ArticleThe Journal of biological chemistry2014
The Rts1 regulatory subunit of PP2A phosphatase controls expression of the HO endonuclease via localization of the Ace2 transcription factor.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 9 citations in OpenAlex.
- Inferring gene regulatory networks using transcriptional profiles as dynamical attractors.PLoS computational biology · 2023Article
- A Stat1 bound enhancer promotes Nampt expression and function within tumor associated macrophages.Nature communications · 2021Article
- PP2A Functions during Mitosis and Cytokinesis in Yeasts.International journal of molecular sciences · 2019Review
- Ser/Thr protein phosphatases in fungi: structure, regulation and function.Microbial cell (Graz, Austria) · 2019Review
- Yeast Lacking the PP2A Phosphatase Regulatory Subunit Rts1 SensitizesFrontiers in genetics · 2019Article
- Article
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7 authors at 3 institutions in 1 country.
Funding
Abstract
The RTS1 gene encodes a subunit of the PP2A phosphatase that regulates cell cycle progression. Ace2 and Swi5 are cell cycle-regulated transcription factors, and we recently showed that phosphorylation of Ace2 and Swi5 is altered in an rts1 mutant. Here we examine expression of Ace2 and Swi5 target genes and find that an rts1 mutation markedly reduces expression of the HO gene. The decreased HO expression in an rts1 mutant is significantly restored by an additional ace2 mutation, a surprising result because HO is normally activated by Swi5 but not by Ace2. Ace2 normally accumulates only in daughter cells, and only activates transcription in daughters. However, in an rts1 mutant, Ace2 is present in both mother and daughter cells. One of the genes activated by Ace2 is ASH1, a protein that normally accumulates mostly in daughter cells; Ash1 is a transcriptional repressor, and it blocks HO expression in daughters. We show that in the rts1 mutant, Ace2 accumulation in mother cells results in Ash1 expression in mothers, and the Ash1 can now repress HO expression in mothers.
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