k: kidney From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 77. # k: kidney location: 3-64. origin: Spontaneous. discoverer: Bridges, 12f26. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 72 (fig). Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 214 (fig.), 227. phenotype: Eye size reduced by indentation of front margin. Tuft of vibrissae and hairs below eye. Penetrance varies with allele as does expression; moderate alleles overlap wild type significantly. RK3. allele origin discoverer ref ( phenotype ________________________________________________________ k1 spont Bridges, 12f26 1, 4 moderate *k2 spont Goldschmidt, 1927 2 moderate k3 spont Gottschewski, 1937 2 weak k6b spont G.L. Lee 3 strong kD spont Puro, 60c11 5 | ( 1 = Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 72 (fig.); 2 = Gottschewski and Ma, 1937, Z. Indukt. Abstamm. Vererbungsl. 73: 584-97; 3 = Lee, G.L., 1972, DIS 48: 18; 4 = Morgan, Bridges, and Sturtevant, 1925, Bibliogr. Genet. 2: 214 (fig.), 227; 5 = Puro, 1964, DIS 39: 65. | Derivative of k1; phenotype described separately below. # kD: kidney-Dominant phenotype: Eyes of heterozygote reduced at anterior edges. Expression variable; in extreme cases, eye size about one- third normal. kD/k more extreme. Eyes of homozygote reduced about as much as kD/k but occasionally one or both eyes miss- ing; antennae usually slightly deformed with thickened aris- tae. RK1. # kar: karmoisin location: 3-51.7. phenotype: Eye color like st but less bright. Ocelli white. Eyes contain 29% wild-type brown pigment (Nolte, 1954, J. Genet. 52: 111-26). Larval Malpighian tubes of kar1 but not kar2 considerably lighter than wild type; difficult to clas- sify in living larvae (Brehme and Demerec, 1942, Growth 6: 351-56). Phenoxazinone synthetase level subnormal in mutants; maybe a structural gene for this enzyme; 3- hydroxykynurenine accumulates (Sullivan, Kitos, and Sullivan, 1974, J. Exp. Zool. 188: 225-34). RK1. cytology: Placed in 87C8 by Gausz, Bencze, Gyurkovics, Ash- burner, and Ish-Horowicz (1979, Genetics 93: 917-34). alleles: Many deficiencies have been given allelic designations in the past; they are tabulated under Df(3R)kar. Alleles believed unaccompanied by deficiencies are summarized in the accompanying table. allele origin discoverer ref ( cytology __________________________________________________ kar1 spont Pariser 2 kar2 spont Bridges kar5l Gelbart 3 Tp(3;1) kar6l In(3R) karD | X ray Henikoff 4 In(3R) karH4 X ray Henikoff 4 In(3R) karH6 X ray Henikoff 4 In(3R) karS Schalet TM3 karSz1 EMS 1 karSz2 EMS 1 karSz3 EMS 1 karSz4 EMS 1 karSz5 / EMS 1 karSz6 EMS 1 karSz7 EMS 1 karSz8 / EMS 1 karSz9 EMS 1 karSz10 EMS 1 karSz11 / EMS 1 karSz12 / EMS 1 karSz13 / EMS 1 ( 1 = Gausz, Bencze, Gyurkovics, Ashburner, Ish-Horowicz, and Holden, 1979, Genetics 93: 917-34; 2 = Gottschewski, 1935, DIS 4: 15; 3 = Hall and Kankel, 1976, Genetics 83: 517-35; 4 = Henikoff, 1979, Genetics 93: 105-15. | Described more fully below. / Independently induced Df(3R)kar with the same identifying Sz number tabulated under deficiencies. # karD phenotype: karD/+ flies exhibit bright red eyes characteristic of kar homozygotes; ocelli not completely colorless; seem to variegate, Addition of an extra Y chromosome to karD/+ shifts the phenotype toward wild type. Homozygotes show reduced via- bility. cytology: Associated with In(3R)karD=In(3R)81F;87C8 which variegates for a recessive lethal as well as for kar. # karmoisin ghost: see sad # Kartal: see Fs(3)Sz27 # Kavar: see Fs(3)Sz14 # kay: kayak location: 3-99. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). Roark, Mahoney, Graham, and Lengyel, 1985, Dev. Biol. 109: 476-88. phenotype: Homozygous lethal; embryo open dorsally. alleles: Two. cytology: Placed in 99A-100A. # kdn: knockdown (J.C. Hall) location: 1- (between cv and v). origin: Induced by ethyl methanesulfonate. discoverer: Christensen. references: Ganetzky and Wu, 1982, Genetics 100: 587-614. phenotype: Temporary paralysis following mechanical shock; sen- sitive only to initial shock, refractory thereafter. The bang-sensitive phenotype is suppressed by napts at its permis- sive temperature; the electrophysiology of the larval neu- romuscular junction appears normal. alleles: One mutant allele, called kdnPC64. other information: Could be allelic to rex. # kdu: kudu location: 2-{22}. origin: Hybrid dysgenesis. references: Berg and Spradling, 1989. phenotype: Recessive female-sterile mutation; eggs have fused or thin membranes. cytology: Placed in 28A. #*ke: kidney eye location: 1-28.6. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1959, DIS 33: 87. phenotype: Eyes small and extremely rough; anterior border indented, giving a kidney shape. Wings small, abnormal, outspread, or upheld. Veins thick and often interrupted or fail to reach wing margin, which is usually incised. Deformed antennae. Bristles straggly; occasionally, one is missing. Flies short lived; 50% die less than 24 hr after eclosion. Sterile, probably because they are too weak to mate. RK3. # kel: kelch location: 2-{53}. origin: Induced by ethyl methanesulfonate. discoverer: Schupbach. references: Steward and Nusslein-Volhard, 1986, Genetics 113: 665-78. phenotype: Recessive female sterile. Nurse cell cytoplasm not incorporated in oocyte. Small eggs "open" at anterior pole since egg membranes are not deposited around whole oocyte. cytology: Located in 36E4; included in Df(2L)H20 = Df(2L)36A8- 9;36E3-4 and Df(2L)TW330 = Df(2L)36E4-F1;37D1-2. # Keled: see Fs(3)Sz15 # Ketel: see Fs(2)Sz7 # Keve: see Fs(3)Sz16 # kf: see cut # Kf1: Kynurenine formamidase 1 location: 3-{62-70}. references: Moore and Sullivan, 1975, Biochem. Biophys. Acta 397: 486-77. 