m: miniature From Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237. # m: miniature location: 1-36.1 phenotype: Wing size reduced, only slightly longer than abdomen and with normal proportions. Angle between L2 and L5 reduced. Wings dark gray and less transparent than normal. Wing cells smaller than normal (Dobzhansky, 1929, Arch. Entwicklungsmech. Organ. 115: 363-79). In poor cultures, wings may become divergent and stringy. Cell expansion inhibited in prepupae and pupae [Waddington, 1940, J. Genet. 41: 75-139 (fig.)]. Different m mutants complement slightly; m/dy is wild type. RK1. alleles: allele origin ( discoverer ref | comments ________________________________________________________________________ m1 spont Morgan, 10h 19 m2 X ray Glass, 1929 9 In(1)dl49 *m17e spont Bridges 4 *m20f spont Morgan 4 *m20k spont Bridges 4 *m21e spont Bridges 4 *m22e spont Bridges 4 *m23e spont Bridges 4 *m23g spont Plunkett 4 *m25d spont Morgan 4 *m25g spont Fogg 4 *m27e spont Bridges 4 *m38d spont Bridges 4 *m20a spont Mohr 4, 20 m31a X ray Oliver, 31a 4, 22 m33c X ray Oliver, 33c 4, 22 m33d X ray Oliver, 33d 4, 22 *m34a spont Tanaka 4 m36f spont Spencer 36f30 4, 25 m37d spont Nordenskold, 37d14 4, 21 m37i spont Braun 4 m57 X ray Mayo, 57i 18 m59 spont Karwinkel, 59a 3 m60 / ray Ives, 60l 12 m61 / ray Ives, 61e 13 m66d X ray 26, 27 T(1;Y;3)? wings at 45 angle with body; post scutellars erect, male sterile m68 NNG Kaufman 14 female sterile; shows partial dominance m71c Gelbart 8 m73a spont 1 m74f EMS 6 long-winged allele m81 Behnel 2 in Basc; female sterile m259-4 X ray Demerec, 33i 5 Df(1)10C2-3;10E2-3 mD X ray Slatis, 48k17 5, 23, 24 partial dominant | mhow spont Waddle 28 held out wings mI spont Gassparian 7 mi27 spont Green 10 mu derivative | mK X ray Krivshenko, 55l3 5, 11, 17, 29 In(1)10E;20B; v-type position effect mu Green 10 mutable allele | mPS / ray 15, 16 homozygous females poorly fertile ms19 spont Green 10 mu derivative | ( 1 = Anxolabehere and Periquet, 1973, DIS 50: 21; 2 = Behnel, 1982, DIS 58: 183-84; 3 = Burdick, 1961, DIS 35: 45; 4 = CP552; 5 = CP627; 6 = Craymer, 1980, DIS 197; 7 = Gassparian, 1973, DIS 50: 22-23; 8 = Gelbart, 1974, Genetics 76: 51-63; 9 = Glass, 1935, DIS 4: 9; 10 = Green, 1975, Mutat. Res. 29: 77-84; 11 = Hartman-Goldstein and Wargent, 1975, Chromosome, 52: 349-62; 12 = Ives, 1961, DIS 35: 46; 13 = Ives, 1962, DIS 36: 38; 14 = Kaufman, 1969, DIS 44: 44; 15 = Keller and Nash, 1960, DIS 34: 51; 16 = Keller and Nash, 1960, DIS 34: 47; 17 = Krivshenko, 1956, DIS 30: 75; 18 = Mayo, 1958, DIS 32: 82; 19 = Morgan and Bridges, 1916, Carnegie Inst. Wash. Publ. No. 237; 20 = Mohr, 1923, Z. Indukt. Abstamm. Vererbungsl. 32: 215; 21 = Nordenskold, 1939, DIS 12: 49; 22 = Oliver, 1937, DIS 7: 19; 23 = Slatis, 1949, DIS 23: 63; 24 = Slatis and Wil- lermet, 1954, Genetics 39: 45-58; 25 = Spencer, 1937, DIS 7: 14; 26 = Thompson and Braver, 1969, DIS 44: 43; 27 = Thompson and Braver, 1971, DIS 46: 40; 28 = Waddle, 1977, DIS 52: 3; 29 = Wargent, and Hartmann-Goldstein, 1974, Heredity 33: 317-26. | More complete description below. cytology: Placed in 10E1-2 by Lefevre [Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 31-66]. other information: The miniature-dusky region has been subdi- vided into four recombinationally separable sites (Dorn and Burdick, 1962, Genetics 47: 503-18). # mD: miniature-Dominant phenotype: Wings of homozygote smaller than m/m. mD/+ wings intermediate between homozygote and wild type. Viability 20- 50% normal in males and 5% in homozygous females; most die in embryo. Fertility low in homozygous females. Wing size of mD/m and mD/dy intermediate between mD/+ and mD/mD. RK2. # mi: miniature-intermediate origin: Stable spontaneous derivative produced repeatedly by mu. phenotype: Wing length intermediate between that of mu and wild type. Resembles dy73 but complements dy73 and is mutant in combination with mu. Phenotype more extreme in combination with Df(1)m-fw. # mK: miniature of Krivshenko phenotype: Variegated-type position effect; enhanced by In(2LR)RevB = In(2LR)40;52C-E; In(1)mK = In(1)10E;20B; in turn enhances RevB (Wargent and Hartmann-Goldstein, 1974, Heredity 33: 317-26). # mu origin: A spontaneous derivative of dy73, which was accompanied by reversion of dy73. phenotype: A strong allele that mutates at an inordinately high rate, both germinally and somatically, to two different states, mi and ms. # ms: miniature-subliminal origin: Stable spontaneous derivative produced repeatedly by mu. phenotype: Hemizygotes, homozygotes, and heterozygotes with dy73 are wild type. In heterozygous combination with either mu or Df(1)m-fw displays a dy-like phenotype. # M: Minute Minutes are a class of genes, which, when the wild-type allele is present in hemizygous condition (not including X- linked Minutes in males), produce a characteristic phenotype consisting of short slender bristles and delayed development. That is, heterozygotes for deficiencies or loss of function alleles of these loci exhibit the Minute phenotype. Many of the early Minutes were mapped crudely, and those with similar map positions were seldom tested for complementation. As most of these Minutes have long since been lost, experimental establishment of allelism is not possible. Furthermore the results of deficiency analysis are also ambiguous; a Minute phenotype of a deficiency heterozygote indicates the presence of "at least one," not "only one" M gene. Given these uncer- tainties, tentative designations of allelism have been made, with the caveat that complementation tests have not or cannot be done. Furthermore inviability of trans heterozygotes does not invariably indicate allelism (Moscoso del Prado and Ripoll, 1983, Genet. Res. 42: 59-63). The existence of a Minute locus more frequently inferred from the phenotype of a deficiency heterozygote than a point mutant. Trans-acting suppressors turn out to be duplications of the locus on the M+ homologue (Schultz, Baker, 1972, DIS 49: 59; Broderick and Roberts, 1982, Genetics 102: 71-74). Phenotype of flies heterozygous for two different Minutes no more extreme than that of the more extreme mutant of the combination (Schultz, 1929, Genetics 14: 366-419); however, see M(3)65F and M(3)69E. Homozygotes and hemizygotes for mutant alleles are late embryonic or early larval lethals (reviewed by Wright, 1970, Adv. Genet. 