ACE2 is required for daughter cell-specific G1 delay in Saccharomyces cerevisiae

Tracy L. Laabs, David D. Markwardt, Matthew G. Slattery, Laura L. Newcomb, David J. Stillman, Warren Heideman

Research output: Contribution to journalArticlepeer-review

63 Scopus citations


Saccharomyces cerevisiae cells reproduce by budding to yield a mother cell and a smaller daughter cell. Although both mother and daughter begin G 1 simultaneously, the mother cell progresses through G1 more rapidly. Daughter cell G1 delay has long been thought to be due to a requirement for attaining a certain critical cell size before passing the commitment point in the cell cycle known as START. We present an alternative model in which the daughter cell-specific Ace2 transcription factor delays G1 in daughter cells. Deletion of ACE2 produces daughter cells that proceed through G1 at the same rate as mother cells, whereas a mutant Ace2 protein that is not restricted to daughter cells delays G 1 equally in both mothers and daughters. The differential in G 1 length between mothers and daughters requires the Cln3 G 1 cyclin, and CLN3-GFP reporter expression is reduced in daughters in an ACE2-dependent manner. Specific daughter delay elements in the CLN3 promoter are required for normal daughter G1 delay, and these elements bind to an unidentified 127-kDa protein. This DNA-binding activity is enhanced by deletion of ACE2. These results support a model in which daughter cell G1 delay is determined not by cell size but by an intrinsic property of the daughter cell generated by asymmetric cell division.

Original languageEnglish (US)
Pages (from-to)10275-10280
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number18
StatePublished - Sep 2 2003


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