1978, Biochem. Genet. 16: 619-34. phenotype: The structural gene for one of the two forms of kynurenine formamidase found in Drosophila melanogaster [aryl- formylamine amidohydrolase (EC 3.5.1.9)]. Formamidase I is a dimer of 34,000 subunit molecular weight, which catalyzes the conversion of N-formylkynurenine to kynurenine. Biochemical characterization by Moore and Sullivan. cytology: Localized to 91B-93F by dosage response to segmental aneuploidy. # Kf2 location: 2-{13-21}. references: Moore and Sullivan, 1975, Biochem. Biophys. Acta 397: 468-77. 1978, Biochem. Genet. 16: 619-34. phenotype: Structural gene for the second form of kynurenine formamidase in Drosophila melanogaster. Formamidase II is monomeric with a molecular weight of 31,000. Amino acid com- positions of formamidase I and II are virtually indistinguish- able, suggesting that they are duplicate genes. They do not interconvert in vitro. The supposed duplicate nature of the coding sequence postulated as the explanation of the inability to recover mutants defective in the conversion of N- formylkynurenine to kynurenine. cytology: Dosage studies in segmental aneuploids place the structural gene in 25A-27E. #*Kg: Kugel location: 3-47.5 [changed from 48.2 in order to lie 0.1 unit to left of Ki; as determined using KgV (Craymer, 1980, DIS 55: 199)]. origin: Spontaneous. discoverer: Benz, 1953. references: 1956, Rev. Suisse Zool. 63: 208-16. phenotype: Larva, pupa, and adult shorter and thicker than nor- mal. Most striking in pupa. Homozygote more extreme than heterozygote. Homozygote viability 68% of wild type and fer- tility somewhat reduced. RK2. # KgV: Kugel of Valencia origin: X ray induced. discoverer: Valencia, 1964. synonym: ChV: Chubby of Valencia. references: 1968, DIS 43: 60. Craymer, 1980, DIS 55: 198. phenotype: Larvae, pupae, and adults short and thickset; espe- cially easy to score preadult stages. Homozygous males viable and fertile. # Ki: Kinked location: 3-47.6 [Location in 3R demonstrated by mitotic recom- bination. (Merriam and Garcia-Bellido, 1972, DIS 44:51) and by recovery in newly induced C(3R)RM but not C(3L)RM chromo- somes (Lutolf, 1971, Experientia 27: 1357)]. origin: Spontaneous. discoverer: R. F. Grell, 57l. references: 1958, DIS 32: 80. phenotype: All bristles and hairs of heterozygote shortened and twisted. Resembles sn. Viability and fertility excellent; classification easy. Homozgyote has more extreme bristle and hair effects. Expression much reduced in flies raised at 18 (Hardy). Ki+ an excellent marker for cuticular clones in Ki/+ heterozygotes. Viability somewhat reduced but fertility near normal. RK1 as heterozygote. alleles: Ki72 induced by ethyl methanesulfonate (Garcia-Bellido and Dapena, 1974, Mol. Gen. Genet. 128: 117-30). cytology: Placed in 83DE by deficiency analysis (Roehrdanz and Lucchesi, 1980, Genetics 95: 355-66). other information: Very closely linked to the triplo-lethal region of 83DE; attempts to revert Ki by deletion unsuccessful (Kaufman, 1978, Genetics 90: 579-96), and Ki frequently deleted simultaneously with Tpl (Roehrdanz and Lucchesi). # kidney: see k # kidney eye: see ke # killer of males: see km # Killer of prune: see awdK # Kin: Kinesin location: 2-{78}. discoverer: Christensen. references: Saxton, Porter, Cohn, Scholey, Raff, and McIntosh, 1988, Proc. Nat. Acad. Sci. USA 85: 1109-13. Yang, Saxton, and Goldstein, 1988, Proc. Nat. Acad. Sci. USA 85: 1864-86. Scholey, Heuser, Yang, and Goldstein, 1989, Nature 338: 355- 57. Yang, Laymon, and Goldstein, 1989, Cell 56: 879-89. phenotype: Encodes a protein from Drosophila that behaves simi- larly in its effect on movement of microtubules and is antigenically similar to the heavy chain kinesin of squid and sea urchin (Saxton et al., 1988). The Drosophila kinesin is found in embryos, larvae, adults, and tissue culture cells. Flies deficient for Kin survive through early embryogenesis (Saxton). molecular biology: Antiserum recognizing the heavy chain of Drosophila melanogaster kinesin was employed in the isolation of cDNA clones. The complete nucleotide and predicted protein sequence of a 3.8 kb cDNA clone were obtained (Yang et al., 1988, 1989); this clone produced a protein synthesized in vitro that, like heavy chain kinesin in other organisms, binds to microtubules in the presence of the non-hydrolyzable analo- gue of ATP, AMP-PNP, but not in the presence of ATP or 0.1 M KCl. The cDNA is 3547 nucleotides long and has one long open reading frame; the predicted protein has a molecular weight of 110,428 daltons and is made up of 975 amino acids. Analysis of the protein indicates the presence of a 50 kd globular amino-terminal domain with sites for microtubule and nucleo- tide binding (the motor domain), a 50-60 kd (-helical coiled- coil stalk region, and a short carboxy-terminal region that is also globular and interacts with light chains (Yang et al., 1989). These structural elements show good correlation with the corresponding structure of mammalian, squid, and sea urchin kinesin heavy chains observed under the electron micro- scope (Amos, 1987, J. Cell Science 87: 105-11; Hirakawa, Pfister, Yorufuji, Wagner, Brady, and Bloom, 1989, Cell 56: 867-78; Scholey et al., 1989). # Kinked: see Ki # kinked femur: see kf under ct # kis: kismet (J.A. Kennison) location: 2-0 (between net and art). origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1984. synonym: Su(Pc)21AB. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Isolated as a dominant suppressor of Pc alleles. Homozygous lethal. Duplications for kismet strongly enhance the dominant Pc phenotypes. kismet mutations suppress the antennal transformations of AntpB, Antp73b, and AntpNs, as well as the transformations caused by ectopic expression of Antp protein under the control of a heat-inducible promoter. kismet mutations in mitotic clones induced during larval stages transform the fifth abdominal segment into a more ante- rior segmental identity. alleles: Eight alleles induced by ethyl methanesulfonate [including three on Dp(2;Y)L124], two by gamma irradiation, and one associated with an insertion of a P-element derived ry vector. cytology: Located in 21B6-7 based on its failure to complement Df(2L)net - PMF = Df(2L)21A1;21B7-8 and Df(2L)net - PMC = Df(2L)21A1;21B6-7 but not Df(2L)net - PM47C = Df(2L)21A1;- 21B6-7. # kisS: kismet-Spradling origin: P-element-induced insertion. discoverer: Spradling. other information: ry+ transformant that fails to complement kismet mutations for viability. Failure to complement kismet mutations is revertable at high frequency in the presence of P-element transposase. #*kk: kinky location: 1-42. origin: Spontaneous. discoverer: Philip. references: 1937, DIS 8: 10. phenotype: Bristles slightly bent or forked. RK3. other information: May be an allele of fw. # kkv: krotzkopf verkehrt location: 3-49. origin: Induced by ethyl methanesulfonate. references: Jurgens, Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). phenotype: Homozygous lethal; head skeleton crumbled; denticle bands narrower; embryo rarely inverted in egg case. alleles: Twenty including one weak and one temperature sensi- tive. # KL: Male fertility complex in the long arm of the Y chromosome synonym: Mutants in the Y-linked male-fertility genes have in the past been symbolized ms(Y) followed by an identifying sym- bol; this convention fails to indicate allelic relations among independently recovered Y-linked sterile mutants. Accord- ingly, mutant terminology now uses the symbol of the fertility gene involved with the particular allele designated by the previously used identifying symbol as a superscript. e.g., ms(Y)G9 now is kl-3G9. references: Brosseau, 1960, Genetics 45: 257-74. Kennison, 1981, Genetics 98: 529-48. 1983, Genetics 103: 219-34. Hazelrigg, Fornili, and Kaufman, 1982, Chromosoma 87: 535-59. Gatti and Pimpinelli, 1983, Chromosoma 88: 349-73. Bonaccorsi, Pisano, Puoti, and Gatti, 1988, Genetics 120: 1015-34. The male fertility complex of the long arm of the Y chromo- some, originally called K1 by Stern (1929, Z. Indukt. Abstamm. Vererbungsl. 51: 253-353) and subsequently called KL by Bros- seau comprises four male-fertility genes designated kl-1, kl- 2, kl-3, and kl-5 (kl-4 described by Brosseau, has not been confirmed). These loci have been defined by complementation analysis (Brosseau), by segmental aneuploidy (Kennison) and by cytological localization of male-sterile, Y-chromosome break- points (Gatti and Pimpinelli). # kl-1 phenotype: Males deficient or mutant at kl-1 are sterile. One allele of Brosseau's, probably kl-1B13, studied by Kiefer, produces motile sperm which are transferred to females but do not reach the female sperm-storage organs; substantial amounts of sperm degeneration observed [Kiefer, 1969, Genetics 61: 157-66 (fig.)]. The spermatogenic lesion resembles the late phenotypes of other sterile mutants suggesting that the primary departure from normality has been overlooked. Cross sections of sperm tails nonuniform within a cyst and the number of tails at various levels in a bundle varies. The minitubules, which fill the interstices among the individual- ized sperm tails of mature bundles, not formed. [Hardy, Tokuyasu, and Lindsley, 1981, Chromosoma 83: 593-617 (fig.)]. alleles: In addition to the alleles tabulated, Williamson (1972, Mol. Gen. Genet. 119: 43-47) reported fifteen non- complementing and five complementing alleles, all induced by ethyl methanesulfonate. origin allele treatment treated discoverer synonym ref ( _______________________________________________________________ kl-1B13 X ray y+Y Brosseau ms(Y)L13 2, 3 kl-1B25 X ray y+Y Brosseau 25 2 kl-1B29 X ray y+Y Brosseau 29 2 kl-1B30 X ray y+Y Brosseau 30 2 kl-1B33 X ray y+Y Brosseau 33 2 kl-1E3 EMS BSYy+ Kennison ms(Y)E3 6 kl-1E4 EMS BSYy+ Kennison ms(Y)E4 6 kl-1G6 / ray BSYy+ Kennison ms(Y)G6 6 kl-1G16 | / ray BSYy+ Kennison ms(Y)G16 5 kl-1G17 / / ray BSYy+ Kennison ms(Y)G17 5 kl-1ts1 EMS Y E91 1 kl-1ts2 EMS Y A141 1 kl-1X1 X ray BSYy+ Lms1A12 4 kl-1X2 X ray BSYy+ Lms1A18 4 kl-1X3 X ray BSYy+ Lms1A22 4 kl-1X4 X ray BSYy+ Lms1B8 4 ( 1 = Ayles, Sanders, Kiefer, and Suzuki, 1973, Dev. Biol. 32: 239-57; 2 = Brosseau, 1960, Genetics 45: 257-74; 3 = CP627; 4 = Hazelrigg, Fornili, and Kaufman, 1982, Chro- mosoma 87: 535-59; 5 = Kennison, unpublished information; 6 = Kennison, 1983, Genetics 103: 219-34. | Induced on the same chromosome with kl-5G16. / Induced on the same chromosome with kl-3G17. cytology: Y-h14. # kl-2 phenotype: Males deficient or mutant for kl-2 are sterile; pri- mary ultrastructural lesion not identified. Such sterile males lack a 300-325 kilodalton sperm polypeptide thought to be a structural component of the axoneme (Goldstein, Hardy, and Lindsley, 1982, Proc. Nat. Acad. Sci. USA 79: 7404-09; Hardy, Lindsley, Livak, Lewis, Sivertsen, Joslyn, Edwards, and Bonaccorsi, 1984, Genetics 107: 591-610). alleles: In addition to the alleles tabulated, Williamson (1972, Mol. Gen. Genet. 