hybridization. molecular biology: Genes cloned, presumably by differential screen of pre- and post-fusion stages of myocytes in culture. # mfd: myofibrillar-defective (J.C. Hall) location: 1- {38}. phenotype: Deletion of salivary segment 11A6-7 leads to inabil- ity to jump or fly, hemizygosity for this variant allows via- bility, and the phenotypic defects induced by the deletion are recessive; myofibrils or thoracic muscles shortened; spots are missing in two dimensional gel analysis of proteins from fibrillar and tubular muscles; these differences from wild type apparently due to blocking of phosphorylation of proteins in these muscles; such proteins are very likely myosins that become phosphorylated during the first day after eclosion (in wild-type), in parallel with the gradual development of flying and jumping ability (Hiromi, Ohmura, Masaki, Hirose and Hotta). cytology: Maps to 11A6-7; synthetic deletion, constructed using T(1;Y)'s, is the only mfd variant. # mfs(2)31: male-female-sterile (2) in region 31 location: 2-41.35 [based on 23 recombinants between J (2-41.0) and msf(2)31 with da (2-41.3) as a middle marker]. origin: Induced by ethyl methanesulfonate. synonym: mfs48. references: Sandler, 1977, Genetics 86: 567-82. Lindsley, Goldstein, and Sandler, 1980, DIS 55: 84-85. phenotype: Homozygotes have short thin bristles; relative via- bility 25% at 25; hemizygotes lethal. Both males and females sterile at 25 but some fertility observed in flies raised at 23. Males raised at 28.5 have no motile sperm and some sper- matids have micronuclei, and occasionally two basal bodies and axonemes are observed. cytology: Placed in 31B-32A based on its lethality in combina- tion with Df(2L)527 = Df(2L)31B-D;31F-32A # mfs(2)350 location: 2-50.7. references: Fukunaga, 1980, J. Hered. 71: 349-52. phenotype: Homozygous males and females sterile in certain cytoplasmic constitutions, fertile in others. Gonads rudimen- tary, although some males have normal testes without motile sperm. # mfs(2)7601: see Dox-A2mfs1 # mfs(3)73A location: 3- {45}. origin: Induced by ethyl methanesulfonate. discoverer: Hoffmann. cytology: Placed in 73A10-B1 between the right breakpoints of Df(3L)st7P and Df(3L)st-g24. # mfs(3)G: male-female-sterile of Gill location: 3-59. origin: X ray induced. discoverer: Gill, 59a. synonym: fs(3)459a. references: 1960, Anat. Record 138: 351. 1961, Ph.D. Thesis, Yale Univ. 1962, DIS 36: 37. 1963, J. Exp. Zool. 152: 251-77 (fig.). phenotype: Oogenesis incomplete; follicles usually cease development early in vitellogenesis (at or before stage 9); occasional breakthrough produces adult fly. Primary compound chambers in which two, occasionally three, incipient cysts are enclosed occur in about 10% of the cases. Male sterile. Adult fat body hypertrophied; body size reduced. Occasion- ally, metathoracic legs with tibiae more curved than normal and tarsi crooked. Viability low. RK3. # mgr: merry-go-round location: 3-51.3. origin: X-ray induced. references: Gonzalez, Casal, and Ripoll, 1988, J. Cell Sci. 89: 39-47. phenotype: Most characteristic abnormality is appearance of mitotic and meiotic figures in which all the chromosomes are arranged in a circle. Other mutant traits include metaphase arrest, polyploid cells, postmeiotic cysts with 16 nuclei, and spermatids carrying four times the normal complement of chro- mosomes. The circular mitotic figures (CMF's) are caused by monopolar spindles. The wild-type allele of mgr apparently is necessary for correct centrosome behavior. # mgt: midget location: 1-48.7. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 71. phenotype: Small fly with delayed eclosion. Not easily classi- fied. Male fertile and viability about 20% wild type. Expression more extreme in female and viability further reduced. RK3. other information: One allele each induced by CB. 3025 and X rays; two alleles induced by CB. 1506. # mh: maternal haploid location: 1-. origin: Induced by ethyl methanesulfonate. synonym: fs(1)A1182. references: Gans, Audit, and Masson, 1975, Genetics 81: 683- 704. Zalokar, Audit, and Erk, 1975, Dev. Biol. 47: 419-32. Santamaria and Gans, 1980, Nature (London) 287: 143-44. Santamaria, 1983, Dev. Biol. 96: 285-95. phenotype: Homozygous mh females are fertile at 18 but at 25 they are sterile; irrespective of the males used in cross, nuclei of developing embryos appear to be X-bearing and haploid. 183/200 eggs developed to blastoderm; gastrulation was abnormal; 22 embryos gave evidence of segmentation and muscular movement. Nuclei from such embryos injected into normal early embryos are capable of developing into patches of tissue, some of which produce structures of normal number and size and are presumably diploid, some of which produce increased numbers of smaller-than-normal structures and are presumably haploid, and a few of which are mixed. Haploid tissue with female phenotype found in basistarsus, tergites, and terminalia. Nuclear division cycles of haploid embryos 2.1 min. longer than wild type; such embryos undergo an extra nucleus division in the syncitial blastoderm, possibly to achieve a proper nuclear: cytoplasmic ratio prior to cellular- ization (Edgar, Kichle, and Schuberger, 1986, Cell 44: 365- 72). Haploid cell cultures established from 25 embryos (Debec, 1978, Nature 274: 255-56). Haploid cells and their diploidized derivatives lack centrioles (Debec, Szollosi, and Sollosc, 1982, Biology of the Cell 44: 133-38). # Mhc: Muscle myosin heavy chain location: 2-52. origin: A number of mutants have been induced by ethyl methanesulfonate. references: Mogami and Hotta, 1981, Mol. Gen. Genet. 183: 409-17. Bernstein, Mogami, Donady, and Emerson, 1983, Nature 302: 393-97. Rozek and Davidson, 1983, Cell 32: 23-34. Mogami, O'Donnell, Bernstein, Wright, and Emerson, 1986, Proc. Nat. Acad. Sci. USA 83: 1393-97. Bernstein, Hansen, Becker, Wassenberg, Roche, Donady, and Emerson, 1986, Mol. Cell. Biol. 6: 2511-19. Rozek and Davidson, 1986, Proc. Nat. Acad. Sci. USA 83: 2128-32. Wassenberg, Kronert, O'Donnell, and Bernstein, 1987, J. Biol. Chem. 262: 10741-47. Homyk and Emerson, 1988 Genetics 119: 105-21. O'Donnell and Bernstein, 1988, J. Cell Biol. 107: 2601-12. Chun and Falkenthal, 1988, J. Cell Biol. 107: 2613-21. George, Ober, and Emerson, 1989, Mol. Cell Biol. 9: 2957-74. Hess, Kronert, and Bernstein, 1989, Cellular and Molecular Biology of Muscle Development (Kedes and Stockdale, eds.). A.R. Liss, New York, pp. 621-31. O'Donnell, Collier, Mogami, and Bernstein, 1989, Genes Dev. 3: 1233-44. Kazzaz and Rozek, 1989, Dev. Biol. 133: 550-61. phenotype: Structural gene for the heavy chain of muscle myosin (MHC). Heterozygotes for dominant flightless mutant alleles are characterized by erect wings and disrupted myofibrils in the indirect flight muscles. Segmental-deficiency heterozy- gotes for the locus are also flightless with disrupted myofi- brils. Flight can be rescued in heterozygotes for most alleles by addition of a second Mhc+ allele to the complement, or by making the fly simultaneously hemizygous for Act88F [Beall, Sepanski, and Fyrberg, 1989, Genes Dev. 3: 131-40 (fig.)]