# z: zeste location: 1-1.0 (to the right of pn and kz). references: Gans, 1948, DIS 22: 69-70. Gans-David, 1949, Bull. Biol. France Belg. 83: 136-57. Gans, 1953, Bull. Biol. France Belg., Suppl. 38: 1-90. Green, 1967, Biol. Zentralbl. 86 (suppl.): 211-20. Judd, Shen, and Kaufman, 1972, Genetics 91: 139-56. Kaufman, Tasaka, and Suzuki, 1973, Genetics 75: 299-321. Sorsa, Green, and Beermann, 1973, Nature (London), New Biology 245: 34-37. Jack and Judd, 1979, Proc. Nat. Acad. Sci. USA 76: 1368-72. Babu and Bhat, 1980, Development and Neurobiology of Droso- phila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York and London, pp. 35-40. Gelbart and Wu, 1982, Genetics 102: 179-89. Green, 1984, Mol. Gen. Genet. 194: 275-78. Hazelrigg, Levis, and Rubin, 1984, Cell 36: 469-81. Lifschytz and Green, 1984, EMBO J. 3: 999-1002. Pirrotta and Brockl, 1984, EMBO J. 3: 563-68. Mariani, Pirrotta, and Manet, 1985, EMBO J. 4: 2045-52. Gunaratne, Mansukhani, Lipari, Liou, Martindale, and Goldberg, 1986, Proc. Nat. Acad. Sci. USA 83: 701-05. Benson and Pirrotta, 1987, EMBO J. 6: 1387-92. Hazelrigg, 1987, TIG 3: 43-47. Pirrotta, Manet, Hardon, Bickel, and Benson, 1987, EMBO J. 6: 791-99. Benson and Pirrotta, 1988, EMBO J. 7: 3907-15. Biggin, Bickel, Benson, Pirrotta, and Tjian, 1988, Cell 53: 713-22. Mansukhani, Crickmore, Sherwood, and Goldberg, 1988, Mol. Cell. Biol. 8: 615-23. Pirrotta, Bickel, and Mariani, 1988, Genes Dev. 2: 1839-50. Goldberg, Colvin, and Mellin, 1989, Genetics 123: 145-55. phenotype: The regulatory gene zeste interacts with the white locus as well as with the bithorax and decapentaplegic com- plexes, changing the phenotypic expression of these loci. z1 was the first mutant allele identified (Gans, 1948, 1953); the homo- or hemizygotes of this neomorphic mutant show a lemon yellow eye color when carrying two paired copies of w+ or of the rightmost w+ alleles [as in z1 w+/z1 w+ females or z1/Y males with a w+ duplication (Jack and Judd, 1979)]. z1 w+/Y males without the duplication, z1/z1 females heterozygous for a w allele belonging to one of the right-hand (zeste- suppressing) subloci, or z+/z1 females are wild type. An intralocus duplication for a right sublocus of white produces mottling in z1 males. z1 eye color develops autonomously in mosaics and in eye-disk transplants. It is not affected by the number of Y chromosomes in the genotype. A third chromo- some mutant wo interacts with z1 or z58g to lighten eye color, producing z/z;wo/wo white-eyed females and z/Y;wo/wo males with a slight deviation from wild-type eye color (Rayle, 1969, DIS 44: 98; Kaufman et al., 1973). z1 has no effect on the expression of the white gene in ocelli, testes, or larval Mal- phigian tubules. The first za mutant was also identified by Gans. These mutants are wild type in za/Y males and za/za, za/Df(1)z, and z+/za females. The heteroallelic combination of z1/za, how- ever, results in yellow-eyed flies. Complementation between wsp and other white alleles does not occur in za mutants, although it does occur in z+ or z1 flies (Babu and Bhat, 1980). za-type alleles, including zae(bx), as well as the partial revertant of z1, z11G3, enhance the mutant phenotype of certain heteroallelic combinations of BXC alleles that show transvection (partial complementation) when paired; z+ and z1, however, do not affect these BXC alleles (Kaufman et al., 1973; Gelbart and Wu, 1982; Mariani et al., 1985; Pirrotta et al., 1987). All zeste mutant alleles tested enhance certain heteroallelic mutant combinations that show transvection in dpp (Gelbart and Wu, 1982). The zop mutants (Lifschytz and Green, 1984), unlike z1, require only one copy of w+ for expression of a zeste eye color in homo- and hemizygotes. Heterozygotes over z+ are zeste if they have two copies of w+, but are wild type if there is only one copy. Another mutant, zv77h, requires only one copy of w+ in males. The eyes are brown variegated in hemi- and homozygous zv77h females and zv77h/Y males, but