119: 43-47) reported five ethyl- methanesulfonate induced complementing alleles. origin allele treatment treated discoverer synonym ref ( _________________________________________________________________ kl-2B37 X ray y+Y Brosseau ms(Y)L37 2, 3, 4 kl-2B38 X ray y+Y Brosseau ms(Y)L38 2, 3, 4 kl-2E5 EMS BSYy+ Kennison ms(Y)E5 5 kl-2E6 EMS BSYy+ Kennison ms(Y)E6 5 kl-2E7 EMS BSYy+ Kennison ms(Y)E7 5 kl-2E8 EMS BSYy+ Kennison ms(Y)E8 5 kl-2G7 EMS BSYy+ Kennison ms(Y)G7 5 kl-2G8 EMS BSYy+ Kennison ms(Y)G8 5 kl-2ts1 | EMS Y A66 1 kl-2ts2 | EMS Y A82 1 kl-2ts3 | EMS Y A145 1 kl-2X1 X ray BSYy+ Lms2A48 4 ( 1 = Ayles, Sanders, Kiefer, and Suzuki, 1973, Dev. Biol. 32: 239-57; 2 = Brosseau, 1960, Genetics 45: 257-74; 3 = CP627; 4 = Hazelrigg, Fornili, and Kaufman, 1982, Chro- mosoma 87: 535-59; 5 = Kennison, 1983, Genetics 103: 219- 34. | Listed as involving either kl-2 or kl-4. cytology: Y-h10. # kl-3 phenotype: Males mutant for kl-3 fail to assemble the outer dynein arms associated with the peripheral nine microtubule doublets of the sperm-tail axoneme [Hardy, Tokuyasu, and Lindsley, 1981, Chromosoma 83: 593-617 (fig.)]. Such males also fail to produce a kl-3-specific 300-325 kilodalton sperm polypeptide presumed to be a component of the outer dynein arms (Goldstein, Hardy, and Lindsley, 1982, Proc. Nat. Acad. Sci. USA 79: 7404-09). Such mutants display an exceedingly low level of fertility at 25 but not at 18 immediately upon eclosion, but not thereafter (Kennison, 1983, Genetics 103: 219-34). Deficiencies for kl-3 are completely sterile, and in addition to the above mutant phenotype, they fail to elaborate the loops (ribbon-like structure) observed in the primary spermatocyte nuclei of normal males by light micros- copy and the reticular material ordinarily observed by elec- tron microscopy in spermatocyte nuclei (Hardy et al., 1981). The kl-3 loops are visible in living spermatocytes and in fixed cells stained with the protein-specific dye CBB; these loops are also demonstrated by the polyclonal antibody Sph-155 but do not react with monoclonal antibody S5 (Bonaccorsi et al., 1988). alleles: In addition to the alleles tabulated, Williamson (1972, Biol. Gen. Genet. 119: 43-47) reported 23 non- complementing and nine complementing alleles induced by ethyl methanesulfonate. origin allele treatment treated discoverer synonym ref ( _________________________________________________________________ kl-3B11 X ray y+Y Brosseau ms(Y)L11 1, 2, 3 kl-3B20 X ray y+Y Brosseau ms(Y)L20 2 kl-3B27 X ray y+Y Brosseau ms(Y)L27 2 kl-3B41 X ray y+Y Brosseau ms(Y)L41 2 kl-3E9 EMS BSYy+ Kennison ms(Y)E9 5 kl-3E10 EMS BSYy+ Kennison ms(Y)E10 5 kl-3E11 EMS BSYy+ Kennison ms(Y)E11 5 kl-3G9 / ray BSYy+ Kennison ms(Y)G9 4 kl-3G10 / ray BSYy+ Kennison ms(Y)G10 5 kl-3G11 / ray BSYy+ Kennison ms(Y)G11 5 kl-3G17 | / ray BSYy+ Kennison ms(Y)G17 4 kl-3X1 X ray BSYy+ Lms3A1 3 kl-3X2 X ray BSYy+ Lms3A40 3 kl-3X3 X ray BSYy+ Lms3A51 3 kl-3X4 X ray BSYy+ Lms3B10 3 ( 1 = Brosseau, 1960, Genetics 45: 257-74; 2 = CP627; 3 = Hazelrigg, Fornili and Kaufman, 1982, Chromosoma 87: 535-59; 4 = Kennison, unpublished information; 5 = Kennison, 1983, Genetics 103: 219-34. | Induced on the same chromosome with kl-1G17. cytology: Y-h7. # kl-4 Existence inferred by Brosseau (1960, Genetics 45: 257-74) on the basis of the failure of a kl-3- Y to complement a kl-5- Y for male fertility. No single site mutant or breakpoint interrupting kl-4 alone reported by Brosseau, Kennison (1983, Genetics 103: 219-34), Hazelrigg, Fornili and Kaufman (1982, Chromosoma 87: 535-59), or Gatti and Pimpinelli (1983, Chro- mosoma 88: 349-73). Williamson (1972, Mol. Gen. Genet. 119: 43-47), on the other hand reported seven noncomplement- ing and seven complementing alleles induced by ethyl methanesulfonate. # kl-5 phenotype: Males mutant for kl-5 fail to assemble the outer dynein arms associated with the A tubules of the peripheral doublets of the sperm tail axoneme [Hardy, Tokuyasu, and Lindsley, 1981, Chromosoma 83: 593-617 (fig.)]. Such males also fail to produce kl-5-specific 300-325 kilodalton sperm polypeptide considered to be a component of the outer arms (Goldstein, Hardy, and Lindsley, 1982, Proc. Nat. Acad. Sci. USA 79: 7404-09). kl-5 mutants exhibit very low level of fertility at 25 but not at 18 and in young but not older males (Kennison, 1983, Genetics 103: 219-34). Deficiencies for kl-5 completely sterile, and in addition to the mutant pheno- type they fail to produce aggregates of tubuli normally seen in thin sections of primary spermatocyte nuclei (Hardy et al.). Within the kl-5 fertility region of the spermatocyte nucleus, a loop-forming site has been demonstrated by its reaction with the monoclonal antibody S5 (Bonaccorsi et al., 1988). These loops are stained with the protein-specific dye CBB, but are not visible in living preparations. alleles: In addition to the alleles tabulated, Williamson (1972, Mol. Gen. Genet. 119: 43-47) reported 26 non- complementing and 9 complementing alleles induced by ethyl- methanesulfonate. origin allele treatment treated discoverer synonym ref ( _______________________________________________________________ kl-5B3 X ray y+Y Brosseau ms(Y)L3 2, 3 kl-5B28 X ray y+Y Brosseau ms(Y)L28 2 kl-5B34 X ray y+Y Brosseau ms(Y)L34 2 kl-5E12 EMS BSYy+ Kennison ms(Y)E12 6 kl-5E13 EMS BSYy+ Kennison ms(Y)E13 6 kl-5E14 EMS BSYy+ Kennison ms(Y)E14 6 kl-5E15 EMS BSYy+ Kennison ms(Y)E15 6 kl-5E16 EMS BSYy+ Kennison ms(Y)E16 6 kl-5E17 EMS BSYy+ Kennison ms(Y)E17 6 kl-5G12 / ray BSYy+ Kennison ms(Y)G12 6 kl-5G13 / ray BSYy+ Kennison ms(Y)G13 6 kl-5G14 / ray BSYy+ Kennison ms(Y)G14 6 kl-5G15 / ray BSYy+ Kennison ms(Y)G15 6 kl-5G16 | / ray BSYy+ Kennison ms(Y)G16 6 kl-5ts1 EMS Y A12 1 kl-5ts2 / EMS Y B119 1, 4 kl-5ts3 EMS Y H39 1 kl-5X1 X ray BSYy+ Lms4A3 