15: 262-85). M/+/+ triploids are normal in phenotype, whereas M/M/+ triploids are lethal (Schultz). Heterozygotes often display secondary effects such as small body size, large and somewhat rough eyes, missing aristae, thin-textured wings with tendency to plexus venation, missing bristles (usually postverticals), and low fertility, espe- cially in females. The developmental delay exhibited by M/+ individuals is attributable to increased cell cycle times com- pared to that of wild type; this feature is autonomous such that +/+ cells produced by mitotic exchange in an M/+ fly proliferate more rapidly than the surrounding cells, leading to increased size of M+ clones, and facilitating ascertainment of mitotic recombination events (Morata and Ripoll, 1975, Dev. Biol. 42: 211-21); this observation was interpreted by Stern (1936, Genetics 21: 625-730) as increased incidence of somatic crossing over in the M-bearing chromosome arm of M/+ flies. Overgrowth of M+ clones used extensively in somatic genetic studies of development. Most Minutes enhance domi- nance of such venation characters as px and net or of such bristle characters as sc. Dominant lethal effects are fre- quent, in combination with Dl, J, and occasionally D. At least one Minute locus shown to encode a ribosomal protein (Kongsuwan, Yu, Vincent, Frisardi, Rosbash, Lengyel, and Mer- riam, 1985, Nature 317: 555-58), and presumably most if not all the others do as well. A consequent reduction in the rate of protein synthesis is postulated to lengthen the cell cycle and to limit the rate of bristle elaboration, which is postu- lated to require maximum rates of synthesis (Atwood). Since many Minute loci have been named according to the let- tered subdivision of the polytene map to which they have been localized, this revision attempts to standardize that mode of designation for all confirmed loci. Further restriction of designations to single lettered subdivisions should accompany revised localizations. # Mzw: see M(G6PD) # m-like: see dy31d # M-pro: see T(1;4)M-pro # M(1) The following table summarizes the Minute loci inferred to exist on the X chromosome on the basis of the phenotypes of females carrying mutations or deficiencies. The loci included are confirmed; others that have been claimed, but not con- firmed are included among the entries that follow the table. genetic cytological locus location location included in excluded from synonym ref ( ____________________________________________________________________________ M(1)1B 1-0.1 1B11-12 Df(1)y74k24.1 Df(1)svr M(1)Bld 7 M(1)3E 1-{5} 3E3-4 Df(1)N264-76 Df(1)N264-38 1, 6 M(1)5A 1-{13} 5A6-13 YPXDW14 YPXDB119 M(1)30? 4, 6 M(1)5D6A 1-13.7 5D5-6A Df(1)5D;6A YPXDD10 M(1)30? 3, 4, 6 M(1)7BC 1-{21} 7B-C YPXDS27 YPXDB123 4 M(1)7C 1-{22} 7C-E3 YPXDW31 YPXDB17 4 M(1)8F 1-30.0 8F1-2 Df(1)v+75d M(1)14-171 5 M(1)11F 1-{42} 11F1-4 Df(1)wy2 Df(1)N12 7 M(1)13A 1-{49} 12F6-13B6 YPXDS29 YPXDB128 4 M(1)14C 1-{54} 14B13-D1 Df(1)r75c Df(1)r-D1 M(1)19-153 5 M(1)15D 1-56.6 15D M(1)o 3 M(1)18C 1-62.7 18B9-D YPXDV6 YPXDB50 M(1)n 4 ( 1 = Demerec, Kaufmann, Fano, Sutton, and Sansome, 1942, Car- negie Inst. Wash. Year Book 41: 191; 2 = Lefevre, Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 32-66; 3 = Lefevre, 1974, Cold Spring Harbor Symp. Quant. Biol. 38: 591-99; 4 = Merriam et al.; 5 = Schalet, 1986, Mutat. Res. 163: 115-44; 6 = Schultz, 1929, Genetics 14: 366-419; 7 = Scott, 1987, Ph.D. Thesis, University of California at San Deigo; 8 = Voelker. # M(1)1B discoverer: Patterson. synonym: Vi: Viability. references: 1932, Z. Indukt. Abstamm. Vererbungsl. 60: 125-36. phenotype: Heterozygous deficiency for locus is extreme Minute of low viability. In Patterson's work, the nonappearance of Minutes led him to postulate a factor for viability (Vi). Eclosion delayed 76 hr (Ferrus, 1975, Genetics 79: 589-99). RK3A. alleles: Single ethyl-nitrosourea-induced mutant allele recovered by Voelker in a screen for lethals in the vicinity of su(s). Lethality occurs between the first larval instar and pupation (Eberl, Hilliker, and Voelker, 1988, DIS 67: 36). molecular biology: Both the recessive lethality of M(1)1BB46 and the Minute phenotype of Df(1)su(s)83 are rescued by a P- element transformant containing a 10 kb fragment of genomic DNA from immediately to the left of the su(s) gene. M(1)1B function is apparently encoded by a ~3.5 kb message (Voelker, Huang, Wisely, Sterling, Bainbridge, and Hiraizumi, 1989, Genetics 122: 625-42). cytology: Associated with the XP2RD element of T(1;2)Bld = T(1;2)1C3-4;60B12-13 when the 2RPXD element is replaced by a normal second chromosome. # M(1)3E: Minute (1) in region 3E location: 1-{5}. discoverer: Demerec, 1938. references: Demerec, Kaufman, Fano, Sutton, and Sansome, 1942, Year Book - Carnegie Inst. Washington 41: 191. phenotype: Identified on basis of slight Minute phenotype, barely distinguishable from wild type, associated with defi- ciencies that include region 3E. RK3A. cytology: Found and located in salivary chromosome bands 3E3-4 on the basis of slight M phenotype of females heterozygous for Df(1)N264-76 = Df(1)3B4-C1;3E4-5 and non-M phenotype of females heterozygous for Df(1)N264-38 = Df(1)2D3-4;3E2-3 and Df(1)N264-117 = Df(1)3A6-7;3E2-3. Also identified in a seg- mental deficiency scan of the X by Merriam and colleagues. # M(1)4BC: Minute (1) in region 4BC location: 1-{6.8}. discoverer: Demerec, 1938. references: Demerec, Kaufmann, Fano, Sutton, and Sansome, 1942, Year Book - Carnegie Inst. Washington 41: 191. phenotype: Strong Minute; easily distinguishable from wild type. RK2A. cytology: Inferred to be in salivary gland chromosome region 4B5 through 4C6 on the basis of extreme M phenotype of females heterozygous for Df(1)N264-73 = Df(1)3C3-4;4C6-7 versus slight M phenotype [M(1)3E] of Df(1)N264-42 = Df(1)3C4-5;4B4-6. How- ever, no minute phenotype observed in a segmental - deficiency scan of 3F through 4F by Merriam and Colleagues. As M(1)4BC was inferred only deficiencies