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The Rts1 regulatory subunit of PP2A phosphatase controls expression of the HO endonuclease via localization of the Ace2 transcription factor.

Authors
  • Parnell, Emily J1
  • Yu, Yaxin1
  • Lucena, Rafael2
  • Yoon, Youngdae3
  • Bai, Lu4
  • Kellogg, Douglas R2
  • Stillman, David J5
  • 1 From the Department of Pathology, University of Utah Health Sciences Center, Salt Lake City, Utah 84112.
  • 2 the Department of Molecular, Cell and Developmental Biology, University of California, Santa Cruz, California 95064, and.
  • 3 the Center for Eukaryotic Gene Regulation, Department of Biochemistry and Molecular Biology, and.
  • 4 the Center for Eukaryotic Gene Regulation, Department of Biochemistry and Molecular Biology, and Department of Physics, The Pennsylvania State University, University Park, Pennsylvania 16802.
  • 5 From the Department of Pathology, University of Utah Health Sciences Center, Salt Lake City, Utah 84112, [email protected].
Type
Published Article
Journal
Journal of Biological Chemistry
Publisher
American Society for Biochemistry and Molecular Biology
Publication Date
Dec 19, 2014
Volume
289
Issue
51
Pages
35431–35437
Identifiers
DOI: 10.1074/jbc.M114.611715
PMID: 25352596
Source
Medline
Keywords
Language
English
License
Unknown

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. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.

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