Ace2 and Cln3 are required for daughter cell-specific G1 delay in S.
cerevisiae.
Warren Heideman, David Markwardt, Tracy
Laabs
Pharmaceutical Sciences, University of Wisconsin, 777 Highland
Ave, Madison, WI 53705, USA
Saccharomyces cerevisiae cells reproduce
by budding to yield a small daughter cell and a larger mother cell at
the end of mitosis. The mother cell then progresses through G1 more
rapidly than the daughter cell, and enters S phase first. CLN3 and BCK2
are thought to play important roles in regulating progress through G1.
We hypothesized that differential regulation of CLN3 or BCK2 between
mother and daughter cells could account for the difference in G1 length.
Deletion of CLN3 produced a defect in daughter cell G1 delay, while
replacement of 5' regulatory sequences from CLN3 with heterologous
promoters produced a more profound defect. This defect occured with wide
variety of heterologous promoters of varying strength, and was not
caused by CLN3 overexpression. We find no evidence to link BCK2 to this
process. These results are consistent with a model in which mother and
daughter cells differentially regulate CLN3 via 5' elements. In support
of this model, deletion of ACE2, a gene that encodes a daughter-specific
zinc finger protein also blocks daughter cell G1 delay. These results
suggest a model in which the longer G1 phase observed in daughter cells
is determined by an intrinsic property of the daughter cells.
Surprisingly, strains in which mother and daughter cells bud
simultaneously can have normal size distributions.
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