including both 3E and 4BC, perhaps deficiency for 4BC acts as an enhancer of M(1)3E; how- ever Merriam and colleagues fail to report such an enchance- ment. # M(1)5A phenotype: Identified by extreme Minute phenotype and very low viability of segmental deficiencies for 5A6-13. other information: Possibly the same as the lost M(1)30, a spontaneous deficiency, which included cv at 5B, recovered by Schultz (1929, Genetics 14: 366-419). # M(1)5D6A other information: Considered the same as the lost spontaneous Minute, M(1)30 (CP627; Lefevre, 1973, Cold Spring Harbor Symp. Quant. Biol. 38: 591-99; Merriam et al.); M(1)30 was associ- ated with Df(1)M30, which included cv at 5B. # M(1)8F origin: Spontaneous. phenotype: Readily classified Minute found between lz and v (Schalet, 1986, Mutat. Res. 163: 115-44). cytology: Since the proximal breakpoint of Df(1)lz5, which is M+, is listed as 8F-9A (CP627), and the cytology of another M+ deficiency Df(1)C52 is listed as Df(1)8F3-9D6 (Mason, Green, Shaw, and Boyd, 1981, Mutat. Res. 81: 329-43), M(1)8F is probably located at 8F1-2 (Schalet, 1986). # M(1)11F phenotype: Identified on the basis of the slightly finer bris- tles and protracted development of Df(1)C246/+ females (Cray- mer and Roy, 1955, DIS 55: 204). other information: Tentatively equated to M(1)k by Craymer and Roy; however, genetic map position of M(1)k discordant with cytological position of Df(1)C146; also M(1)k described as strong Minute. # M(1)14C origin: Spontaneous. phenotype: Moderate Minute. cytology: Located in the 14B13 to 14D1-2 interval since allelic to Df(1)r75c = Df(1)14B13;15A9 but not to Df(1)r-D1 = Df(1)14D1-2;15D1-2 (Schalet, 1986, Mutat. Res. 163: 115-44). # M(1)15D phenotype: Eclosion delayed 35 hr (Ferrus, 1975, Genetics 79: 589-99). alleles: allele origin discoverer synonym ref ( ______________________________________________________ M(1)15D1 spont Bridges, 24B24 M(1)o 1 M(1)15D2 spont Spencer, 32i28 M(1)oSp 1, 2, 3 M(1)Sp ( 1 = CP627; 2 = Spencer, 1935, DIS 3: 28; 3 = Spencer, 1937, DIS 7: 14. M(1)18C1: Minute (1)18C1 Edith M. Wallace, unpublished. # M(1)18C phenotype: Heterozygous females have Minute bristles. Lethal in males. Viability and fertility low. Pupation delayed about 42 hr at 25 (Brehme). Wing cells smaller than normal (Brehme, 1941, J. Exp. Zool. 88: 135-60). RK2. allele origin discoverer synonym ref ( comments ______________________________________________________________________ M(1)18C1 spont Bridges, 1923 M(1)n 1, 2, 4 *M(1)18C2 | spont Curry, 36f10 M(1)n36 2, 3 weak M in C(1)RM M(1)36f ( 1 = Bridges, 1925, Proc. Nat. Acad. Sci. USA 11: 701-06; 2 = CP627; 3 = Curry, 1937, DIS 7: 14; 4 = Morgan, Stur- tevant, and Bridges, 1924, Carnegie Inst. Wash. Year Book 23: 231-36. | Allelism inferred from locations of M(1)18c2 at 62. # M(1)30: see M(1)5D6A # M(1)34i28: see M(1)oSp # M(1)36f: see M(1)18C # M(1)Bld: see M(1)1B #*M(1)k location: 1-36.3 discoverer: Bridges, 23d28. phenotype: A strong Minute. RK2. other information: Placed approximately 0.1 cm to the right of m in 10E1-2 in a cross of a type in which the v - g distance was normal. However, no Minute phenotype discovered by Mer- riam and colleagues in a segmental - deficiency scan of 9A- 12F. The original mutant may have been a gain-of-function allele of a haplo-sufficient gene. # M(1)n: see M(1)18C # M(1)o: see M(1)15D # M(1)oSp: see M(1)15D # M(1)Sp: see M(1)15D # M(2) Fifteen second-chromosome Minute loci considered to be well established and localized are tabulated below; additional information provided in entries that follow the table. Several described Minutes that are less well established are also included among the subsequent entries. genetic cytological locus location location included in excluded from synonym ref ( ____________________________________________________________________________ M(2)21AB 2-{0} 21AB Df(2L)a1 Su(2)5 M(2)21C 2-0.0 21C1-2 Df(2L)al Df(2L)S5 4 M(2)24D 2-{12} 24D4-8 Df(2L)sc19-1 Df(2L)dp-h28 M(2)LS2 2, 5, 9, 10 M(2)24F 2-12.9 24F1-25A1 Df(2L)sc19-6 Df(2L)ed-sz1 M(2)z 2, 5, 9, 10 M(2)25C 2-15.0 25B9-C3 Df(2L)sc19-7 Df(2L)sc19-10 M(2)S1 2, 5, 9, 10 M(2)30A 2-{40.5} 30A Df(2L)J4 Df(2L)J2 M(2)e, 2, 8 M(2)LS3 M(2)36F 2-54 36F2-6 Df(2L)TW202 Df(2L)hk18 M(2)m 5, 2 M(2)39F 2-54.3 39E-40A Df(2L)TW161 Df(2L)TW65 M(2)H 11 M(2)41A 2-55.1 41A M(2)S2 2 M(2)44C 2-57 44C 2PYDH136 2PYDB26 M(2)38b 2, 12 Df(2R)cn9 M(2)53 2-77.5 52D-53E YP2DR14 4P2DC4 M(2)S7 5 M(2)56CD 2-87.5 56C-D YP2DB184 YP2DG100 M(2)b 5, 7 M(2)56F 2-92.3 56F5-15 Df(2R)017 M(2)173 2, 3, 5 M(2)58F 2-101.2 58F Df(2R)M58F M(2)l 1, 6, 7 M(2)60E 2-108 60E Df(2R)M60E M(2)c ( 1 = Bridges, 1937, Cytologia, Fujii Jub., Vol. 2: 745-55; 2 = CP627; 3 = Duttagupta and Shellenbarger, 1980, Develop- ment and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York and London, pp. 25-33; 4 = Lewis, 1945, Genetics 30: 137-66; 5 = Linds- ley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Mik- los, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero, 1972, Genetics 71: 157-84; 6 = Morgan, Bridges, and Schultz, 1937, Carnegie Inst. Wash. Year Book 36: 298-305; 7 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 231; 8 = Schultz, 1929, Genetics 14: 366-419; 9 = Semeshin and Szidonya, 1985, DIS 61: 148-54; 10 = Szidonya and Reuter, 1988, Genet. Res. 51: 197-208; 11 = Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85; 12 = Yannopoulos, Stamatis, Zacharo- poulou, and Pelecanos, 1981, Mutat. Res. 83: 383-93. # M(2)21AB location: 2-0.0 (3.8 cm to the left of shv). origin: Induced by ethyl methanesulfonate. synonym: Su(z)5. references: Persson, 1976, Hereditas 82: 57-62. 