wild type in homozygous zv77h Dp(1;1)w+2 females and zv77h Dp(1;1)w+2/Y males, this allele responding to an increase in w+ dosage in a manner con- trary to that of z1 (Green, 1984). Diepoxy-butane-induced mutations (including multilocus dele- tions) have been generated in an attempt to obtain a null allele of zeste (Goldberg et al., 1989). Some of the females that were completely deficient for z [Df(1)z-deb3/Df(1)z-deb3, for example] survived and were fertile, indicating that the product of the zeste gene is not required for viability or female fertility. alleles: Zeste mutants and rearrangements are described in the following table. Deficiencies for zeste are listed as rear- rangements. See end of text for more detailed descriptions of certain alleles. allele origin discoverer ref ( comments _________________________________________________________________________________________________________________________ z1 spont Gans, 46b 5-9, 10- eye color wild type in males; lemon yellow at 25, 13, 16, 17 mottled yellow and brownish red at 19 in homozygous females z1-35 Jack 11 no detectable DNA rearrangements z1-42 Jack 11 no detectable DNA rearrangements z11G3 X ray Gans 9, 11, 13, eye color wild type in z males and homozygous (from z1) 15, 17 and heteroallelic z females z31 HD Simmons 11 z32 HD Simmons 11 z58g spont Gloor 11, 12 eye color wild type in males, lemon yellow in homozygous females; z58g/zp69a zeste mottled; z58g/z11G3 wild type; z58g/za zeste; no detectable DNA rearrangement z59d Green, 59d15 11, 12 z+/z59d females have orange mottled eyes; Dp(1;1)2F5-3A1;3A4-5 z78c Jack 11 no detectable DNA rearrangements z81E Green 16 recombinant between z1 and zv77h z+64b9 X ray Green 1, 2, 18 z+64b9/Y males and z+64b9/z+64b9 females wild type; In(1)3C1-2;12B z+64b13 X ray Green 1, 2 z+64b13/Y males and z+64b13/z+64b13 females wild type za X ray Gans 3-5, 9, za/Y males, z+/za and za/za females wild type; 11, 12 enhances certain genotypes in BXC and dpp that show transvection za68k EMS Gelbart 9, 13 za68k/Y males and za68k/za68k females wild type; enhances certain genotypes in BXC and dpp that show transvection za691 EMS Gelbart 9, 13 za691/Y males and za691/za691 females wild type; enhances certain genotypes in BXC and dpp that show transvection za692 EMS Gelbart 9, 11, 13 za692/Y males and za692/za692 females wild type; enhances certain genotypes in BXC and dpp that show transvection; no detectable DNA rearrangements za693 EMS Gelbart 9, 11, 13 za693/Y males and za693/za693 females wild type; enhances certain genotypes in BXC and dpp that show transvection za694 EMS Gelbart 9, 13 za694/Y males and za694/za694 females wild type; enhances certain genotypes in BXC and dpp that show transvection; no detectable DNA rearrangements zae(bx) | / ray Lewis 3, 9, 11, males and females wild type in eye color; 13, 14, 17 enhances most bx alleles; In(1)3A3;4F zae(bx)2 X ray Lewis 14 like zae(bx); salivary chromosomes appear normal zop6 induced in Lifschytz 15, 17 two w+ genes not essential for zeste mutant z1 by EMS expression in zop6/zop6 and zop6/Df(1)z females or zop6w+/Y males zop11 same as Lifschytz 15 intermediate between z1 and zop6 (same eye color in zop6 zop11w+/Y and zop6w+/Y males, but z+/zop11 females with two copies of w+ have brown eyes); no detectable DNA rearrangements zp69a Gelbart 13 hemizygous males wild type; homozygous females brown mottled on yellow ("peppered"); with z1, eyes uniform zeste; with za, eyes zeste mottled z~~1 HD Pirrotta 16, 17 like za (with some variegation); P element in- sertion at coordinate 0 on molecular map in females; revertants obtained z~~2 HD Pirrotta 16 like za except eyes more orange; P element in- sertion at coordinate 0 on molecular map in females zRN4 X ray Green 15 partial revertant of zop6 zv77h HD Green 10, 11, 17 brown variegated eye color darkening toward posterior in zv77hw+/Y males and zv77hw+/zv77h w+ females; lighter at 28 ( 1 = Arcos-Teran, 1972, Chromosoma 37: 233-96; 2 = Arcos- Teran and Beermann, 1968, Chromosoma 25: 377-91; 3 = Babu and Bhat, 1980, Development and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall eds.). 