microbiology, Vol 142, 2655-2662, Copyright © 1996 by Society for General Microbiology

ARTICLES

Cell cycle studies on the mode of action of yeast K28 killer toxin

MJ Schmitt, P Klavehn, J Wang, I Schonig and DJ Tipper
Institut fur Mikrobiologie und Weinforschung, Johannes Gutenberg- Universitat Mainz, Germany.

The virally encoded K28 killer toxin of Saccharomyces cerevisiae kills sensitive cells by a receptor-mediated process. DNA synthesis is rapidly inhibited, cell viability is lost more slowly and cells eventually arrest, apparently in the S phase of the cell cycle with a medium-sized bud, a single nucleus in the mother cell and a pre- replicated (1n) DNA content. Cytoplasmic microtubules appear normal, and no spindle is detectable. Arrest of a sensitive haploid yeast strain by alpha-factor at START gave complete protection for at least 4 h against a toxin concentration that killed non-arrested cells at the rate of one log each 2.5 h. Cells released from alpha-factor arrest were killed by toxin at a similar rate; arrest occurred with medium- sized buds within the same cell cycle. Cells arrested by hydroxyurea, with unreplicated DNA, or by the spindle poison methylbenzimidazol-2yl- carbamate, with unseparated chromosomes, both arrest at the checkpoint at the G2/M boundary; these arrested cells were not protected against toxin, losing about one log of viability every 4 h. Following release from the cell cycle block, a majority of these toxin-exposed cells progressed through the cell cycle and arrested in the following S- phase, again with medium-sized buds. Killing by K28 toxin apparently requires entry into the nuclear division and bud cycles, but can result from inhibition of either early or late events in these cycles. Morphogenesis in moribund cells is uniformly blocked in early S-phase with an immature bud. Toxin action causes either independent blockage of both DNA synthesis and the budding cycle, or inhibits some unknown step required for both events.

This article has been cited by other articles:

				F. Breinig, T. Sendzik, K. Eisfeld, and M. J. Schmitt Dissecting toxin immunity in virus-infected killer yeast uncovers an intrinsic strategy of self-protection PNAS, March 7, 2006; 103(10): 3810 - 3815. [Abstract] [Full Text] [PDF]

				I. Ivanovska and J. M. Hardwick Viruses activate a genetically conserved cell death pathway in a unicellular organism J. Cell Biol., August 1, 2005; 170(3): 391 - 399. [Abstract] [Full Text] [PDF]

				J. Reiter, E. Herker, F. Madeo, and M. J. Schmitt Viral killer toxins induce caspase-mediated apoptosis in yeast J. Cell Biol., January 31, 2005; 168(3): 353 - 358. [Abstract] [Full Text] [PDF]

				A. Eiden-Plach, T. Zagorc, T. Heintel, Y. Carius, F. Breinig, and M. J. Schmitt Viral Preprotoxin Signal Sequence Allows Efficient Secretion of Green Fluorescent Protein by Candida glabrata, Pichia pastoris, Saccharomyces cerevisiae, and Schizosaccharomyces pombe Appl. Envir. Microbiol., February 1, 2004; 70(2): 961 - 966. [Abstract] [Full Text] [PDF]

				D. Jablonowski and R. Schaffrath Saccharomyces cerevisiae RNA Polymerase II Is Affected by Kluyveromyces lactis Zymocin J. Biol. Chem., July 12, 2002; 277(29): 26276 - 26280. [Abstract] [Full Text] [PDF]

				F. Riffer, K. Eisfeld, F. Breinig, and M. J. Schmitt Mutational analysis of K28 preprotoxin processing in the yeast Saccharomyces cerevisiae Microbiology, May 1, 2002; 148(5): 1317 - 1328. [Abstract] [Full Text] [PDF]

				E. R. Sumner and S. V. Avery Phenotypic heterogeneity: differential stress resistance among individual cells of the yeast Saccharomyces cerevisiae Microbiology, February 1, 2002; 148(2): 345 - 351. [Full Text] [PDF]