Gene Dmel\w

Apparently wild type but, in combination with g, produces a more orange eye than g alone. RK3.

The white locus is involved in the production and distribution of ommochrome (brown) and pteridine (red) pigments found in the compound eyes and ocelli of adult flies as well as the pigments in adult testis sheaths and larval Malpighian tubules; the specific function of the protein it encodes is still unknown, but it is believed to be a membrane-associated ATP-binding transport protein for pigment precursors in both the ommochrome and pteridine pathways (Sullivan and Sullivan, 1975; Mount, 1987; Dreesen et al., 1988; Tearle et al., 1989). w1 was the first mutant found in Drosophila melanogaster (Morgan, 1910; Morgan and Bridges, 1916). Mutant alleles do not appreciably affect the viability and fertility of the flies. Extreme white alleles as well as white deficiencies remove both brown and red pigments, the w1 allele having very little, if any, pteridine (Hadorn and Mitchell, 1951); isoxanthopterin is present in considerable quantity during pupation but is eliminated during the first three days of adult life (Hadorn, 1954, Experientia 10: 483-84). Hypomorphic alleles are visibly lighter in combination with w1 than when present as homozygotes. Intermediate white alleles result in partial loss of ommochromes and pteridines; some alleles also affect the distribution of these pigments in the compound eyes (Lewis, 1956; Green, 1959a, 1959c). Although the mutants are positively phototactic, they show no optomotor responses (Kalmus, 1943, J. Genet. 45: 206-13). Wild-type alleles are incompletely dominant over mutant alleles, w/w+ heterozygotes, though visibly indistinguishable from w+/w+, have less red pigment (Muller, 1935; Ziegler-Gunder and Hadorn, 1958; Green, 1959b). Mutant larval disks transplanted into wild-type host develop autonomously (Beadle and Ephrussi, 1936). Early genetic studies identified mutations separable by intralocus recombination into at least seven groups spanning 0.03 cm (Lewis, 1952; MacKendrick and Pontecorvo, 1952; Green, 1959a; Judd, 1959). Mutants occupying the centromere-proximal sites apparently play a regulatory role (Judd, 1976). Subsequent molecular analysis has localized the proximal mutations to the 5' end of the transcription unit (we) and the upstream flanking sequences (wsp) (Judd, 1987). Mutations at the distal sites have been mapped to the protein coding exons and the introns between them. The proximally-located regulatory mutants (we, for example) do not show dosage compensation; they suppress the zeste gene, and some of them (the wsp alleles) affect the distribution of the red and brown screening pigments of the eyes. Most of the distally-located structural mutants show dosage compensation, wa/Y males having the same eye color as wa/wa females, and do not suppress (but may interact with) zeste. Green (1959a) found that wi fails to show dosage compensation and does not suppress zeste; but wh exhibits both zeste suppression and dosage compensation. In spite of their heterogeneity, the alleles at the white locus fail to complement each other except for wsp which partially complements all other w alleles except in the presence of za [Babu and Bhat, 1980, Development and Neurobiology of Drosophila, (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York and London, pp. 35-40)]. Some white alleles (wc for example) are extremely unstable (Green, 1976); w1 is slightly unstable, giving rise to we and wh, mutants with darker eyes than w1. The locus is characterized by asymmetrical recombination involving transposons; the mutants wr,def and wr,dup are the result of such exchange (Davis et al., 1987). Some P-element white transformations show reproducible patterns of pigmentation which can be altered by the trans-acting gene zeste (Rubin et al., 1985).