1980, Plenum Press, New York and London, pp. 35-40; 4 = Babu and Bhat, 1980, Mol. Gen. Genet. 183: 400-02; 5 = Bingham, 1980, Genetics 95: 341-53; 6 = Gans, 1948, DIS 22: 69-70; 7 = Gans, 1953, Bull. Biol. France Belg., Suppl. 38: 1-90; 8 = Gans-David, 1949, Bull. Biol. France Belg. 83: 136-57; 9 = Gelbart and Wu, 1982, Genetics 102: 179-89; 10 = Green, 1984, Mol. Gen. Genet. 194: 275-78; 11 = Gunaratne, Mansukhani, Lipari, Liou, Martindale, and Goldberg, 1986, Proc. Nat. Acad. Sci. USA 83: 701-05; 12 = Jack and Judd, 1979, Proc. Nat. Acad. Sci. USA 76: 1368-72; 13 = Kaufman, Tasaka, and Suzuki, 1973, Genetics 75: 299-321; 14 = Lewis, 1959, DIS 33: 96; 15 = Lifschytz and Green, 1984, EMBO J. 3: 999-1002; 16 = Mariani, Pirrotta, and Manet, 1985, EMBO J. 4: 2045- 52; 17 = Pirrotta, Manet, Hardon, Bickel, and Benson, 1987, EMBO J. 6: 791-99; 18 = Sorsa, Green, and Beermann, 1973, Nature (London) New Biology 245: 34-37. | Synonym: e(bx). cytology: Located in salivary chromosome band 3A3 on the basis of its inclusion in Df(1)w258-11 = Df(1)3A3-4;3C2-3 and Df(1)64C = Df(1)3A3-4;3C2-3 (Gans, 1953, Judd, Shen, and Kauf- man, 1972, Genetics 71: 139-56), but not in Df(1)K95 = Df(1)3A3-6;3B1. Also located in 3A3 by in situ hybridization to In(1)zae(bx) (Mariani et al., 1985). molecular biology: The wild type allele of zeste and some of the zeste mutants have been cloned and the cDNA sequenced (Mariani et al., 1985; Gunaratne et al., 1986; Pirrotta et al., 1987). Cloning has been accomplished by microdissection of the salivary 3A1-4 region followed by microcloning and chromosome walking; also by "transposon tagging" of the locus with P elements, recovering the sequences flanking the 3A3-4 P insertion. Probes from the 3' or 5' end of the gene were used to isolate cDNA clones; the length of the longest clone was just over 2300 nucleotides (Pirrotta et al., 1987). No detectable DNA rearrangements were found in many of the mutants (Gunaratne et al., 1986). A transcript of 2.2-2.4 kb was found at all postzygotic stages of development in wild type and most mutant individuals; shorter transcripts were found in zae(bx), z~~1, and zv77h. Transcription is most abundant in maternal RNA; it declines during larval growth, but increases again in third instar larvae and pupae (Pirrotta et al., 1988). The gene is transcribed along the X from distal to proximal. The z+ transcript includes three exons and two introns; no differences in exon size or position could be detected in the RNA of the mutants z1, zop6, or za. P fac- tor mediated germ-line transformation to wild-type eye color was carried out in a z1 Dp(1;1)w+ strain (Gunaratne et al., 1986); in other transformation experiments, yellow-eyed transformants were produced by injecting zop6 DNA in a P ele- ment vector into a y za strain (Pirrotta et al., 1987). The zeste protein predicted from the nucleotide sequence of wild type zeste cDNA has an amino terminal region with both basic and acidic residues, a second region that is acidic, a third region with few basic or acidic residues but many glu- tamines and alanines, and a carboxy terminal region with many basic and acidic residues (Pirrotta et al., 1987). The pro- tein binds directly to specific DNA sequences of the white, Ultrabithorax, decapentaplegic, Antennapedia, and engrailed regulatory regions (Benson and Pirrotta, 1987, 1988; Biggin et al., 1988; Mansukhani et al., 1988). Anti-zeste antibodies interact with approximately 60 specific bands in polytene chromosomes; this number is drastically increased by heat shock (Pirrotta et al., 1988). other information: Inversions, translocations, and transposi- tions with breaks in 3C3, induced as derivatives of z1 chromo- somes carrying tandem duplications of w+, result in a range of zeste phenotypes in males and females, the eye colors being