The [KIL-d] cytoplasmic genetic element of yeast results in epigenetic regulation of viral M double-stranded RNA gene expression

Abstract

[KIL-d] is a cytoplasmically inherited genetic trait that causes killer virus-infected cells of Saccharomyces cerevisiae to express the normal killer phenotypes in a/alpha cells, but to show variegated defective killer phenotypes in a or alpha type cells. Mating of [KIL-d] haploids results in "healing" of their phenotypic defects, while meiosis of the resulting diploids results in "resetting" of the variegated, but mitotically stable, defects. We show that [KIL-d] does not reside on the 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 transmitted during cytoduction without causing defects in killer virus expression. Subsequently, mating of these cytoductants followed by meiosis generates spore clones expressing variegated defective phenotypes. Cytoduction of wild-type cytoplasm into a phenotypically defective [KIL-d] haploid fails to heal, nor does simultaneous or sequential expression of both MAT alleles cause healing. Thus, healing is not triggered by the appearance of heterozygosity at the MAT locus, but rather requires 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.