*e(g): enhancer of garnet
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: white-Dominant-zeste-like
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).