zeste, zeste variegated, zeste halo, and wild type (Green, 1967, 1984). E(z) and Su(z) loci have been described (Green, 1967; Kalisch and Rasmuson, 1974, Hereditas 78: 97-104; Pers- son, 1976, Hereditas 82: 111-20). # z1 phenotype: Two synapsed copies of w+ required for expression of zeste eye color (Gans, 1953). Ocelli wild type in color, as are testes and larval Malpighian tubules. Supports transvec- tion at Ubx but not at dpp. molecular biology: Comparison between the sequences of z+ and za shows many polymorphisms concentrated in the middle, repetitive part of the gene (Pirrotta et al., 1987). There are no changes in the 5' flanking region or in the untranslated leader. Most of the changes do not affect the predicted amino acid sequence since they are in the introns or in the third position of the codons; the change from A to T (Lys to Met in the middle repetitive part of the protein) is believed to have an important effect on the properties of the mutant product (Pirrotta et al., 1987). # z11G3 phenotype: Partial revertant of z1 showing wild-type eye color in hemizygous males and homozygous females (Gans, 1953). Almost complete complementation of z1 eye color. Does not support transvection at dpp or Ubx. molecular biology: The sequence of z11G3 is identical to that of z1 except that three nucleotides have been deleted, remov- ing a tyrosine from the amino acid sequence (Pirrotta et al., 1987). # za phenotype: Hemizygous males and homozygous females said to be wild type in eye color (Gans); however, on closer inspection they are seen to have a diluted eye color that becomes brown with age (Pirrotta et al., 1987). z1/za females have zeste eyes; za wDZL/za wch females have light brown eyes. Does not support transvection at dpp or Ubx. molecular biology: No detectable rearrangements except for a DNA insertion (about 15 kb) of unknown significance (Gunaratne et al., 1986). # zae(bx) phenotype: Mostly wild type, but slight eye color variegation in homozygous females (Lewis, 1959, DIS 33: 96). z1/zae(bx) females zeste. Does not support transvection at dpp or Ubx. molecular biology: Lacks about 800 nucleotides of the zeste coding region, but otherwise the 5' half of the mutant gene is normal (Pirrotta et al., 1987). The transcript of 1.4-1.8 kb (Mariani et al., 1985; Gunaratne et al., 1986) ends shortly after the 3A3 breakpoint of the inversion [breakpoint placed on molecular map of zeste at about +2.0 kb, the origin being the first EcoRI site in clone CS1014 (Gunaratne et al., 1986)]. # zop6 phenotype: Eye color zeste in hemizygous males and homozygous females with only one copy of w+; homozygous females with two copies of w+ also zeste. Heterozygous z+/zop6 females wild type if one copy of w+, but zeste if two copies; zop6 reverts to weaker alleles after EMS or X rays (Lifschytz and Green, 1984). molecular biology: Carries all the polymorphisms in the z1 sequence as well as the change from Lys to Met; also a C to T mutation causing a proline to leucine change in the middle region of the protein, increasing its hydrophobic nature (Pir- rotta et al., 1987). # z~~1 phenotype: Hemizygous males and homo- or hemizygous females almost wild type in eye color. Supports transvection at Ubx (Pirrotta et al., 1987). molecular biology: P element insertion at coordinate 0 on molecular map of Mariani et al. (within 10 kb of this origin and in the same orientation as the coordinates of Gunaratne et al.) plus a deletion of about 300 nucleotides (Pirrotta et al., 1987); otherwise, coding region like that of z+. # zv77h phenotype: Eye color diluted, turning brownish with age in hem- izygous males and hemi- and homozygous females with a normal complement of w+ genes. za/zv77h females are wild type; z1/zv77h females are zeste; zv77h hemizygous males and homozy- gous females carrying a w+ duplication in each X are wild type. molecular biology: Carries deletion of about 320 nucleotides and addition of seven nucleotides in the first exon; P element was probably inserted, followed by excision of the P and the flanking deletion (Pirrotta), the deletion removing the AUG start codon. # zl: see wzl # zm: see wzm #*Z: Zerknittert location: 1-5.5. references: Gruneberg, 1931, Biol. Zentralbl. 