1977, DIS 52: 1. phenotype: Body size and bristles reduced in heterozygotes; irregular facets in upper half of eye. Heterozygous females virtually sterile at temperatures above 18; surviving offspr- ing frequently have missing legs or halteres, somewhat nar- rowed wings, and reduced bristles. Homozygotes lethal. Selected on the basis of a dominant suppressor of zeste pheno- type. Characterized by relatively frequent reversions of all features of the phenotype save homozygous lethality. One such revertant found to be deficient for the tip of 2L, suggesting a gain of function rather than haplo insufficiency as the nature of the mutation (Kennison). cytology: Salivary-gland chromosomes appear normal. Placed in 21A-B on the basis of complementation by M(2)21AB of Df(2L)al, Df(2L)S2, and Df(2L)S3, the recovery of 0/196, 0/284, and 0/642 recombinants with net, al, and ex, respectively, and a position 3.8 cM from shv; complements l(2)gl. # M(2)21C phenotype: Identified by virtue of the extreme Minute phenotype of Df(2L)al/+. # M(2)24F phenotype: Medium Minute with good characteristics. About two days delay in puparium formation (Dunn and Mossige, 1937, Hereditas 23: 70-90). RK2. alleles: Three alleles are listed in the following table. allele origin discoverer synonym ref ( ________________________________________________ M(2)24F1 spont Schultz M(2)z 2 M(2)24F2 X ray Green M(2)zG1 1 M(2)24F3 X ray Green M(2)zG2 1 ( 1 = Persson, 1977, DIS 52: 1; 2 = Schultz, 1929, Genetics 14: 366-419. #*M(2)25C origin: X ray induced. discoverer: Schultz, 33a12. phenotype: Small-bristled Minute with heavy body. Classifica- tion good. Viability and fertility fairly good. RK2. # M(2)29: see M(2)56F # M(2)30A location: 2-40.5 [based on cytological position immediately to the left of J (2-41); originally mapped to 46_5]. phenotype: M(2)30A1 is a medium Minute with delayed hatching. 50% of females and 10% of males show abnormal abdomen effect. Most females sterile and remainder produce few progeny. RK3(A). alleles: Four presumptive alleles, but no complementation stu- dies done. Allelism based on similarity of genetic positions of M(2)30A1 = 46_5, M(2)30A2 = 43, and M(2)30A3 = 46_5; also both M(2)30A1/+ and M(2)30A4/+ described as female sterile. allele origin discoverer synonym ref ( comments ______________________________________________________________________ *M(2)30A1 spont Bridges, 20b25 M(2)e 2 moderate allele *M(2)30A2 spont Bridges, 24l16 M(2)t, M(2)et 1 weak allele M(2)30A3 X ray Schultz, 34k21 M(2)S11, M(2)eS 1 moderate allele M(2)30A4 X ray Sandler M(2)fs 3 ( 1 = CP627; 2 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 231; 3 = Sandler, 1977, Genetics 86: 567-82. cytology: Placed in 30A based on inclusion in Df(2R)J4 = Df(2R)31A-B;31F-32A, but not in Df(2R)J2 = Df(2R)31B;32A. Also distal to the breakpoint of T(Y;2)L52 = T(Y;2)30F-31A. other information: Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero (1972, Genetics 71, 157-84) placed M(2)e in 28D-29F, where reexamination of the data sug- gests no M locus exists; their M(2)LS3 presumably corresponds to M(2)e = M(2)30A. # M(2)33a: see Df(2R)M60E # M(2)36F phenotype: Medium to strong Minute. Eclosion of heterozygous deficiency delayed 30 hr (Ferrus, 1975, Genetics 79: 589-99). alleles: allele origin discoverer synonym ref ( comments ______________________________________________________________________ *M(2)36F1 spont Bridges, 23g12 M(2)m 1, 2 strong Minute *M(2)36F2 spont Schultz, 24l28 M(2)ms, M(2)s 1, 4 medium Minute *M(2)36F3 X ray Schultz, 33b3 M(2)mS13, 1 strong Minute M(2)S13 M(2)36F4 X ray Green M(2)mG 3 M(2)36F5 X ray Green M(2)HG 3 ( 1 = CP627; 2 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 231; 3 = Persson, 1977, DIS 52: 1; 4 = Schultz, 1929, Genetics 14: 366-419. cytology: Originally assigned its present chromosomal position on the basis of its extreme phenotype and that of the combina- tion Df(2L)G/Dp(2;Y)H plus its genetic map position estimated to be 2-54 by Bridges, even though the appropriate complemen- tation tests not performed. Allelisms inferred from similari- ties in genetic map positions: M(2)36F2 = 54.5; M(2)36F3 = 50; M(2)36F3 complemented by Dp(1;Y)G, but not by Dp(1;Y)H; M(2)36F4 fails to complement Df(2L)M36-56 and M(2)36F5 fails to complement Df(2L)M36F-S5. # M(2)38b: see M(2)44C # M(2)39F phenotype: Originally identified on the basis of the weak Minute phenotype of heterozygotes for the Df(2L)H segregant from Tp(2;Y)H = Tp(2;Y)37B1-2;40B2-3. alleles: allele origin discoverer synonym ref ( ______________________________________________________ *M(2)39F1| X ray Schultz, 33a9 M(2)HS5 1, 2 M(2)S5 M(2)39F2/ X ray Schultz, 33b7 M(2)HS12 1 M(2)S12 ( 1 = CP627; 2 = Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85. | Originally complemented M(2)36F; current stocks labelled M(2)HS5 do not; they are Df(2L)M36F-S5 (Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85). / Allelism inferred from weak phenotype and inseparability from pr. #*M(2)40c location: 2-65_5. origin: Spontaneous. discoverer: Ives, 40c. references: 1941, DIS 14: 39. phenotype: Medium Minute with probable eye effect. RK2. cytology: Crossing over normal. Genetic map position of 65_5 places M(2)40c in the vicinity of vg. Tentatively placed in the region deleted by the segmental deficiency formed from T(Y;2)D19 and T(Y;2)G53 [= Df(2R)48E;50A] [Pasztor, 1976, Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 185-206]; this region encroached upon from the right by Df(2R)vgC = Df(2R)49B2-3;49E1-F1, which has no Minute phenotype, thus restricting the tentative position of M(2)40c to 48E-49B. alleles: Besides the original allele, a second allele, M(2)40c2 (= M(2)40cG), tentatively identified as an allele by genetic map position, X ray induced by Green (Persson, 1977, DIS 52: 1). # M(2)41A phenotype: Medium Minute. Originally identified by virtue of Minute phenotype of Df(2R)M41A10; most recurrences shown to be deficiencies. Eclosion of heterozygous deficiency delayed 13 hr (Ferrus, 1975, Genetics 79: 589-99). alleles: Formerly listed alleles of M(2)41A known to be defi- ciencies by virtue of failing to complement mutants in adja- cent loci are listed with the deficiencies. allele origin discoverer synonym comments ________________________________________________________________ M(2)41A1 X ray Schultz, 33a M(2)S23, M(2)S3 no b-pr recombination M(2)41A2 X ray Schultz, 32k31 M(2)S29, M(2)S9 cytology: Placed in 41A, i.e., in the proximal heterochromatin of 2R, based on the normal polytene configuration but reduced amount of heterochromatin at the base of 2R in ganglion pro- phase figures of Df(2R)M41A10. # M(2)44C phenotype: Extreme Minute with small bristles and compact body. Viability