5 kl-5X2 X ray BSYy+ Lms4A36 5 kl-5X3 X ray BSYy+ Lms4B5 5 ( 1 = Ayles, Sanders, Kiefer, and Suzuki, 1973, Dev. Biol. 32: 239-57; 2 = Brosseau, 1960, Genetics 45: 257-74; 3 = CP627; 4 = Goldstein, Hardy, and Lindsley, 1982, Proc. Nat. Acad. Sci. USA 79: 7405-09; 5 = Hazelrigg, Fornili, and Kaufman, 1982, Chromosoma 87: 535-59; 6 = Kennison, unpublished information. | Induced on same chromosome with kl-1G16. / Produces normal quantities of its high-molecular-weight polypeptide at restrictive temperature; however, outer-arm assembly defective. cytology: Y-h1-2 and h3. # kls: klarsicht location: 3-0.0. discoverer: Nusslein-Volhard. phenotype: Maternal effect mutant; without effect on viability or fertility of homozygotes. Homozygous females produce eggs with clear distinction between yolk and germ layers. Facili- tates in vivo observation of developmental processes. # kmA: killer of males location: 2-45. origin: Induced by ethyl methanesulfonate. references: Pierre, 1972, DIS 48: 16. phenotype: Homozygous males die during embryogenesis. # kmB location: 2-20. origin: Induced by ethyl methanesulfonate. references: Pierre, 1972, DIS 48: 16. phenotype: Homozygous males die during embryogenesis. # kn: knot location: 2-72.3. discoverer: Nichols-Skoog, 31h1. references: Diaz-Benjumea, Gaitan, and Garcia-Bellido, 1989, Genome 31: 612-19. phenotype: Veins L3 and L4 shifted closer together in region of anterior crossvein, which is either extremely thick or elim- inated by regional fusion of L3 and L4. Frequently, extra crossvein between L3 and L4 near end of wing. Shift in posi- tions of sensilla and extra chaetae accompanies shift in vein positions. Wing narrowed. Head narrowed and flattened, so the long axis of eye is at oblique angle. May overlap wild type at high temperatures and in late counts. Best at 19. RK2. cytology: Located in 51C-E (MacIntyre). # kni: knirps location: 3-{46}. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard and Wieschaus, 1980, Nature (Lon- don) 287: 795-801 (fig.). Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). Carroll and Scott, 1986, Cell 45: 113-26. Jackle, Tautz, Schuh, Seifert, and Lehmann, 1986, Nature (Lon- don) 324: 668-70. Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. Nauber, Pankratz, Kienlin, Seifert, Klemm and Jackle, 1988, Nature (London) 336: 489-92. Pankratz, Hoch, Seifert, and Jackle, 1989, Nature (London) 341: 337-40. Rothe, Nauber, and Jackle, 1989, EMBO J. 8: 3087-94. phenotype: Zygotic gap gene whose mutants are homozygous lethal; their denticle belts in segments one through seven are fused into a single field (Nusslein-Volhard and Wieschaus, 1980), but the head, thorax, eighth abdominal segment, and tail region appear normal. Embryos homozygous for a strong kni mutant show a wide band of ftz staining instead of the normal number of ftz stripes (Carroll and Scott, 1986). alleles: The following alleles are listed by Tearle and Nusslein-Volhard, 1987: allele origin synonym comments ______________________________________ kni1 EMS kni5F kni2 EMS kni7G strong kni3 EMS kni14F weak kni4 EMS kni17 kni5 EMS kni19 strong kni6 EMS kni301 strong kni7 EMS kni357 strong kni8 X ray kniFC13 ( strong kni9 EMS kniIL strong kni10 EMS kniIID strong kni11 EMS kniIIE strong kni12 EMS kniIIV ( Also see Nauber et al., 1988. cytology: Placed in 77E1-2 by in situ hybridization of cloned DNA to salivaries (Nauber et al., 1988). Included in Df(3L)ri79c = Df(3L)77B-C;77F-78A (Jurgens et al., 1984). molecular biology: The 77E1 region was microcloned and used to start a chromosome walk (Nauber et al., 1988). Breakpoints of chromosomal aberrations involving kni were located on the molecular map. Two transcripts of 2.2 and 2.5 kb were identi- fied; the smaller transcript is expressed transiently at the blastoderm stage, but the larger one continues to be expressed after gastrulation. These transcripts are not present in embryos homozygous for kniFC13, a small molecular deletion of 2 kb. Genomic and cDNA sequences and predicted amino acid sequences were determined (Nauber et al., 1988). Analysis of the DNA sequences showed three exons interrupted by two introns of 733 bp and 214 bp. A protein of 429 amino acids would be encoded by the single open reading frame of 1,287 bp. This protein shows similarity in the N terminus to proteins of the vertebrate nuclear hormone receptor family (Nauber et al., 1988). The zinc-finger domain of knirps and its amino-acid motif, the kni box, show 80-88% identity with the correspond- ing domains of egon and knrl, two genes that also map in the 77-79 region [Oro, Ong, Margolis, Posakony, McKeown, and Evans, 1988, Nature (London) 336: 493-96; Rothe et al., 1989]. # knickkopf: see knk # knirps: see kni # knirps-related: see knrl # knk: knickkopf location: 3-49. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95 (fig.). phenotype: Homozygous lethal; head skeleton defective; denticle bands narrowed; embryo rarely inverted in egg case. alleles: Four, including one weak and one temperature-sensitive allele. cytology: Placed in 85E1-10 based on its inclusion in Df(3R)GB104 = Df(3R)85D11-13;85E10 and Df(3R)by62 = Df(3R)85D11-14;85E16 but not Df(3R)by416 = Df(3R)85D10-12;- 85E1-2. #*kno: knobbyhead location: 1-63.9. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1951. references: 1958, DIS 32: 70. phenotype: Abnormal head with one or both eyes irregularly shaped, often drastically reduced in size. Occipital region frequently has hairy tufts, often carried on protuberances. Males highly infertile; viability about 10% wild type. RK2. other information: One allele induced by D-1:6- dimethanesulfonyl mannitol (CB. 2511). # knockdown: see kdn # knot: see kn # knrl: knirps-related location: 3-{46}. origin: Isolated from a genomic library using a a human retinoic acid receptor cDNA probe (Oro et al., 1988) or a Dro- sophila kni zinc-finger probe (Rothe et al., 1989). references: Oro, Ong, Margolis, Posakony, McKeown, and Evans, 1988, Nature (London) 336: 493-96. Rothe, Nauber, and Jackle, 1989, EMBO J. 8: 3087-94. phenotype: Expressed maternally at low levels in very early stages; expression increases during early embryogenesis and continues in larvae and adults (in contrast to kni, which is first expressed zygotically and does not continue beyond embryonic stages) (Oro et al., 1988; Rothe et al., 1989). alleles: No loss-of-function alleles isolated. cytology: Located in 77E1-2 by in situ hybridization; location not distinguishable by this technique from that of kni. molecular biology: Gene cloned and sequenced (Oro et al., 1988). One clone of 3,505 bp contains an open reading frame encoding 647 amino acids showing 85% identity with the predicted knirps gene product and 47% identity with the human retinoic acid receptor. The genes knrl, kni, and egon show more than 80% sequence identity in the first part of the zinc-finger domain and share a kni box downstream from this domain (Rothe et al., 1989). In the carboxyl-terminal region, however, there is little sequence similarity between knrl and the other receptors. # kohtalo: see kto # Kompolt: see Fs(2)Sz8 # Kpn: see awdK Kr: Kruppel location: 2-107.6 (mapped with respect to sp and If). discoverer: Graber. references: Gloor, 1950, Arch. Julius Klaus-Stift. Vererbungs- forsch. Sozialanthropol. Rassenhyg. 25: 38-44 (fig.). 1954, Arch. Julius Klaus-Stift. Vererbungsforsch. Sozialanth- ropol. Rassenhyg. 29: 277-87. Nusslein-Volhard and Wieschaus, 1980, Nature (London) 287: 795-801 (fig.). Jurgens, Wieschaus, Nusslein-Volhard and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Wieschaus, Nusslein-Volhard, and Kluding, 1984, Dev. Biol. 104: 172-86. (fig.). Knipple, Seifert, Rosenberg, Preiss, and Jackle, 1985, Nature (London) 317: 40-44. Preiss, Rosenberg, Kienlin, Seifert, and Jackle, 1985, Nature (London) 313: 27-32. Rosenberg, Preiss, Seifert, Jackle, and Knipple, 1985, Nature (London) 313: 703-06. Jackle, Tautz, Schuh, Seifert, and Lehmann, 1986, Nature (Lon- don) 324: 18-25. Rosenberg, Schroder, Preiss, Kienlin, Cote, Riede, and Jackle, 1986, Nature (London) 319: 336-39. Schuh, Aicher, Gaul, Cote, Preiss, Maier, Seifert, Nauber, Schroder, Kemler, and Jackle, 1986, Cell 47: 1025-32. Gaul and Jackle, 1987, Cell 51: 549-55. Gaul, Seifert, Schuh, and Jackle, 1987, Cell 50: 639-47. Gaul, Redemann, and Jackle, 1989, Proc. Nat. Acad. Sci. USA 86: 4599-4603. Gaul and Jackle, 1989, Development 107: 651-62. Stanojevic, Hoey, and Levine, 1989, Nature (London) 341: 331-35. Treisman and Desplan, 1989, Nature (London) 341: 335-37. phenotype: The wild-type allele of Kruppel controls the development of the thoracic and abdominal segments of Droso- philia; homozygous mutants show a gap in the larval pattern in these regions (Nusslein-Volhard and Wieschaus, 1980; Knipple, et al., 1987). Kr/+ adult sometimes has thoracic malforma- tion; a leg or a wing may be absent; penetrance low. Hetero- zygous larvae show small defects in denticle bands of thorax and abdomen as do heterozygous deficiencies for Kr; penetrance about 80%. Homozygotes are embryonic lethal. Kr1 homozygotes exhibit shortened germ band of but three to four segments with three to four tracheal pits; visible beginning at 7h of embryogenesis; head and gnathal segments apparently normal. At later stages only three to four abdominal and thoracic seg- ments clearly visible; normal telson and segments 8 and 7 fol- lowed by enlarged sixth, a rudimentary fifth and apparently mirror image sixth segment. Weak and intermediate mutant alleles lack the mirror-image duplications (Gaul and Jackle, 1987, Trends Genet. 3: 127-30). Ventral chain of ganglia disconnected; tracheal system defective; Malpighian tubules missing; salivary glands normal. Homozygotes for hypomorphic alleles display more nearly complete segmentation. Homozygous M+ Kr clones develop normally in all parts of adult cuticle of M/+ flies. Metamorphic potential of Kr/Kr embryos cultured in female abdomens restricted in that wing-disc-derived struc- tures not observed. Germline clones of homozygous Kr cells capable of normal oogenesis; no maternal effect of Kr+ observed. Requirement for Kr+ function apparently restricted to early embryogenesis. Kr affects ftz producing abnormal intensity and spacing of ftz stripes in thorax and anterior abdomen (Carroll and Scott, 1986, Cell 45: 113-26). alleles: Twentyfour alleles are listed in the following table. Deficiencies are listed in the rearrangement section. molecular allele origin synonym ref ( phenotype | cytology biology / _________________________________________________________________________ Kr2 EMS 3, 5 S Kr3 EMS 3, 5 S Kr5 EMS 6A69 5 S Kr7 EMS 3, 5 S Kr8 EMS 3, 5 S Kr9 EMS 3-5 S; no MT cys -> ser Kr11` X ray UR1 3 S In(2R)58A;60F3 ~0 to +9 Kr12` X ray API 3 S +1 to >+34 Kr13` X ray AK1 3 S T(Y;2)60F3-5 Kr15 spont KrJ1 3, 5 S +5 to >+34 Kr16 EMS KrIIIA102 3, 5 I Kr17 EMS KrIV 1, 3, 5 I phe -> ile Kr18 EMS KrVI 3, 5 I Kr19 EMS KrI066 1-3, 5 W; MT short gly -> glu Kr20 EMS KrIIE57 3, 5 W Kr21 EMS KrV 1-3, 5 W; MT variable cys -> stop Kr22 EMS KrVII 3, 5 W Kr23 EMS KrVIII 3, 5 W Kr24 EMS KrIX 3, 5 W Kr25 EMS KrX 1-3, 5 W; MT variable tyr -> asn Kr26 EMS KrXI 3, 5 W Kr27 EMS KrXII 3, 5 W Kr28 P Kr21-11 2 S Kr29 P