51: 219-25. 1934, DIS 2: 8. phenotype: Wings may be crumpled or incompletely unfolded, but majority overlap wild type. Viability 10% wild type. RK3. # z2: see under ANTC # Z600 location: 3-[42]. references: Schultz and Butler, 1989, Genes Dev. 3: 232-42. Schultz, Schlomchik, Cherbas, and Cherbas, 1989, Dev. Biol. 131: 515-23. phenotype: Member of cluster of genes that includes Eip28/29 and Gdl. Believed to play role in processes of early develop- ment. cytology: Located in 71C3-D4 (Schultz and Butler, 1989). molecular biology: Gene cloned, partially sequenced, and a 600-nucleotide transcript (missing sequences from the 5 end) detected in zygotes (Schultz et al., 1989; Schultz and Butler, 1989). Z600 is located upstream to the neighboring gene GdlM and overlaps it. The Z600 gene is expressed abundantly in very early embryos and again at a lower level in adults; the transcript is expressed at a higher level in oviposited eggs than in ovaries The gene is 1780 bp long, with three exons of 453, 295, and 506 bp and two introns of 56 and 410 bp. # zen: see under ANTC # zen-2: see z2 under ANTC # Zerind: see Fs(3)Sz25 # Zerknittert: see Z # zerknullt: see zen under ANTC # zeste: see z # zip: zipper location: 2-107.6. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus and Kluding, 1983, DIS 59: 158-60. Nusslein-Volhard, Wieschaus and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Cote, Preiss, Haller, Schuh, and Jackle, 1987, EMBO J. 6: 2793-2801. Zhao, Cote, Jahnig, Haller, and Jackle, 1988, EMBO J. 7: 1115-19. phenotype: The wild-type allele of zipper is expressed in the nervous system during development and was believed to encode an integral membrane protein necessary for normal axon pat- terning (Zhao et al., 1988); however it has more recently been shown to encode the heavy chain of cytoplasmic myosin (Kierhart). The mutants are embryonic lethals; abnormalities include a small hole in the ventral thorax, distortion of ven- tral denticle rows, and defects in head involution and dorsal closure (Nusslein-Volhard et al., 1984; Cote et al., 1987). These defects vary in different alleles and in different embryos from the same egg laying (Cote et al., 1987). The nervous system of mutant embryos also differentiates abnor- mally, showing local defects in the fasciculation pattern of axons (Zhao et al., 1988), as indicated by antibody stains for neurons and their axons. These CNS abnormalities can be detected after germ band shortening and, together with the molecular data, suggested that neurological rather than epidermal defects are the primary ones in zip mutants (Cote et al., 1987). alleles: zip1 (isolation number ID16), a strong allele showing severe cuticular and neurological defects, zip2 (isolation number IIF107), a weaker allele, and 16 discarded alleles have been reported. cytology: Located in 60E9-F1 since uncovered by Df(2R)gsb = Df(2R)60E9-10;60F1-2, but not by Df(2R)SB1 = Df(2R)60E10- F1;60F5. molecular biology: The 60E9-60F1 region of 2R was cloned by microdissection and the clones were used to start a chromosome walk (Cote et al., 1987). On the molecular map, the zip region lies between the proximal breakpoint of Df(2R)gsb at -55 to -49 kb ("-" values to the left) and the proximal break- point of Df(2R)SB1 at 0 to +3.5 kb ("+" values to the right). A transcript of 2.4 kb was demonstrated by northern blot analysis. The transcript accumulates in the mesodermal- neuroblast region (not in the ectoderm) at the extended germ band stage, but becomes restricted to neural tissue (brain and ventral nerve cord) from the time of germ band shortening up to hatching, not appearing in the precursor cells of the cuti- cle (Cote et al., 1987). zip cDNA has been sequenced and the putative amino acid sequence of the protein determined (Zhao et al., 1988). There is a single open reading frame of 1500 bp which encodes a polypeptide of 500 amino acids with several domains, including a putative signal sequence and a transmembrane domain. other information: Shown to be the same as Mhc-c, and is a synonym thereof (Kierhart). # Zolta: see Fs(3)Sz32 # Zombor: see Fs(3)Sz36 # Zw: Zwischenferment location: 1-62.9 (Eanes); located between car and sw. discoverer: Young. references: Young, Porter, and Childs, 1964, Science 143: 140-41. Young, 1966, J. Hered. 