varies with modifiers. M(2)44C/stw is non-stw; M(2)44C/M(2)p is viable. RK3. cytology: Tentatively placed in 44C based on its genetic map position, and the Minute phenotype of the segmental deficiency between T(Y;2)B26 and T(Y;2)H136 [= Df(2R)43E-F;44C], but not of Df(2R)cn9 = Df(2R)42E;44C. alleles: M(2)44C1 is the original spontaneous allele isolated by Curry (33b18); a second allele, M(2)44C2 X ray induced by Green (Persson, 1977, DIS 52: 1). # M(2)47: see M(2)56F # M(2)50J: see Df(2R)M41A50J # M(2)51: see M(2)56F # M(2)53 origin: X ray induced (occurred as a mosaic). discoverer: Schultz, 33a2. phenotype: Bristles very small; aristae often reduced; venation plexus like. Ecloses 24 hr late (Ferrus, 1975, Genetics 79: 589-99). Viability about 70% of wild type and variable. Fertility good. RK2. cytology: Salivary chromosomes apparently normal. other information: May be the same as RpA1. # M(2)56CD phenotype: Bristles extremely small. Abnormal abdomen effects in 90% of females and 40% of males. RK2. other information: The first Minute found in chromosome 2. # M(2)56F phenotype: Moderate Minute; expression enhanced when heterozy- gous to l(2)56Fb; enhances expression of cp (Schultz, 1929, Genetics 14: 366-419) and suppresses extra-sex-comb phenotype of Msc and Pc (Sinclair, Suzuki, and Grigliatti, 1981, Genet- ics 97: 581-606). alleles: Identified through recovery of M(2)56F1, which although cytologically normal fails to complement mutant alleles that complement each other, l(2)56Fa, l(2)56Fb, and M(2)56F; accordingly M(2)56F1 considered a deficiency [Df(2R)173]. M(2)56F4 and M(2)56F5 lethal in combination with Df(2R)017and Df(2R)173, but survive as homozygotes exhibiting Minute-like bristles; enhance Minute phenotype when heterozy- gous to other M(2)56F alleles and to each other, except that M(2)56F4 and M(2)56F7 complement. allele origin discoverer synonym ref ( comments _______________________________________________________________ M(2)56F1 Csik M(2)173 1, 3 multilocus; cytology normal M(2)56F2 EMS M(2)29 2, 5 noncomplementing M(2)56F3 EMS M(2)47 2, 5 noncomplementing M(2)56F4 EMS M(2)51 2, 5 recessive; complementing M(2)56F5 EMS M(2)2362 2, 5 recessive, noncomplementing M(2)56F6 EMS M(2)D741 2, 5 noncomplementing M(2)56F7 EMS M(2)U 2, 5 complementing M(2)56F8 X ray Green M(2)173G 4 ( 1 = Csik, 1930, Magy. Biol. Kutatointez. Munkai 3: 438-53; 2 = Duttagupta and Shellenbarger, 1980, Development and Neu- robiology of Drosophila (Siddiqi, Babu, Hall and Hall, eds.). Plenum press, New York and London, pp. 25-33, 1980; 3 = Gottschewski, 1935, DIS 4: 15; 4 = Persson, 1977, DIS 52: 1; 5 = Shellenbarger and Duttagupta, 1978, Mutat. Res. 52: 395-407. # M(2)58F phenotype: Identified by the strong Minute phenotype of Df(2R)M58F. Heterozygosity for null allele as represented by the deficiency characterized by a two-day delay in eclosion (at 25) owing to delay in puparium formation (Dunn and Mos- sige, 1937, Hereditas 23: 745-55); delay 19 hr according to Ferrus (1975, Genetics 79: 589-99). Eyes somewhat rough; veins often show plexus; abdominal sclerites often abnormal; ocelli often reduced. Viability 80-90% wild type and fertil- ity low. Presumed mutant allele, M(2)58F1, displays 13 hr delay in puparium formation at 25 (Brehme, 1939, Genetics 24: 131-61); slight delay in time of second larval molt. Viabil- ity, fertility, and classification excellent. Homozygote lethal in first larval instar. alleles: M(2)58F1 (formerly M(2)l' or M(2)l2), spontaneous with apparently normal polytene chromosomes, Schultz (26a7); M(2)58F2, / ray induced, with Minute phenotype suppressed by SM5, as if this Minute lies within the 58B-F segment dupli- cated in SM5 (Kennison: M located between Pu2 and PinB). # M(2)60E phenotype: Fairly strong Minute; slow development; good viabil- ity and fertility [description based on Df(2R)M60E = Df(2R)60E2-3;60E11-12]. Eclosion of Df(2R)M60E/+ delayed 49 hours (Ferrus, 1975, Genetics 79: 589-99). alleles: allele origin discoverer synonym ref ( _____________________________________________________ *M(2)60E1 spont Sturtevant, 20a7 M(2)c 1, 2, 3 M(2)60E2 X ray Green M(2)cG 4 ( 1 = Bridges, 1937, Cytologia, Fujii Jub., Vol. 2. 745-55; 2 = CP627; 3 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 231; 4 = Persson, 1977, DIS 52: 1. # M(2)115: see Df(2)M60E # M(2)173: see M(2)56F # M(2)2362: see M(2)56F # M(2)a: see M(2)60E # M(2)b: see M(2)56CD # M(2)B: see Df(2L)M24E-B # M(2)c: see M(2)60E # M(2)C: see Df(2L)M24E-C #*M(2)d location: 2-72. discoverer: Bridges, 20b25. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 231-34. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 231. phenotype: Heterozygote has no effect except when also hetero- zygous for M(3)d. The double heterozygote has Minute bristles in about 95% of flies. Probably lethal in homozygote. RK3. # M(2)D: see Df(2R)M41A-D # M(2)0741: see M(2)56F # M(2)e: see M(2)30A # M(2)fs: see M(2)30A # M(2)H: see M(2)39F # M(2)l: see M(2)58F M(2)LS1: not a Minute (Spencer, Hoffmann, and Gelbart, 1982, Cell 28: 451-61). # M(2)LS2: see M(2)24E # M(2)LS3: see M(2)30A # M(2)m: see M(2)36F #*M(2)p location: 2- (to the right of msf at 2-55.2). discoverer: Bridges, 24b6. references: Curry, 1939, DIS 12: 46. Morgan, Schultz, Bridges, and Curry, 1939, Year Book - Carne- gie Inst. Washington 38: 273-77. phenotype: Bristles small. Survives in combination with M(2)44C; not tested against Minutes further to the right. RK3(A). other information: May also have a second Minute factor to left of pr. Crossing over possibly reduced. # M(2)pD: see Df(2R)M41A-D # M(2)s: see M(2)36F2 # M(2)S1: see M(2)25C # M(2)S2: see Df(2R)M41A # M(2)S3: see M(2)41A # M(2)S4: see Df(2R)M41A4 # M(2)S5: see M(2)39F # M(2)S6: see M(2)36F # M(2)S7: see M(2)53 # M(2)S8: see Df(2R)M41A8 # M(2)S9: see M(2)41A # M(2)S10: see Df(2R)M41A10 # M(2)S11: see M(2)30A # M(2)S12: see M(2)39F # M(2)S13: see M(2)36F # M(2)t: see M(2)30A # M(2)U: see M(2)56F # M(2)vg11: see Df(2R)M-vg11 # M(2)z: see M(2)25A #*M(2) Minute mutations in the second chromosome that are lost and were never characterized are tabulated below. Mutant origin discoverer ref ( comments __________________________________________________________________ *M(2)28 Schultz 3 moderate, in In(2R)Cy *M(2)33d X ray Oliver, 33d14 2 In(2L+2R)Cy *M(2)34b X ray Oliver, 34b3 2 In(2L+2R)Cy *M(2)34d X ray Oliver, 34d25 2 In(2L+2R)Cy *M(2)34k X ray Oliver, 34k22 2 In(2L+2R)Cy *M(2)38k spont Mosssige, 38k4 1 ( 1 = CP627; 2 = Oliver, 1939, DIS 12: 48; 3 = Schultz, Genetics 14: 366-419. # M(3)1: see M(3)99B # M(3)6: see M(3)69E # M(3)33d: see M(3)69E # M(3)33j: see M(3)69E # M(3)36e: see M(3)96C # M(3) 18 third-chromosome Minute loci are tabulated; additional information provided in entries that follow the table. genetic cytological locus location location included inexcluded from synonym ref ( _____________________________________________________________________________ M(3)62A 3-{0} 61F-62A YP3DD8 YP3DA114 M(3)LS1 3 M(3)62F 3-{2} 62E-63A YP3DB21 YP3DD8 M(3)LS2 3 M(3)63B 3-{5} 63B6-C1 Df(3L)HR298Df(3L)HR232 M(3)LS3 3 M(3)65F 3-{23} 65F10-11 Dp(3;3)MS3 Dp(3;3)MS2 M(3)S37 6 M(3)hS37 6 M(3)67C 3-28.9 67C1-10 Dp(3;3)MS6 M(3)i55 Dp(3;3)MS7 M(3)69E 3-40.2 69E2-69F Df(3L)VW3 3PYDR7 M(3)h 1, 6 M(3)76A 3-44.3 76A3-B2 Df(3L)VW1 YP3DL131 M(3)S34 1, 7, 8 M(3)80 3-{47} 79E5-80F YP3DG72 YP3DJ162 M(3)LS4 3, 10 M(3)82BC 3-47 82A-82C YP3DJ17 YP3DA154 M(3)S39 3 M(3)85E 3-{50} 85E2-F1 Df(3R)by10 M(3)LS5 2, 3, 4 Df(3R)by62 M(3)86D 3-50.0 86D1-4 Df(3R)M86D M(3)S31 1, 3, 4 M(3)95A 3-79.7 94D-94E Dp(3;3)M95A M(3)w, M(3)B, 9, 11 M(3)Fla M(3)96A 3-{84} 95E6-96A5 YP3DH173 YP3DG73 3 M(3)96C 3-84.5 96C1-5 YP3DB217 YP3DH135 M(3)be 2 M(3)96CF 3-90.2 96C-97A YP3DH135 YP3DR87 M(3)j 2 M(3)99B 3-101.2 99B5-9 Dp(3;Y)L127Dp(3;1)46A M(3)1 5 M(3)99D 3-{101} 99D1-9 Dp(3;1)R14 Dp(3;1)R10 5 M(3)99E 3-106.2 99E4-F1 Dp(3;1)124PYP3DG116 M(3)g 5 M(3)100CF 3-105 100C-tip YP3DL129 M(3)f 5 ( 1 = Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91; 2 = CP627; 3 = Gonzalez, Molina, Casal, and Ripoll, 1989, Genetics 123: 371-77; 4 = Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Geth- mann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould- Somero, 1972, Genetics 71: 157-84; 5 = Kemphues, Raff, and Kaufman, 1983, Genetics 105: 345-56; 6 = Kongsuwan, Della- valle, and Merriam, 1986, Genetics, 112: 539-50; 7 = Mos- coso del Prado and Ripoll, 1983, Genet. Res. 42: 59-63; 8 = Schalet, 1960, DIS 34: 55; 9 = Schultz, 1929, Genetics 14: 366-419 10 = Stern, 1927, Naturwissenschaften 15: 745 11 = Sinclair, Suzuki, and Grigliatti, 1981, Genetics 97: 581-606; 12 = Vassin, Vielmetter, and Campos-Ortega, 1985, J. Neurogenet. 2: 291-308. # M(3)65F origin: X ray induced. discoverer: Schultz, 33a12. phenotype: Extreme Minute with fine bristles and small body. RK3. other information: Considered to be allelic to M(3)69E [M(3)h in CP627] on the basis of lethality of the trans heterozygote; however, Moscoso del Prado and Ripoll (1983, Genet. Res. 42: 59-63) demonstrated that the two Minutes occupy different cytological positions, thus rendering fallible the rule that double Minute genotypes are no more severe in phenotype than the more severe member of the pair, and suggesting some cau- tion in concluding allelism based on lethality of trans heterozygotes. # M(3)67C phenotype: Moderate alleles have good heterozygous viability; extreme alleles very late eclosing [45 hr according to Ferrus (1975, Genetics 79: 589-99)] with poor viability, and females usually sterile. Viability further reduced in presence of su(f) alleles (Girton, Langer, Cejka, 1986, Roux's Arch. Dev. Biol. 195: 334-37). alleles: Most assignments of allelism based on map positions in the vicinity of 3-30; M(3)67C4 through M(3)67C7 assigned on the basis of complementation results (Moscoso del Prado, 1983, Genet. Res. 42: 59-63; Persson, 1977, DIS 52: 1). allele origin discoverer synonym ref ( comments ________________________________________________________________________ *M(3)67C1 spont Bridges, 23d23 M(3)i 1 medium Minute *M(3)67C2 spont Bridges, 24b28 M(3)iq, 1 extreme Minute M(3)q *M(3)67C3 spont Schultz, 33a6 M(3)iS33, 1 extreme Minute M(3)S33 M(3)67C4 EMS M(3)i55 2, 3 M(3)67C5 X ray Green M(3)iG1 4 M(3)67C6 X ray Green M(3)iG2 4 M(3)67C7 X ray Green M(3)iG3 4, 3 M(3)67C8 | DEB Leicht l(3)dt0A4 non Minute? M(3)67C9 | EMS Leicht l(3)e80A6-1 non Minute? ( 1 = CP627; 2 = Morata and Ripoll, 1975, Dev. Biol. 42: 211-21; 3 = Moscoso del Prado, 1983, Genet. Res. 42: 59-63; 4 = Persson, 1977, DIS 52: 1. | Tentative assignments; these two recessive lethal alleles fail to complement each other, and M(3)67C9 fails to comple- ment M(3)67C4. # M(3)69E phenotype: Moderate alleles have good viability and fertility; puparium formation delayed two days (Dunn and Mossige, 1937, Hereditas 23: 70-90; Ferrus, 1975, Genetics 79: 589-99). Extreme alleles have low viability, flimsy or waxy wings with plexus effects along vein L2 and at posterior crossvein; eyes may be small and rough. alleles: M(3)69E4 and M(3)69E5 both lethal in trans heterozy- gotes with M(3)69E1, but see M(3)66A; allelism of M(3)69E2 and M(3)69E3 inferred from genetic map positions. Df(3L)M69E con- sidered an allele in CP627. allele origin discoverer synonym ref ( comments ___________________________________________________________________________ *M(3)69E1 spont P. R. Sturtevant *M(3)h 1, 2, 3, 5 medium Minute *M(3)69E2 heat Ives, 33d30 *M(3)h33d 3, 6 extreme Minute M(3)69E3 X ray Schultz, 33a12 M(3)hS38 3 extreme Minute M(3)69E4 spont Bridges, 25dt8 M(3)hv, 3 medium Minute M(3)v M(3)69E5 spont Sturtevant, 25g19 M(3)hy, 3, 4, 5, 7 medium Minute M(3)y ( 1 = Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 244; 2 = Coyne, 1935, DIS 4: 59; 3 = CP627; 4 = Mos- coso del Prado and Ripoll, 1983, Genet. Res. 42: 59-63; 5 = Mossige, 1938, Hereditas 23: 70-90; 6 = Plough and Ives, 1934, DIS 1: 33; 7 = Stern, 1927, Naturwissenschaften 15: 740-46. # M(3)76A origin: X ray induced. discoverer: Schultz, 33a6. phenotype: Slight Minute; overlaps wild type; in existing lines bristles appear normal, but recessive lethal effect at 44.3 remains. RK3. # M(3)80 synonym: M(3)Q-III, M(3)LS4Q-III. phenotype: Originally identified by virtue of the Minute pheno- type of the segmental deficiency for 79E5 to the chromo- center. An EMS-induced temperature-sensitive