Kr62-14 2 W ( 1 = Gaul, Redemann, and Jackle, 1989, Proc. Nat. Acad. Sci. USA 86: 4599-4603; 2 = Harbecke and Janning, 1989, Genes Dev. 3: 114-22; 3 = Preiss, Rosenberg, Kienlin, Seifert, and Jackle, 1985, Nature (London) 313: 27-32; 4 = Redemann, Gaul, and Jackle, 1988, Nature (London) 332: 90-92; 5 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. | S = Strong alleles: segments T1-3 and A1-5 deleted; A6 and sometimes A7 and 8 duplicated with reverse polarity. I = Intermediate alleles: segments T1-3 and A1-4 deleted; duplicated segments not observed. W = Weak alleles: seg- ments T2 and 3 and A1 deleted; A2-4 variably deleted depend- ing on allele. MT = Malpighian tubules. / Approximate extents of molecular deletions on coordinates of Preiss et al., 1985; amino acid substitutions in zinc-finger region (Gaul et al., 1989) as indicated by sequence analysis. ` Recovered as revertants of If. cytology: Placed in 60F3 based on proximal breakpoint of In(2R)KrUR1 and the 2R breakpoint of T(Y;2)KrAK1; mutant phenotype associated with five Kr deficiencies (Preiss et al., 1985). molecular biology: Kr was cloned by microdissection from the salivary band 60F3 followed by chromosome walking. A physical map was constructed from 50 kb of the Kr region in a series of overlapping clones (Preiss et al., 1985). Kr+ activity con- tained in a 4 kb subsegment (approximate coordinates +5 to +9) was identified by the region of overlap between molecular deletions Kr11 and Kr15. DNA sequencing indicates a single open reading frame of 1,398 bp split by a 372 kb intron and encoding a putative protein of about 466 amino acids (Rosen- berg et al., 1986). The protein shares structural elements with the DNA-binding zinc-finger domain of TFIIIA, a Xenopus transcription factor [Schuh et al., 1986; Gaul et al., 1987; Stanojevic et al., 1989, Nature (London) 341: 331-35]. This gene product binds to the sequence AAGGGGTTAA, the binding sites being located upstream of the hb promoter (Stanojevic et al., 1989; Treisman and Desplan, 1989). One cloned segment rescues Kr embryos when injected and identifies a 2.5 kb blastoderm-specific polyadenylated RNA (Preiss et al., 1985). Injection of anti-sense RNA into wild-type embryos produces Kr/Kr phenocopies (Rosenberg et al., 1985). Transcripts are first detected at the syncytial blastoderm stage, and can be demonstrated at the cellular blastoderm in the central part of the embryo (Knipple et al., 1985). In the absence of hb expression, the Kr+ transcript domain extends anteriorly up to segment A3 (Jackle et al., 1986); in the absence of kni expression, the extent of this domain is posterior to its nor- mal boundary. At the start of gastrulation, an anterior tran- script domain appears between head and thorax. Later, the transcripts are restricted to certain cells of the the brain and nervous system, to the mesoderm, and to the Malpighian tubules (Knipple et al., 1985). At the beginning of germ-band shortening, there is a very low level of transcript accumula- tion throughout the embryo. The protein domain of Kr involves the activity of maternal effect genes and two adjacent gap genes, hb and kni (Gaul et al., 1987). The Kr protein can be detected in the middle of the embryo (by antibody staining) at syncytial blastoderm and is demonstrated in a wide band of increasing density during cellular blastoderm (Gaul and Jackle, 1987, 1989). Antibody staining is strongest in the center of the domain, growing weaker toward the anterior and posterior margins. The band in the middle of the embryo decreases in width at the end of cellularization and two more protein domains have been established as a stripe and a poste- rior cap. Domains of protein expression in hb and Kr overlap in wild-type embryos (Gaul and Jackle, 1989) as do the protein domains of Kr and kni [Hulskamp, Pfeifle, and Tautz, 1990, Nature (London) 346: 577-80]. # krotzkopf verkehrt: see kkv # KS: Male fertility complex on the short arm of the Y chromosome synonym: see KL. references: Brosseau, 1960, Genetics 45: 257-74. Kennison, 1981, Genetics 98: 529-48. 1983, Genetics 103: 219-34. Hazelrigg, Fornili, and Kaufman, 1982, Chromosoma 87: 535-59. Gatti and Pimpinelli, 1983, Chromosoma 88: 349-73. The male fertility complex of the short arm of the Y chromo- some, originally called K2 by Stern (1929, Z. Indukt. Abstamm. Vererbungsl. 51: 253-353) and subsequently called KS by Bros- seau (1960, Genetics 45: 257-74), contains two complementing units designated ks-1 and ks-2. # ks-1 phenotype: Males deficient for ks-1 sterile. Cross sectional profiles of sperm tails in coiled bundles abnormal in outline; minute tubules ordinarily present among individualized sperm- tails in coiled bundles missing; replaced by membrane bound vesicles [Hardy, Tokuyasu, and Lindsley, 1981, Chromosoma 83: 593-617 (fig.)]. Within the ks-1 fertility region of the spermatocyte nucleus, a loop-forming site has been demon- strated by antibody staining using the monoclonal S5 (Bonac- corsi et al., 1988). The loops are not visible in living preparations, but like the kl-5 loops, can be stained with the dye CBB. alleles: In addition to the alleles tabulated, Williamson (1972, Mol. Gen. Genet. 