57: 58-60. Steele, Young, and Childs, 1968, Biochem. Genet. 2: 159-75. Seecof, Kaplan, and Futch, 1969, Proc. Nat. Acad. Sci. USA 62: 528-35. Gvozdev, Birstein, Polu-Karova, and Kakpakov, 1971, DIS 46: 68. Bowman and Simmons, 1973, Biochem. Genet. 10: 319-31. Faizullin and Gvozdev, 1973, Mol. Gen. Genet. 126: 233-45. Lucchesi and Rawls, 1973, Biochem. Genet. 9: 41-51. Maroni and Plaut, 1973, Genetics 74: 331-42. Geer, Bowman, and Simmons, 1974, J. Exp. Zool. 187: 77-86. Stewart and Merriam, 1974, Genetics 76: 301-09. 1975, Genetics 79: 635-47. Gvozdev, Gerasimova, Kogan, and Braslavskaya, 1976, FEBS Lett. 64: 85-88. Gvozdev, Gerasimova, Kogan, and Rosovsky, 1977, Mol. Gen. Genet. 153: 191-98. Hughes and Lucchesi, 1977, Science 196: 1114-15. Gvozdev, Gerasimova, Rosovsky, Kogan, and Braslavskaya, 1978, DIS 53: 143-44. Hughes and Lucchesi, 1978, Biochem. Genet. 16: 1023-29. O'Brien and MacIntyre, 1978, The Genetics and Biology of Dro- sophila (Ashburner and Wright, eds.). Academic Press, London, New York, San Francisco, Vol. 2a, pp. 395-551. Geer, Lindel, and Lindel, 1979, Biochem. Genet. 17: 881-95. Gerasimova and Rosovsky, 1979, Dev. Genet. 1: 97-107. Lucchesi, Hughes, and Geer, 1979, Curr. Top. Cell. Regul. 15: 143-54. Bijlsma, 1980, Biochem. Genet. 18: 699-715. Laurie-Ahlberg, Maroni, Bewley, Lucchesi, and Weir, 1980, Proc. Nat. Acad. Sci. USA 77: 1073-77. Cavener and Clegg, 1981, Proc. Nat. Acad. Sci. USA 78: 4444- 47. Gvozdev, Gerasimova, Kogan, Rosovsky, and Smirnova, 1981, DIS 56: 53-55. Williamson and Bentley, 1981, Genetics 97: s113. Eanes, 1983, Biochem. Genet. 21: 703-11. Williamson and Bentley, 1983, Biochem. Genet. 21: 1153-66. Eanes, 1984, Genetics 106: 95-107. Ganguly, Ganguly, and Manning, 1985, Gene 35: 91-101. Eanes and Hey, 1986, Genetics 113: 679-93. Miyashita, Laurie-Ahlberg, Wilton, and Emigh, 1986, Genetics 113: 321-35. Fouts, Ganguly, Gutierrez, Lucchesi, and Manning, 1988, Gene 63: 261-75. Lucchesi and Manning, 1988, Insect Biochem. 18: 515-19. Merriam, 1988, DIS 67: 111-36 (clone list). phenotype: Structural gene for glucose 6-phosphate dehydro- genase (Zwischenferment of Warburg) [G6PD (E.C. 1.1.1.49)], the first enzyme in the oxidative part of the pentose phos- phate shunt. Electrophoretic variants ZwA and ZwB have been described in Drosophila melanogaster (Young et al., 1964; Young, 1966). The G6PD produced by ZwA shows faster migration in starch gel (Young et al., 1964) or acrylamide gel (Peeples, Barnett, and Oliver, 1967, J. Hered. 58: 243-45) than that produced by ZwB. A ZwA/ZwB female shows fast- and slow- migrating bands but no hybrid band of intermediate mobility (Young et al., 1964; Steele et al., 1968; Hori and Tanda, 1980, Jpn. J. Genet. 55: 211-23). The B variant in both homo- and heterozygotes is characterized by a double band and shows more heat stability than the A variant (Steele et al., 1968). A dominant sex-linked modifier of the electrophoretic mobility of G6PD, M(G6PD), has been described by Komma (1968, Biochem. Genet. 1: 229-37). A regulatory element that affects the activity level of G6PD has been reported by Itoh and Hori (Jpn. J. Genet. 60: 441-53). The molecular weight of the A variant of G6PD approximates 147,000 and that of the B variant 317,000 according to Steele et al. (1968), who used the elec- trophoretic starch gel method and observed that the B form can dissociate and produce some A-like form. Lee, Langley, and Burkhart (1978, Anal. Biochem. 