allele recovered and described by Sinclair, Suzuki, and Grigliatti (1981, Genetics 97: 581-606). Heterozygotes raised at 22 normal in phenotype; those raised at 29 display small bristles, rough eyes, prolonged developmental time, reduced viability, and interact with several unrelated mutations; at 29 but not at 22, in the presence of M(3)80/+, vg/+ and cp/+ exhibit reduced viability and incomplete wing margins; enhances J34e/+, Ly/+, Dfd/+, and DlD/+ such that they are lethal or weakly viable; also suppresses extra-sex-comb phenotypes of PC and Msc. These effects are similar to those shown by other minutes at all temperatures. The temperature sensitive periods of these effects reflect the time of action of the modified genes (Sinclair, Grigliatti, and Kaufman, 1984, Genet. Res. 43:257-75). M(3)80 homozygotes reared at 22 display moderate small bristle and rough eye phenes, as well as prolonged development; homozygotes lethal when reared at 29. Homozygous females fertile, but switching to 29 blocks egg production; males at 22 are poorly fertile and become sterile upon switching to 29. Temperature-pulse experiments yield a number of abnormal phenotypes which differ depending on the stage and duration of the pulse; described by Sinclair et al. other information: As there is apparently but a single mutant allele, we designate it M(3)801, sinking to synonomy the specific designation Q-III, used by the authors. May be the same as Rp21. # M(3)82BC origin: X ray induced. discoverer: Schultz, 33a3. phenotype: Extreme Minute with small body. Low viability and fertility. RK3. # M(3)85E other information: Identified by virtue of the Minute phenotype of the segmental deficiency produced between T(Y;3)G42 and T(Y;2)L17 [Df(3R)85E2-4;86A] and equated to M(3)S31 (Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero, 1972, Genetics 71: 157-84). M(3)S31 subse- quently shown to lie in 86D (Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91), and this Minute deficiency mapped to 85E2-F1 and renamed M(3)LS5 (Kemphues, Raff, and Kaufman, 1983, Genetics 105: 345-56). # M(3)86D phenotype: Fine-bristled Minute with medium viability. RK3. other information: Identified by virtue of Minute phenotype of Df(3R)M86D = Df(3R)86D1;86D4; no mutant alleles identified. This Minute erroneously designated M(3)S35 (Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Geth- mann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero, 1972, Genetics 71: 157-84). # M(3)95A phenotype: Strong Minute; eclosion delayed 40 hours (Ferrus, 1975, Genetics 79: 589-99). alleles: allele discoverer synonym ref ( comments __________________________________________________________ M(3)95A1 Schultz, 1925 M(3)w 7, 8 strong Minute M(3)95A2 Csik M(3)w124, 5, 6 strong Minute M(3)124 M(3)95A3 Burkart M(3)wB, 3 moderate Minute M(3)B M(3)95A4 Bridges, 38c6 M(3)wB2, 4 moderate Minute M(3)B2 M(3)95A5 Mossige, 35d M(3)wFla, 1, 2 strong minute M(3)Fla ( 1 = Bryson, 1937, DIS 7: 18; 2 = Bryson, 1939, DIS 12: 50; 3 = Burkart, 1935, DIS 4: 15; 4 = CP627; 5 = Csik, 1930, Magy. Biol. Kutatointez. Munkai 3: 438-53; 6 = Gottschewski, 1935, DIS 4: 15; 7 = Schultz, 1929, Genetics 14: 366-419; 8 = Stern, 1927, Naturwissenschaften 15: 740-46. cytology: Placed in 95A1 by Broderick and Roberts and in 94D-E by Vassin. # M(3)96A phenotype: Heterozygotes for 3PYDG73 YP3DH173 display slender bristles; viability and developmental time, however, normal. # M(3)96C phenotype: Medium Minute of excellent viability. Eclosion delayed 31 hr (Ferrus, 1975, Genetics 79: 589-99). M(3)96C2 reported to show plexus effect along vein L2 and at posterior crossvein. RK2. alleles: Allelism based on similarity of genetic map positions which put M(3)96C1 at 87_ and M(3)96C2 at 84.5. allele origin discoverer synonym ref ( ___________________________________________________ *M(3)96C1 spont Stern, 26a20 M(3)be 1 M(3)96C2 spont Bridges, 36e22 M(3)be36e M(3)36e ( 1 = Stern, 1927, Naturwissenschaften 15: 740-46. # M(3)96CF phenotype: Extreme Minute; very small bristles; late eclosing; females sterile or of very low fertility; males have fair via- bility and fertility. M(3)96CF2 described as having broad wings with plexus of veins and somewhat abnormal abdominal bands. alleles: Allelism of M(3)96CF1 and M(3)96CF2 inferred from genetic map positions of 90.2 and 90_10, respectively. allele origin discoverer synonym ref ( comments _____________________________________________________________________ M(3)96CF1 Bridges, 23dt2 M(3)j lethal with l(3)PR M(3)96CF2 spont Spencer, 36c21 M(3)jSp 1 M(3)Sp ( 1 = Spencer, 1937, DIS 7: 14. # M(3)99B origin: Spontaneous. discoverer: Bridges, 19b8. references: Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 206-7 (fig.). phenotype: Bristles slender and shorter than wild type. Some- what late hatching. Heterozygous deficiency for M(3)99B also displays rough eyes and slightly plexate wings (Kongsuwan, Dellavalle, and Merriam, 1986, Genetics 112: 539-50). RK2. other information: First Minute found. # M(3)99D phenotype: Identified by the phenotype of heterozygotes for a synthetic deficiency; no mutant alleles identified. Strong Minute; small bristles, slightly abnormal wings; eclosion delayed two to three days (Kongsuwan, Dellavalle, and Merriam, 1986, Genetics 112: 539-50). M(3)99D/+ females produce smaller than normal eggs; 10-15% of embryos fail to hatch often displaying fusion and partial deletion of segments post- rior to A3 (Kongsuwan, Yu, Vincent, Frisardi, Rosbash, Len- gyell, and Merriam, 1985, Nature 317: 555-58). molecular biology: Encodes the large ribosomal subunit 49. Transformants carrying 2.1 kb of upstream and 0.6 kb of down- stream sequence in addition to the entire coding sequence of rp49 suppress the mutant phenotype, including the maternal effect, of heterozygous deficiencies for M(3)99D (Kongsuwan et al., 1985). # M(3)99E phenotype: Identified by virtue of moderate Minute phenotype of heterozygotes for a synthetic deficiency (Kongsuwan, Della- valle, and Merriam, 1986, Genetics 112: 539-50). other information: Designated M(3)f by Kongsuwan, Dellavalle, and Merriam, despite the fact that M(3)f was originally recorded as having a strong phenotype. Localized just proxi- mal to the segmental deficiency for 99F-100B designated by Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero (1972, Genetics 71: 157-84) as delet- ing M(3)f+; Kongsuwan et al. found no Minute phenotype associ- ated with deficiencies for that region. Most likely M(3)f corresponded to a mutant or deficiency for M(3)99D or M(3)100CF, both of which are recorded as having strong Minute phenotypes. The description of heterozygotes for deficiencies for M(3)99E correspond more closely to that for M(3)g. # M(3)100CF phenotype: Identified by virtue of the strong Minute phenotype of heterozygotes for terminal deficiency for the region distal to 100C; very few escapers (Kongsuwan, Dellavalle, and Mer- riam, 1986, Genetics 112: 539-50). Reuter, Dorn, Wustmann, Friede, and Rauh (1986, Mol. Gen. Genet. 