THE [KIL-D] CYTOPLASMIC GENETIC ELEMENT OF YEAST RESULTS IN EPIGENETIC REGULATION OF VIRAL M-DOUBLE-STRANDED-RNA GENE-EXPRESSION

[KIL-d] is a cytoplasmically inherited genetic trait that causes kille r virus-infected cells of Saccharomyces cerevisiae to express the norm al killer phenotypes in a/alpha cells, but to show variegated defectiv e killer phenotypes in a or a type cells. Mating of [KIL-d] haploids r esults in ''healing'' of their phenotypic defects, while meiosis of th e resulting diploids results in ''resetting'' of the variegated, but m itotically stable, defects. We show that [KIL-d] does not reside on th e double-stranded RNA genome of killer virus. Thus, the [KIL-d] effect on viral gene expression is epigenetic in nature. Resetting requires nuclear events of meiosis, since [KIL-d] can be cytoplasmically transm itted during cytoduction without causing defects in killer virus expre ssion. Subsequently, mating of these cytoductants followed by meiosis generates spore clones expressing variegated defective phenotypes. Cyt oduction of wild-type cytoplasm into a phenotypically defective [KIL-d ] haploid fails to heal, nor does simultaneous or sequential expressio n of both MAT alleles cause healing. Thus, healing is not triggered by the appearance of heterozygosity at the MAT locus, but rather require s the nuclear fusion events which occur during mating. Therefore, [KIL -d] appears to interact with the nucleus in order to exert its effects on gene expression by the killer virus RNA genome.