Results in nearly wild-type pigmentation of w^sp1, w^sp2, w^sp3, and w^sp4, but not w^sp81d. 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(w^sp) 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(w^sp), lacking repressor function, results in the derepression of the defective enhancers at the time of eye-pigment deposition, leading to increased pigmentation. w^sp81d, a molecular deletion extending more 3' that the other w^sp1 alleles is postulated to be insensitive to the presence or absence of repression owing to loss of the site of interaction between the su(w^sp) gene product and the w locus. Adult transcription of all w alleles, including w⁺, markedly increased by su(w^sp), apparently after pigment deposition, since with the exception of w^sp1 alleles, eye color does not respond to su(w^sp). The latter observation implies a second site of repressor binding specific to adult transcription.