86: 697-706), using gel- filtration chromatography, reported that the B variant has a molecular weight of 240,000. A subunit molecular weight for the purified enzyme was estimated by Lee et al. to be 55,000 and by Hori and Tanda to be 69,000, as if the slow B variant represented a tetramer and the fast A variant a dimer of sin- gle polypeptides (Hori and Tanda, 1980; Miyashita et al., 1986). Significant amounts of the enzyme are found in the fat body and the intestine of Drosophila melanogaster larvae (Cochrane and Lucchesi, 1980, Genetics 94: s20). Enzyme lev- els are raised by dietary sucrose or D-glycerate (Geer, Kamiak, Kidd, Nishimura, and Yemm, 1976, J. Exp. Zool. 195: 15-31; Geer, Woodward, and Marshall, 1978, J. Exp. Zool. 203: 391-402; Cavener and Clegg, 1981; Cochrane, Lucchesi, and Laurie-Ahlberg, 1983, Genetics 105: 601-13). A maternal form of G6PD can be detected up to the early pupal stage (Gerasimova and Smirnova, 1979). Total G6PD activity increases during the larval period, reaches a peak during the third larval instar, drops during pupation, and increases again in the adult (Bijlsma and Van der Meulen-Bruijns, 1979, Biochem. Genet. 17: 1131-44; Williamson and Bentley, 1983). The enzyme shows a characteristic staining pattern in imaginal disks (Cunningham, Smith, Makowski, and Kuhn, 1983, Mol. Gen. Genet. 191: 238-43). Males with one dose of Zw+ and females with two doses have about the same amount of G6PD activity, i.e. show dosage compensation for enzyme activity (Seecof et al., 1969; Gvozdev et al., 1971; Bowman and Simmons, 1973; Faizullin and Gvozdev, 1973; Williamson and Bentley, 1981). Females heterozygous for a Zw deficiency show a corresponding reduction in enzyme activity; males and females with an extra dose of Zw+ show increased enzyme activity (Seecof et al., 1969; Maroni and Plaut, 1973; Stewart and Merriam, 1975). Contribution of each dose of G6PD to the level of enzyme activity is the same in triploid females as in diploid females (Lucchesi and Rawls, 1973). A number of low- and null-activity mutations have been induced at the Zw locus. The mutant alleles are fully viable (Gvozdev et al., 1976; Hughes and Lucchesi, 1977; Bijlsma, 1980; Lucchesi et al., 1979), but the larvae do not grow as well as wild type on a minimal amino-acid diet lacking fatty acids and whole nucleic acids (Geer et al., 1974). Null alleles at the ry locus are also viable, but double mutant combinations of Zw-;ry- do not survive (Lucchesi and Manning, 1988). Although Pgd- flies are lethal, Zw-Pgd- flies carrying null alleles for both G6PD, the first enzyme in the pentose phosphate shunt, and 6PGD, the last enzyme , are viable , presumably because the toxic 6-phosphogluconate is not pro- duced (Hughes and Lucchesi, 1977, 1978; Geer et al., 1979; Lucchesi et al., 1979). Many natural populations throughout the world are polymorphic for the A and B variants (Oakeshott, Chambers, Gibson, Eanes, and Willcocks, 1983, Heredity 50: 67-72). Rare variants from a number of North American populations have been screened by sequential electrophoresis of starch and acrylamid gels to detect molecular heterogeneity (Eanes, 1983, 1984; Eanes and Hey, 1986); the G6PD activity of these lines and also of induced mutants has been measured (see the following table). alleles: The following table includes electrophoretic (wild- type), low activity, and null alleles at the Zw locus. (Synonyms for the Zw+ alleles, ZwA and ZwB, use terminology for allozyme variants from DIS 53: 117). allele origin discov synonym ref ( mobility; suppression of activity | Pgd-lethality _______________________________________________________________________________________________________ ZwA spont Young G6pd6 10-12 fast ZwAF1 nature Eanes 1 >A strong ZwAF2 nature Eanes 1 >A strong ZwAF3 nature Eanes 1 >A strong ZwAF4 nature Eanes 1 >A strong ZwAS1 nature Eanes 1 B moderate ZwBS1 nature Eanes 1 A = faster than ZwA; B = faster than ZwB;