202: 481-87) describe su(var)3-12, which maps to 3-100.2, is associated with a Minute, and is deficient for 100F3-5. other information: The distal segment of 3R tentatively associ- ated with a Minute by Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero (1972, Genetics 71: 157-84) on the basis of their failure to recover terminal deficiencies and the published genetic position of M(3)g at 3-106.2; Kongsuwan, Dellavalle, and Merriam (1986, Genetics 112: 539-50) followed suit, placing M(3)g distal to M(3)f; however, phenotypic considerations suggest the allelic correspondences presented in the table of third-chromosome Minutes. Several Minute mutations in the third chromosome that were never located and are no longer available are tabulated below: mutant origin discoverer ref ( comments _____________________________________________________________________ *M(3)32l X ray Oliver, 32l2 4 suppressed crossingover *M(3)39b Curry, 39b17 1 strong Minute *M(3)54c neutron Mickey, 54c10 2 In(3L)73A9-10;75D7-E1 + In(3LR)61C2-3;80C4-5;93B4-5; 100B8-9 *M(3)bb spont Mossige 3 medium Minute ( 1 = Curry, 1939, DIS 12: 45; 2 = Mickey, 1963, DIS 38: 29; 3 = Mossige, 1946, DIS 20: 68; 4 = Oliver, 1939, DIS 12: 48. # M(3)124: see M(3)95A # M(3)B: see M(3)95A # M(3)be: see M(3)96C #*M(3)d location: 3-95. discoverer: Bridges, 20b25. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 231. phenotype: Part of digenic Minute. Produces no effect except when M(2)d is also heterozygous. Homozygote probably lethal. RK3. # M(3)f: see M(3)100CF # M(3)f: see M(3)S35 # M(3)Fla: see M(3)95A # M(3)g: see M(3)99E # M(3)h: see M(3)69E # M(3)hS37: see M(3)66A # M(3)i: see M(3)67C # M(3)j: see M(3)96CF # M(3)LS1: see M(3)62A # M(3)LS2: see M(3)62F # M(3)LS3: see M(3)63B # M(3)LS4: see M(3)80 # M(3)LS5: see M(3)85E # M(3)q: see M(3)67C # M(3)Q-III: see M(3)80 # M(3)S31: see M(3)86D # M(3)S32 location: 3- (not located). origin: X ray induced. discoverer: Schultz, 33a5. phenotype: Medium Minute. Most flies thickset. RK3. # M(3)S33: see M(3)67C # M(3)S34: see M(3)76A #*M(3)S35 location: 3-64. origin: X ray induced. discoverer: Schultz, 33a11. phenotype: Extreme Minute with small body. RK3. alleles: allele origin discoverer comments ________________________________________________ *M(3)S351 X ray Schultz 3-64 *M(3)S352 ( Moriwaki, 38f2 3-62.4 ( Synonym: M(3)f; M(3)S35f. References: Moriwaki, 1939, DIS 12: 50. other information: Two mutants, both lost, mapped between 60 and 65, yet segmental deficiencies covering the region reveal no Minute phenotypes. # M(3)S36 location: 3- (not located). origin: X ray induced. discoverer: Schultz, 32k26. phenotype: Variable phenotypes appear in stock; Minute and variegated for ss-like. Not studied. RK3. # M(3)S37: see M(3)66A # M(3)S38: see M(3)69E # M(3)S39: see M(3)82BC # M(3)Sp: see M(3)96CF # M(3)v: see M(3)69E # M(3)w: see M(3)95A # M(3)x: Minute (3) with C(3)x location: 3- (on the left arm). origin: Spontaneous in In(3L)P. discoverer: Muller, 1929. phenotype: Rather extreme Minute; expression reduced by H. RK3A. # M(3)y: see M(3)69E # M(4): see Df(4)M101 # M(4)2: see Df(4)M101-2 # M(4)3: see Df(4)M101-3 # M(4)4: see Df(4)M101-4 # M(4)101 location: 4-0. references: Hochman, 1974, Cold Spring Harbor Symp. Quant. Biol. 38: 581-89. phenotype: Medium Minute; viability good; development pro- tracted; eclosion delayed 33 hr (Ferrus, 1975, Genetics 79: 589-99). M(4)101/+/+ triplo-fours are non-Minute (Mohr, 1933, Hereditas 17: 317-32). Homozygous mutants die in embryonic stage (Farnsworth, 1951, Genetics 36: 550). RK2. alleles: Formerly designated alleles nearly all deficiencies; only M(4)10157g has normal polytenes and fails to uncover mutations in neighboring loci (Hochman, Gloor, and Green, 1964, Genetics 35: 109-26). cytology: Placed in 101F2-102A5 on the basis of Df(4)M101-63a = Df(4)101F2-101A1;101A2-5 (Hochman). # M(4)62e: see Df(4)M101-62e # M(4)62f: see Df(4)M101-62f # M(4)63a: see Df(4)M101-63a # M(B): see su(B) # m(Est6): modifier of Esterase 6 location: 3-56.7. origin: Spontaneous. synonym: m-est, M-est. references: Cochrane, 1976, Genetics 83: s16. Cochrane and Richmond, 1979, Biochem. Genet. 17: 167. phenotype: Two alleles; the dominant allele arbitrarily desig- nated m(Est6)+. m(Est6) decreases the electrophoretic mobil- ity of the products of some alleles, but not of others. Also modifies leucine amino peptidase, but not twelve other tested enzymes. Thought to change charge rather than conformation. Evidence that sialylation not involved. # M(g): see e(g) # M(G6PD): Modifier of Glucose 6 Phosphate Dehydrogenase location: 1-65. origin: Spontaneous. synonym: MZw. references: Komma, 1968, Biochem. Genet. 1: 229-37. phenotype: A dominant modifier of the electrophoretic mobility of G6PD encoded by both ZwA and ZwB. Mobility faster in presence of M(G6PD) than in M(G6PD)+ homozygotes. # m(GPDH): see r((GPDH) # M(Sd): Modifier of Sd location: 2-57 (right of Rsp; near cn). origin: Spontaneous. references: Hiraizumi, Martin, and Eckstrand, 1980, Genetics 95: 693-706. phenotype: Enhances segregation distortion in genotypes hetero- zygous for Sd, M(Sd), and Rsps; not the same as E(Sd). Causes high levels of male infertility in genotypes that are hetero- zygous for Sd and M(Sd) and homozygous for Rsps; those males that are fertile produce very few offspring.