Yeast Genetics and Molecular Biology 2000
University of Washington
Seattle, Washington USA
July 2000

Name: Heideman, Warren
Mailing Address: Pharmaceutical Sciences, University of Wisconsin, 425 N Charter St, Madison, WI 53706, USA
Email Address: wheidema@facstaff.wisc.edu
Phone & FAX numbers: 608 262 1795 & 608 262 3397

#003

Loss of upstream CLN3 and BCK2 regulatory sequences produces cells that cannot regulate G1.
Warren Heideman (1), David Markwardt (1), Laura Newcomb (2)
(1) Pharmaceutical Sciences, University of Wisconsin, 425 N Charter St, Madison, WI 53706, USA; (3) Biomolecular Chemistry, University of Wisconsin, 425 N Charter St, Madison, WI 53706, USA

CLN3 and BCK2 are thought to play important roles in regulating the G1 to S transition, termed Start, in the yeast Saccharomyces cerevisiae. We demonstrate that loss of regulatory sequences upstream of the CLN3 and BCK2 coding regions produces cells that are unable to alter the temporal length of G1 in response to different nutrient conditions. Because these cells have a fixed G1 length, they cannot maintain a constant cell size. Cell size in these mutants is proportional to the rate of growth in mass. These mutants are also unable to regulate G1 between mother and daughter cells. Mother and daughter cells in these strains have identical G1 lengths, and bud simultaneously. Mutations that produce a fixed level of CLN3 expression invariably produced cells with a constant temporal G1 length, but did not produce a constant cell size at budding. Our results indicate that rather than setting a cell size that triggers budding, CLN3 regulates cell size by controlling the rate of a process that ends the G1 phase of the cell cycle.

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