. alleles: Of five ethyl-methanesulfonate-induced alleles that are lethal as homozygotes, three have 9-10 kb inserts with some apparently similar restriction sites (Mogami and Hotta; Mogami et al.). Three other ethyl-methanesulfonate-induced mutants, which are homozygous viable, are judged to be allelic based on the failure to obtain recombinants between them and the lethal alleles; as yet no molecular characterization available. allele discoverer synonym ref ( comments | ___________________________________________________________________________ Mhc1 Mogami 5, 6, 7, 8 lethal; 0.1 kb deletion in fifth exon and preceding intron / Mhc2 Mogami 7 lethal; 10 kb insert in intron ~2 kb 3' to Mhc1 Mhc3 Mogami 7 lethal; 10 kb insert in intron ~3 kb 3' to Mhc1 Mhc4 Mogami 7 lethal; 9 kb insert in intron ~5 kb 3' to Mhc1 Mhc5 Grell, 1969 Bsh: Bashed 4, 5 viable / Mhc6 Mogami Ifm(2)1 5, 6 viable Mhc7 Mogami Ifm(2)2 1, 5, 6, 10 viable / Mhc8 Mogami Ifm(2)3 5, 6, 7 lethal; apparent point mutation Mhc9 Mogami 9, 10 viable / Mhc10 Mogami 9, 10 viable / Mhc11 Mogami 9, 10 viable / Mhc12 Sparrow & Ball 9 viable / Mhc13 Sparrow 3 viable; neomorphic / Mhc14 Steward 11 lethal Mhc15 Collier & Finke Stp 2, 5 viable Mhc16 Homyk Nup 5 semilethal / ( 1 = Chun and Falkenthal, 1988, J. Cell Biol. 107: 2613-21; 2 = Collier and Finke, 1984, J. Hered. 75: 477-79; 3 = Fieck, O'Donnell, Sparrow, and Bernstein, 1988, J. Cell Biol. 107: 257a; 4 = Grell, 1969, DIS 44: 46-47; 5 = Homyk and Emerson, 1985, Genetics 119: 105-21; 6 = Mogami and Hotta, 1981, Mol. Gen. Genet. 183: 409-17; 7 = Mogami, O'Donnell, Bernstein, Wright, and Emerson, 1986, Proc. Nat. Acad. Sci. USA 83: 1393-97; 8 = O'Donnell and Bernstein, 1988, J. Cell Biol. 107: 2601-12; 9 = O'Donnell, Mogami, and Bernstein, 1988, J. Cell Biochem. Suppl. 12C: 341; 10 = O'Donnell, Collier, Mogami, and Bernstein, 1989, Genes Dev. 3: 1233-46; 11 = Steward and Nusslein-Volhard, 1986, Genetics 113: 665-78. | Viability notations refer to homozygotes. / Fuller description follows "molecular biology". cytology: Placed in 36A7-C1 on the basis of its inclusion in Df(2L)H20 = Df(2L)36A7-10;36E4-F1 but not in Df(2L)H68 = Df(2L)36B2-C1;37A1-B1 (Steward and Nusslein-Volhard, 1986, Genetics 113: 665-78); located in 36B by in situ hybridiza- tion to salivaries (Bernstein et al., 1983; Rozek and David- son, 1983). molecular biology: Mhc is a single copy gene in Drosophila melanogaster (in contrast to mammals, chickens, and nematodes which have families of myosin heavy chain genes). The Droso- phila Mhc gene has been cloned and the complete nucleotide sequence of the genomic DNA and the derived amino acid sequence of the MHC protein obtained (Bernstein et al., 1983, 1986; Rozek and Davidson, 1983, 1986; George et al., 1989). The gene has a complex exon structure that, by means of regu- lated alternative RNA splicing, enables it to produce a variety of larval and adult muscle isoforms. Its 21 kb tran- scription unit contains 19 exons, 14 single-copy exons and five other exons that are tandemly repeated [two copies of exon 3 (Wassenberg et al., 1987), four of exon 7, three of exon 9, five of exon 11, and two copies of exon 15 (George et al., 1989; Hess et al., 1989)]. In the clones studied by George et al. (1989), the repeated exons are spliced in a mutually exclusive manner, so that only one form of each exon set is included. Exon 18 shows differential splicing by inclusion or exclusion of the exon in pre-mRNA; it is expressed mainly in the thorax of late pupae and adults. Cod- ing sequences for the ATP binding domain have been located in exon 4 (Wassenberg et al., 1987; George et al., 1989); the hydrophobic region next to the ATP-binding domain is encoded by alternative exons 3a/3b as well as by exon 4. Northern blots show transcripts of 6.1 and 6.6 kb in larval stages and transcripts of 6.1, 6.6, and 7.1 kb in adult stages. Posi- tions of the 5' introns are conserved in flies, vertebrates, and nematodes (Wassenberg et al., 1987; George et al., 1989). Fusion genes have been constructed using the 5' end of the E. coli lac-z gene introduced into the genome by P-element gene transfer, and the transformed flies stained for expression of the fusion protein to identify