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The [KIL-d] Cytoplasmic Genetic Element of Yeast Results in Epigenetic Regulation of Viral M Double-Stranded RNA Gene Expression
Zsolt Tallóczya, Sujoy Menona, Lenore Neigebornb, and Michael J. Leibowitza,ca Department of Molecular Genetics and Microbiology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854-5635,
b Department of Biological Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey 08901
c Cancer Institute of New Jersey, New Brunswick, New Jersey 08901
Corresponding author: Michael J. Leibowitz, UMDNJ-Robert Wood Johnson Medical School, 675 Hoes Ln., Rm. 705, Piscataway, NJ 08854-5635., leibowit{at}umdnj.edu (E-mail).
Communicating editor: M. CARLSON
cells, but to show variegated defective killer phenotypes in a or 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.
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