119: 43-47) reported 26 non- complementing and nine complementing alleles induced by ethyl methanesulfonate. _____________________________________________________________ origin allele treatment treated discoverer synonym ref ( _____________________________________________________________ ks-1B2 X ray y+Y Brosseau ms(Y)S2 1, 2 ks-1B4 X ray y+Y Brosseau ms(Y)S4 1 ks-1B6 X ray y+Y Brosseau ms(Y)S6 1 ks-1B7 X ray y+Y Brosseau ms(Y)S7 1 ks-1B8 X ray y+Y Brosseau ms(Y)S8 1 ks-1B10 X ray y+Y Brosseau ms(Y)S10 1 ks-1B11 X ray y+Y Brosseau ms(Y)S11 1 ks-1B12 X ray y+Y Brosseau ms(Y)S12 1 ks-1B13 X ray y+Y Brosseau ms(Y)S13 1 ks-1E1 EMS BSYy+ Kennison 4 ks-1G1 / ray BSYy+ Kennison 4 ks-1X1 X ray BSYy+ Sms1A34 3 ks-1X2 X ray BSYy+ Sms1A35 3 ( 1 = Brosseau, 1960, Genetics 45: 257-74; 2 = CP627; 3 = Hazelrigg, Fornili, and Kaufman, 1982, Chromosoma 87: 535-59; 4 = Kennison, 1983, Genetics 103: 219-34. cytology: Y-h21 and h23. # ks-2 phenotype: Males deficient for ks-2 are sterile. The earliest departure from normal spermiogenesis is the abnormal alignment of the axoneme with the furrow demarcating the two halves of the nebenkern. Subsequent development of the major and minor mitochondrial derivatives and their interactions with endo- plasmic reticulum grossly abnormal [Hardy, Tokuyasu, and Lindsley, 1981, Chromosoma 83: 593-617 (fig.)]. alleles: In addition to the tabulated alleles, Williamson (1972, Mol. Gen. Genet. 119: 43-47) reported eleven noncom- plementing and eleven complementing alleles induced by ethyl methanesulfonate. ___________________________________________________________ origin allele treatment treated discoverer synonym ref ( ___________________________________________________________ ks-2B5 X ray y+Y Brosseau ms(Y)S5 1, 2 ks-2E2 EMS BSYy+ Kennison 5 ks-2G2 / ray BSYy+ Kennison 5 ks-2G3 / ray BSYy+ Kennison ms(Y)G3 4 ks-2X1 X ray BSYy+ Sms2A45 3 ( 1 = Brosseau, 1960, Genetics 45: 257-74; 2 = CP627; 3 = Hazelrigg, Fornili, and Kaufman, 1982, Chromosoma 87: 535-59; 4 = Kennison, unpublished information; 5 = Kennison, 1983, Genetics 103: 219-34. cytology: Y-h25. # KS63: see mud # kto: kohtalo (J.A. Kennison) location: 3-46. origin: Induced by ethyl methanesulfonate. discoverer: Kennison, 1983. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Isolated as a dominant suppressor of Pc mutations. Also suppresses Pcl alleles as well as Msc, Mrt, and AntpScx. Associated with recessive larval lethality. alleles: One mutant allele, called kto1. cytology: Placed in 76B1-76D5 based on Df(3L)kto2 = Df(3L)76B1-2;76D5 (Ashburner). # kudu: see kdu # kug: kugelei location: 3-47. origin: Induced by ethyl methanesulfonate. discoverer: Nusslein-Volhard. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Female sterile. Mature eggs not laid and almost round. alleles: Nineteen alleles. # Kugel: see Kg # Kun: see Fs(3)Sz17 # kurz: see kz # Kynurenine formamidase: see Kf # kz: kurz location: 1-0.9. discoverer: Stern, 26a23. references: Stern, 1930, Z. Indukt. Abstamm. Vererbungsl. 53: 279-86. 1934, DIS 1: 35. Gvozdev, Gostimsky, Gerasimova, Dubrovskaya, and Braslavskaya, 1975, Mol. Gen. Genet. 141: 269-75. Gvozdev, Gerasimova, Kovalev, and Ananiev, 1977, DIS 52: 67- 8. Perrimon, Engstrom, and Mahowald, 1984, Genetics 108: 559-72. Haenlin, Stellar, Pirrotta, and Mohier, 1985, Cell 40: 827- 37. phenotype: In the viable allele kz1, bristle are shorter and finer, like a slight Minute (Stern, 1930, 1934). Postscutel- lars often absent. Mutant hatches somewhat late. Viability fair; both sexes fertile. Recessive lethal alleles are slow to develop. First or second instar larvae stop developing; larvae may survive up to one week in arrested state (Perrimon et al., 1984). All lethal alleles are cell lethal in germ- line clones. kz1 females, heterozygous for a deficiency for the locus or for a lethal allele, emerge occasionally, but only after a delay of several days (Perrimon et al., 1984). allele: allele origin synonym ref ( comments ________________________________________________________ kz1 spont 7, 8 viable; fertile kz2 EMS kz4 1 lethal kz3 EMS kz5 1 lethal kz4 EMS kz17 1 lethal kz5 EMS kz21 1 lethal kz6 EMS kz32 1 lethal kz7 EMS kz34 1 lethal kz8 EMS kz36 1 lethal kz9 EMS kz41 1 lethal kz10 EMS kz47 1 lethal kz11 EMS kz55 1 lethal kz12 EMS kz61 1 lethal kz13 EMS kz63 1 lethal kz14 EMS kz65 1 lethal kz15 EMS kz67 1 lethal kz16 EMS kz77 1 lethal kz17 EMS kz80 1 lethal kz18 EMS kz88 1 lethal kz19 EMS kz97 1 lethal kz20 X ray l(1)C33 4 lethal; T(1;2)2E3;41D kz21 X ray l(1)C115 4 lethal kz22 X ray l(1)GA26 4 lethal; T(1;2)2E3;23C1-2 kz23 X ray l(1)HA90 2, 4, 6 lethal kz24 X ray l(1)RA34 4 lethal kz25 EMS l(1)DC776 5, 6 lethal kz26 EMS l(1)DF942 5, 6 lethal kz27 EMS l(1)EF469 5 lethal kz28 EMS l(1)EF514 5 lethal kz29 EMS l(1)VA217 5 lethal kz30 EMS l(1)VA252 5 lethal kz31 EMS l(1)VA296 5, 6 lethal kz32 EMS l(1)VA337 5 lethal kz33 EMS l(1)VE748 5 lethal kz34 HMS | l(1)HM13 3 lethal kz35 HMS | l(1)HM51 3 lethal kz36 HMS | l(1)HM405 3 lethal kz37 / HD l(1)L271 5 lethal ( 1 = Gvozdev, Gerasimova, Kovalev, and Ananiev, 1977, DIS 52: 67-8; 2 = Haenlin, Stellar, Pirrotta, and Mohier, 1985, Cell 40: 827-37; 3 = Kramers, Schalet, Paradi, and Huiser- Hoogteyling, 1983, Mutat. Res. 107: 187-201; 4 = Lefevre, 1981, Genetics 99: 461-80; 5 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 6 = Perrimon, Engstrom, and Mahowald, 1984, Genetics 108: 559-72; 7 = Stern, 1930, Z. Indukt. Abstamm. Vererbungsl. 53: 279-86; 8 = Stern, 1934, DIS 1: 35. | HMS = hycanthon methanesulfonate. / Discoverer: Sobels. cytology: Placed in polytene band 2E3 by Lefevre (1981, Genet- ics 99: 461-80) and in 2E1-3 by Gvozdev (et al., 1977). molecular biology: The gene kurz was located in a clone micro- dissected from the 2E2-2F3 region of the salivary chromosomes; this clone (cos9), containing a 43 kb insert, was able to res- cue the lethal mutant kz23; viable non-FM7 males were produced from a cross between heterozygous kz23/FM7 females and males carrying the cosmid on an autosome (Haenlin et al., 1985).