sequences involved in muscle- specific expression (Hess et al., 1989). The results indicate that these elements are located 450 nucleotides upstream and 2095 nucleotides downstream of the transcription initiation site. # Mhc1 phenotype: Homozygous embryos show no movement; unable to hatch; ultrastructural observations show complete lack of thick filaments in muscles. Heterozygotes display nearly a 50% reduction in the numbers of thick filaments in indirect flight muscles and the tergal-depressor-of-the-trochanter mus- cle, resulting in disruption of the normal regular array of thick and thin filaments in these muscles. Other less regu- larly organized muscles, although having reduced numbers of thick filaments, appear to function adequately in Mhc1/+ flies (O'Donnell and Bernstein, 1988, J. Cell Biol. 107: 260-12). molecular biology: 101 base pair deletion which removes most of exon 5 and the intron that precedes it. The splice-donor site of exon 4 rather than that of exon 5 appears to interact with the exon-6 splice-acceptor site (O'Donnell and Bernstein, 1988). Deletion generates a nonsense mutation, which likely results in production of an unstable truncated protein. # Mhc5 phenotype: 20% of heterozygotes display indented thorax and erect wings and are flightless; the remainder have normal phenotype but fly poorly. Homozygotes display erect wing phenotype. Judged to be antimorphic since not rescued by addition of Dp(2;3)osp3. Mhc5 interaction in double heterozy- gotes with other flightless mutants observed by Homyk and Emerson (1988, Genetics 119: 105-21). Heterozygous viability severely reduced in combination with hemizygous hdp2, int3, up101; or upx; rare escapers have gnarled legs, walk poorly, and die within two days of eclosion. Females doubly heterozy- gous for Mhc5 and hdp2, int3, up101; or upx have normal via- bility but are completely flightless and display abnormal wing posture. # Mhc6 phenotype: Heterozygotes fly moderately well and display normal wing posture; hemizygotes flightless and occasionally have abnormal wing posture. Double heterozygotes with hdp101, hdp102, int3, up101; or upx; but not hdp2, much more nearly flightless than Mhc6/+; wing posture normal. # Mhc7 phenotype: Indirect flight muscles accumulate little or no MHC, have no thick filaments, and show no organized myofibrils. The four smaller cells of the tergal depressor of the tro- chanter muscle (TDT) display reduction in thick filament number and myofibril size; large TDT cells unaffected. Flies jump 33% as well as wild type. Leg muscle MHC found in normal amounts (O'Donnell et al., 1989). # Mhc8 phenotype: Heterozygotes display indented thorax and erect wings. Judged to be antimorphic since not rescued by addition of Dp(2;3)osp3. Mhc8 interaction in double heterozygotes with other flightless mutants observed by Homyk and Emerson (1988, Genetics 119: 105-21). Heterozygous viability severely reduced in combination with either heterozygous or hemizygous hdp2, int3, and up101; lethal in upx/Y males. No interaction with the following: hdp3, hdp4, hdp5, hdp101, hdp102, up2, up3, or up102. # Mhc9 phenotype: Indirect flight muscles accumulate little or no MHC, have no thick filaments, and show no organized myofibrils. The four smaller cells of the TDT display reduction in thick filament number and myofibril size; large TDT cells unaf- fected. Flies jump 59% as well as wild type. Leg muscle MHC found in normal amounts (O'Donnell et al., 1989). # Mhc10 phenotype: Indirect flight muscles accumulate little or no MHC, have no thick filaments, and show no organized myofibrils. All 32 TDT cells lack thick filaments and lack myofibril organization. Flies cannot jump. Leg muscles accumulate 55% normal amounts of MHC (O'Donnell et al., 1989). molecular biology: Mutation within 3 splice acceptor of exon 15a that encodes the central region of the MHC hinge (Collier, Kronert, O'Donnell, Edwards, and Bernstein, 1990, Genes Dev. 4: 885-95). # Mhc11 phenotype: Indirect flight muscles accumulate little or no MHC, have no thick filaments, and show no organized myofibrils. No apparent effect on TDT; unique among alleles in being capable of jumping. Leg muscle MHC found in normal amounts (O'Donnell et al., 1989). # Mhc12 phenotype: Indirect flight muscles accumulate little or no MHC, have no thick filaments, and show no organized myofibrils. The four smaller cells of the TDT display reduction in thick filament number and myofibril size; large TDT cells unaf- fected. # Mhc13 phenotype: A dominant flightless mutation; in homozygotes but not heterozygotes, the myofibrils of dorsolateral indirect flight muscles, although displaying normal morphology at eclo- sion, degenerate with time so that each cell is composed of a narrow strip of material connected to a bulged-out region. Some areas of the cells contain over-contracted sarcomeres and others show arrays of thick and thin filaments splayed throughout the cytoplasm. Abnormal morphology is recessive. Unlike the situation with other Mhc mutations, the dominant flightlessness of Mhc13 not rescued by the addition of a second dose of Mhc+. # Mhc16 phenotype: Heterozygotes display indented thorax and erect wings; flightless; hemizygotes semilethal, very inactive, have weak mesothoracic legs which are generally folded beneath the thorax; die prematurely after eclosion. Judged to be antimorphic since not rescued by addition of Dp(2;3)osp3. Mhc16 interaction in double heterozygotes with other flight- less mutants observed by Homyk and Emerson (1988, Genetics 119: 105-21). Heterozygous viability severely reduced in combination with hemizygous hdp2, int3, up101; or upx; rare escapers have gnarled legs, walk poorly, and die within two days of eclosion. # Mhc-c: Myosin heavy chain-cytoplasmic (D.P. Kiehart) location: 2-{108}. references: Kiehart and Feghali, 1986, J. Cell Biol. 103: 1517-25. Young, Pesacreta, Rose, and Kiehart, 1987, J. Cell Biol. 105: 172a. Kiehart, Lutz, Chan, Ketchum, Laymon, Nguyen, and Goldstein, 1989, EMBO J. 8: 913-22. Ketchum, Stewart, Stewart, and Kiehart, 1990, Proc. Nat. Acad. Sci. USA 87: 6316-20. Kiehart, Ketchum, Young, Lutz, Alfenito, Chang, Awobuluyi, Pesacreta, Inove, Stewart, and Chen, 1990, Ann. N.Y. Acad. Sci. 582: 233-51. Young, Pesacreta, Rose, and Kiehart, 1991, Development 111: 1-14. phenotype: Encodes a 205 kilodalton myosin heavy chain found in Drosophila cell lines and all Drosophila developmental stages. Antibodies raised against this protein crossreact, but weakly with muscle myosin heavy chain. First appears in preblasto- derm embryos; diffusely distributed until syncytial blastoderm at which time localization to cortex and pole cells observed; at cleavage furrow, canals at the time of cellularization; transiently present at points of invagination during gastrulation (Young et al., 1987, 1991). cytology: Localized to 60E9 by in situ hybridization (Jones and Young). molecular biology: A 50 kb walk that includes the 20.5 kb tran- scription unit for the gene is cloned; in vitro transcription and translation yields a 205 kd protein that reacts specifi- cally with anti-cytoplasmic-myosin serum. Hybridizes with at least 2 ca. 6.3 kilobase messages on Northern blots that result from a differential splice at the 5 end of the gene (Kiehart et al., 1989; Ketchum et al., 1990). other information: Appears to be allelic with zipper. An EMS- induced allele (Mhc-c1) produces a truncated myosin heavy chain on Western blots and fails to complement zip1 and zip2. Western blots also indicate zip2 fails to accumulate myosin heavy chain.