There are many w alleles that show variegated eye color. The wm mutants most commonly used for variegation studies are wm4 and wm264-58. In these alleles, extra heterochromatin partially suppresses eye mottling (Gowen and Gay, 1933, Proc. Nat. Acad. Sci. USA 19: 122-26; Koliantz, Hartmann-Goldstein, and Fuller, 1984, Heredity 52: 203-13; Koliantz and Hartmann-Goldstein, 1984, Heredity 53: 215-22; Baker and Spofford, 1959, Univ. Texas Publ. 5914: 135-54; Spofford, 1959, Proc. Nat. Acad. Sci. USA 45: 1003-07). In wm264-58, variegation less (more wild-type in color) in homozygous females than in heterozygous females. Color variegation found in the testis-sheath as well as the eyes of wm264-58 male flies (Baker, 1968, Adv. Genet. 14: 133-169). In some lines, less variegation when paternally inherited; in others, less variegation when maternally inherited or no parental effect. Mottling in wm4 and wm4h is enhanced by E(var)7 and E(var)c101 (Reuter and Wolff, 1981, Mol. Gen. Genet. 182: 516-19); mottling in wm4 and wm264-58 is suppressed by Su(var) (Spofford, 1962, Genetics 47: 986-87) and a number of other suppressor mutations (Reuter and Wolff, 1981).

Placed on the genetic map of white to the right of wbf and the left of wch. The amount of pigment formed by wa is a function of gene dose: wa/- female < wa/Y male = wa/wa female < wa/wa/wa female < wa/wa male (Muller, 1932). A wa optic disk transplanted into a wild-type host shows autonomous eye color development (Beadle and Ephrussi, 1936). Deficiencies and duplications for wa can be produced as a result of nonhomologous exchanges within the white region. wa gives rise to partial revertants, as wr (Muller), waM (Mossige), and wa57i (Green). Eye color is modified in certain mutant combinations. wa;bw is slightly lighter than wa. wa;st is light pinkish yellow (Mainx, 1938) as is wa v. z wa is lighter than either mutant alone, only slightly darker than wbf (Green, 1959a). wa rb and wa g have nearly white eyes; wa wch, wbf wa, and wa in combination with su(f) all have white eyes. su(wa) wa and su(wa)G wa have browner eyes than wa. The triple mutant su(wa) wa su(f) has eyes only slightly lighter than wa (Levis et al., 1984). wBwx wa is like wa (Judd). wa/+ has lighter eyes than +/+ in v homozygotes (Braver, 1953); Tp(2;3)P darkens wa. Transpositions of wa and the neighboring gene rst+ have been isolated at more than 120 sites in the genome [Ising and Ramel, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 947-54].

Occupies a recombination site between wBwx and wa (Judd, 1959). Spontaneous reversions reported by Redfield (1952, DIS 26: 28). wbf; st has white eyes (Mainx, 1938, Z. Indukt. Abstamm. Vererbungsl. 75: 256-76). Eyes of wbf rb and wbf g are lighter than the eyes of wbf, rb, or g (Green, 1959a).

Located distal to w (MacKendrick and Pontecorvo, 1952) and we (Judd, 1958; Green, 1959a). At 19, eye color as dark as pn; at 30, as light as wbf or wi; sensitivity greatest 40-48 hr after pupation (Ephrussi and Herold, 1945, Genetics 30: 62-70).

Located distal to wbf (Judd, 1957, 1959). Reduces recombination in the y-spl interval. Heterozygotes between wBwx and other white alleles or deficiencies are indistinguishable in eye color from wBwx/wBwx. The double mutant wBwx wcol is lighter than either single mutant, but wBwx/wa and wBwx/wbf are indistinguishable from wa and wbf, respectively.

Maps at the same site as wa. Derivatives of wc may be stable (w+ for example) or mutable (such as wdc and wdi) and include both point mutations and deficiencies (Green, 1967, Genetics 56: 467-82). The mutations take place in both males and females, may occur in clusters, and do not appear to involve recombination. Transpositions of a segment of the w gene that includes wc to different locations on the third chromosome have been recovered and are mutable (Green, 1969, Genetics 61: 423-28; Green, 1976).

Located near wBwx and just distal to wa (Welshons and Nicoletti, 1963, DIS 38: 80). Females heterozygous for wcf and w, wa, wco, wch, wbl, wcol, or wsat have eye color of wcf homozygous females. wcf/+ flies wild-type.

Occupies site proximal to wa and distal to wsp (Lewis, 1956). Eyes light in double mutant with rb or g, white with wa. Enhanced by P and e(we); suppressed by Su(wch), making eyes brownish (Rasmuson, 1970, Hereditas 65: 83-96).

