Results in nearly wild-type pigmentation of wsp1, wsp2, wsp3, and wsp4, but not wsp81d5. No phenotypic effect seen on eight other tested w alleles. The lesions of the spotted alleles map 500 to 1000 base pairs 5' to the w transcription unit and are postulated to affect an enhancer sequence. The normal allele of su(wsp) is postulated to encode a repressor of this enhancing function; the combination of the repressor and defective enhancer produces the spotted phenotype; the mutant allele of su(wsp), lacking repressor function, results in the derepression of the defective enhancers at the time of eye-pigment deposition, leading to increased pigmentation. wsp81d5, a molecular deletion extending more 3' that the other wsp alleles is postulated to be insensitive to the presence or absence of repression owing to loss of the site of interaction between the su(wsp) gene product and the w locus. Adult transcription of all w alleles, including w+, markedly increased by su(wsp), apparently after pigment deposition, since with the exception of wsp alleles, eye color does not respond to su(wsp). The latter observation implies a second site of repressor binding specific to adult transcription.