The determined state of white expression in the Drosophila eye is modified by zeste(1) in the w(zm) family of mutants
1994
Peterson, K.M. (National Inst. of Environmental Health Science, Research Triangle Park, NC (USA). Lab. of Genetics) | Davis, P.S. | Judd, B.H.
Analysis of the white(zeste mottled) (W(zm)) mutant family suggests that the zeste gene product functions in establishing and stabilizing a transeriptionally active chromatin domain for white locus expression. The z(1) mutation reduces expression of paired or proximate copies of white, while single or unpaired copies maintain wildtype levels of expression. The w(zm) mutation, caused by the insertion of the retrotransposon BEL into the 5' intron of white, alters the zeste-white interaction to produce a mottled eye phenotype in hemizygous z(1) w(zm) males. The molecular structure of four w(zm) derivatives was determined. w(zl) results from the insertion of an additional transposable element into the 5' regulatory region of white. w(zvl) is a deletion of sequences upstream of the white locus. Two others, w(halo) and w(cres), result from the transposition of w(zm) plus the entire verticals-roughest region into heterochromatin near the tip of chromosome 3L. They variegate for roughest but not for white; rather, the z(1) effect on w(zm) now causes white expression to become non-autonomous and non-clonal. The analysis of these five mutations shows that the neomorphic zeste(1) product, in combination with structural changes imposed by transposons and intercalary heterochromatin, modifies the determination and stability of white expression. It is proposed that the normal zeste product functions as part of a complex that stimulates transcription by changing chromatin conformation to establish and maintain transcriptionally active domains. The unpairing of homologs is proposed to be one of the initial results of conformational change, providing an explanation for the role of zeste in transvection.
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