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Genetics, Vol. 155, 601-609, June 2000, Copyright © 2000

The [KIL-d] Element Specifically Regulates Viral Gene Expression in Yeast

Zsolt Tallóczya,b, Rebecca Mazara,b, Denise E. Georgopoulosa, Fausto Ramosa,b, and Michael J. Leibowitza,b,c
a UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854-5635,
b Rutgers, The State University of New Jersey
c Cancer Institute of New Jersey, New Brunswick, New Jersey 08901

Corresponding author: Michael J. Leibowitz, UMDNJ-Robert Wood Johnson Medical School, Department of Molecular Genetics and Microbiology, 675 Hoes Lane, Piscataway, NJ 08854-5635., leibowit{at}umdnj.edu (E-mail)

Communicating editor: S. SANDMEYER

The cytoplasmically inherited [KIL-d] element epigenetically regulates killer virus gene expression in Saccharomyces cerevisiae. [KIL-d] results in variegated defects in expression of the M double-stranded RNA viral segment in haploid cells that are "healed" in diploids. We report that the [KIL-d] element is spontaneously lost with a frequency of 10-4–10-5 and reappears with variegated phenotypic expression with a frequency of >=10-3. This high rate of loss and higher rate of reappearance is unlike any known nucleic acid replicon but resembles the behavior of yeast prions. However, [KIL-d] is distinct from the known yeast prions in its relative guanidinium hydrochloride incurability and independence of Hsp104 protein for its maintenance. Despite its transmissibility by successive cytoplasmic transfers, multiple cytoplasmic nucleic acids have been proven not to carry the [KIL-d] trait. [KIL-d] epigenetically regulates the expression of the M double-stranded RNA satellite virus genome, but fails to alter the expression of M cDNA. This specificity remained even after a cycle of mating and meiosis. Due to its unique genetic properties and viral RNA specificity, [KIL-d] represents a new type of genetic element that interacts with a viral RNA genome.




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