Located distal to w1 (MacKendrick and Pontecorvo, 1952). Enhanced by e(we); lightens rb and g (Green, 1959a). wco;st has yellow eyes (Mainx, 1938).

wDZL is located in or immediately proximal to the rightmost set of previously-defined white mutant sites (Bingham, 1981). While this mutant affects the pigmentation of the eyes, it has no effect on the color of the larval Malpighian tubules or the testis sheath of adult males. wDZL shows synapsis-dependent dominance over w+. It is a highly mutable allele (like wc), giving rise spontaneously to w+ and w- derivatives with a frequency of 0.5-1.5%. Interactions between wDZL and z are summarized in the allele table. It was observed that, when carrying the wild-type allele of z, wDZL/w- females have brown eyes; with z1, however, hemizygous wDZL females have yellow eyes (Bingham, 1980, Genetics 95: 341-53).

Placed proximal to wa (Green, 1959a). Amount of pigment formed by we not a function of gene dose: we female = we male < we/we male = we/we female < we/we/we female (Muller, 1932). Mutant enhanced by P, cru, and whg as well as by E(we). Lightens rb and g (Green, 1959a). A we optic disk transplanted into a wild-type host shows autonomous eye color development (Beadle and Ephrussi, 1936).

Placed on the genetic map distal to w1 (MacKendrick, 1953, DIS 27: 100). wi is unstable, reverting spontaneously to w+ with a frequency of 5x10-5 in wi/wi females and 5x10-6 in wi/Y males and wi/Df(1)w females (Lewis, 1959, Genetics 44: 522; Bowman, 1965, Genetics 52: 1069-79). The frequency of germinal reversions and of somatic reversions in larval eye tissue is increased by X rays (Lewis, 1959; Bowman and Green, 1964, Genetics 50: 237). No dosage compensation shown by the mutant (Green 1959a). Recombination between flanking w alleles reduced in wi, but restored in its revertants (Bowman, 1965; Bowman and Green, 1966, Genetica 37: 7-16).

Located proximal to wch and distal to wDZL. wsp affects that deposition of the eye pigments, resulting in a variegated phenotype, but does not affect the pigmentation of the larval Malpiphian tubules. Testis pigmentation varies with different alleles, wsp3 males having unpigmented testes, but wsp1 and wsp2 males showing enhanced testis pigmentation (Davison et al., 1985; Pirrotta, Stellar, and Bozzetti, 1985, EMBO J. 4: 3501-08; Judd, 1987). Partial complementation occurs between wsp alleles and certain other w mutations when they are synapsed; for example, wsp/w, wsp/wch, and wsp/wa females have homogeneous brown eyes (Green, 1959a). The double mutants wa wsp and wch wsp have white and pale yellow eyes, respectively. wsp, when heterozygous with a deficiency for all or part of the w locus, produces a phenotype like that of wsp homozygotes (Green, 1959c). In the presence of z1, two synapsed copies of wsp in trans (or tandemly repeated) result in yellow-eyed females; z1 females with one copy of wsp have wild-type eye color. A specific regulator of the wsp eye phenotype, su(wsp), has been isolated as a partial revertant of wsp1 (Chapman and Bingham, 1985); this suppressor restores wild-type eye color to wsp1, wsp2, wsp3, and wsp4 flies, but not to the wsp81d mutant (Davison et al., 1985).

wzm is located to the right of wa and to the left of w1. It is an unstable white allele, mutating to derivatives, most of which are unstable (Judd, 1963, Proc. Int. Congr. Genet. 11th, Vol. 1: 3-4; 1964, DIS 39: 60). Since all z+ wzm males (as well as z+ wzm/z+ wzm females) have wild-type eye color, the mutant z was used as an indicator of the mutability of wzm strains. Derivatives of wzm (Kalisch and Becker, 1970, Mol. Gen. Genet. 107: 321-35) include wzl (from the z wzm stock), wzmz (from the z wzm stock), and wzmzrb, wzmzz and wzmzw (from the z wzmz stock). Only wzl is stable. The mutants were often recovered in clusters. wzmz reverts to wzm+ (eye color between z wzm and z w+) and the white-eyed wzmzz and ww. Other derivatives (wz, wzh, wzs) were recovered by Judd (1957; 1969, Genetics 61: s29).