Yeast Genetics and Molecular Biology 2002
University of Wisconsin
Madison, Wisconsin USA
July 30 - August 4, 2002


Name: Strich, Randy
Mailing Address: Institute for Cancer Research, Fox Chase Cancer Center, 7701 Burholme Ave, Philadelphia, PA 19111, USA
Email Address: r_strich@fccc.edu
Phone & FAX numbers: 215 728-5321 & 215 379-5715

Abstract #41


Session Title: Cell Cycle and Differentiation
Session Time: Friday, August 2 -- 9:00AM - 10:30AM
Presentation: Platform
Topic: Cell Biology

Removing the Block to Pre-meiotic DNA Re-replication in S. cerevisiae.
Michael Mallory (1), Katrina Cooper (2), Michal Jarnik (1), Randy Strich (1)
(1) Institute for Cancer Research, Fox Chase Cancer Center, 7701 Burholme Ave, Philadelphia, PA 19111, USA; (2) Department of Biochemistry, Hahnemann University, Philadelphia PA

The precise transmission of the genome at each generation is essential for the survival of an organism. In budding yeast, overlapping regulatory systems mediated by cyclin B-cyclin dependent kinase (Cdk) activity restrict mitotic S phase to only once per cell cycle. This study demonstrates that ectopic overexpression of the B-type cyclin Clb1p can recruit approximately 30% of meiotic cells to re-initiate DNA replication and undergo 2-4 additional divisions producing asci containing up to 20 spores. The efficiency of re-replication was directly related to Clb1p levels indicating that this cyclin-Cdk activity is rate limiting. Further characterizations revealed that the additional rounds of DNA replication occur prior to nuclear division and were independent of the Cdk inhibitor Sic1p, an important inhibitor of pre-meiotic S phase. The resulting spore clones are viable, haploid, and demonstrated Mendellian marker segregation indicating that DNA replication was complete and chromosomes segregated normally. This latter observation is consistent with our finding that these cell divisions were coordinated and contained a spindle checkpoint. Since ectopic expression of Clb1p does not alter cell cycle progression in mitotic cells, these results indicate that the checkpoint pathways that block re-replication are different in meiotic and mitotic cells.


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