Tallóczy Z, Menon S, Neigeborn L, Leibowitz M J
Department of Molecular Genetics and Microbiology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854-5635, USA.
Genetics. 1998 Sep;150(1):21-30. doi: 10.1093/genetics/150.1.21.
[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.
[KIL-d]是一种细胞质遗传性状，它使感染杀伤病毒的酿酒酵母细胞在a/α细胞中表达正常的杀伤表型，但在a型或α型细胞中表现出斑驳的缺陷杀伤表型。[KIL-d]单倍体的交配导致其表型缺陷的“修复”，而所得二倍体的减数分裂导致斑驳但有丝分裂稳定的缺陷的“重置”。我们表明，[KIL-d]并不存在于杀伤病毒的双链RNA基因组上。因此，[KIL-d]对病毒基因表达的影响本质上是表观遗传的。重置需要减数分裂的核事件，因为[KIL-d]可以在细胞融合过程中通过细胞质传递而不会导致杀伤病毒表达缺陷。随后，这些细胞融合体交配后再进行减数分裂，产生表达斑驳缺陷表型的孢子克隆。将野生型细胞质导入表型有缺陷的[KIL-d]单倍体中无法修复，同时或顺序表达两个MAT等位基因也不会导致修复。因此，修复不是由MAT位点杂合性的出现触发的，而是需要交配过程中发生的核融合事件。因此，[KIL-d]似乎与细胞核相互作用，以便对杀伤病毒RNA基因组的基因表达发挥作用。
