ArticleProceedings of the National Academy of Sciences of the United States of America2003
ACE2 is required for daughter cell-specific G1 delay in Saccharomyces cerevisiae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 87 citations in OpenAlex.
- Cell cycle-dependent protein dynamics in budding yeast resolved by deconvolution of bulk proteomics.Molecular systems biology · 2026Article
- Cell division timing shapes the morphology and size of nascent multicellular organisms.bioRxiv : the preprint server for biology · 2026Article
- The Cbk1-Ace2 axis guides Candida albicans from yeast to hyphae and back again.Current genetics · 2021Article
- Genetic interaction network has a very limited impact on the evolutionary trajectories in continuous culture-grown populations of yeast.BMC ecology and evolution · 2021Article
- Accumulation of cis- and trans-regulatory variations is associated with phenotypic divergence of a complex trait between yeast species.G3 (Bethesda, Md.) · 2021Article
- The mitotic exit network regulates the spatiotemporal activity of Cdc42 to maintain cell size.The Journal of cell biology · 2021Article
- Article
- A hybrid stochastic model of the budding yeast cell cycle.NPJ systems biology and applications · 2020Article
- A stochastic model of size control in the budding yeast cell cycle.BMC bioinformatics · 2019Article
- Modulation of Cell Identity by Modification of Nuclear Pore Complexes.Frontiers in genetics · 2019Review
- Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast.Aging cell · 2018Article
- Daughter-cell-specific modulation of nuclear pore complexes controls cell cycle entry during asymmetric division.Nature cell biology · 2018Article
- Identification and Mode of Action of a Plant Natural Product Targeting Human Fungal Pathogens.Antimicrobial agents and chemotherapy · 2017Article
- Spatial and temporal signal processing and decision making by MAPK pathways.The Journal of cell biology · 2017Review
- A Stochastic Model of the Yeast Cell Cycle Reveals Roles for Feedback Regulation in Limiting Cellular Variability.PLoS computational biology · 2016Article
- Compartmentalization of a bistable switch enables memory to cross a feedback-driven transition.Cell · 2015Article
- Article
- Regulation of Ace2-dependent genes requires components of the PBF complex in Schizosaccharomyces pombe.Cell cycle (Georgetown, Tex.) · 2015Article
- Uncoupling reproduction from metabolism extends chronological lifespan in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- PP2ARts1 is a master regulator of pathways that control cell size.The Journal of cell biology · 2014Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Saccharomyces cerevisiae cells reproduce by budding to yield a mother cell and a smaller daughter cell. Although both mother and daughter begin G1 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 G1 equally in both mothers and daughters. The differential in G1 length between mothers and daughters requires the Cln3 G1 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.
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