Genetics, Vol 118, 221-234, Copyright © 1988

INVESTIGATIONS

Partial Revertants of the Transposable Element-Associated Suppressible Allele white-apricot in Drosophila melanogaster: Structures and Responsiveness to Genetic Modifiers

S. M. Mount, M. M. Green and G. M. Rubin
Department of Biochemistry, University of California, Berkeley, California 94720, Department of Biological Sciences, Columbia University, New York, New York 10027

The eye color phenotype of white-apricot (w(a)), a mutant allele of the white locus caused by the insertion of the transposable element copia into a small intron, is suppressed by the extragenic suppressor suppressor-of-white-apricot (su(w(a))) and enhanced by the extragenic enhancers suppressor-of-forked su(f)) and Enhancer-of-white-apricot (E(w(a))). Derivatives of w(a) have been analyzed molecularly and genetically in order to correlate the structure of these derivatives with their response to modifiers. Derivatives in which the copia element is replaced precisely by a solo long terminal repeat (sLTR) were generated in vitro and returned to the germline by P-element mediated transformation; flies carrying this allele within a P transposon show a nearly wild-type phenotype and no response to either su(f) or su(w(a)). In addition, eleven partial phenotypic revertants of w(a) were analyzed. Of these, one appears to be a duplication of a large region which includes w(a), three are new alleles of su(w(a)), two are sLTR derivatives whose properties confirm results obtained using transformation, and five are secondary insertions into the copia element within w(a). One of these, w(aR84h), differs from w(a) by the insertion of the most 3' 83 nucleotides of the I factor. The five insertion derivatives show a variety of phenotypes and modes of interaction with su((f) and su(w(a)). The eye pigmentation of w(aR84h) is affected by su(f) and E(w(a)), but not su(w(a)). These results demonstrate that copia (as opposed to the interruption of white sequences) is essential for the w(a) phenotype and its response to genetic modifiers, and that there are multiple mechanisms for the alteration of the w(a) phenotype by modifiers.

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