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

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.