Evidence map›Paper›PMID 30973945›Full record

ArticlePloS one2019

Pop2 phosphorylation at S39 contributes to the glucose repression of stress response genes, HSP12 and HSP26.

Pham Thi Kim Lien, Nguyen Thi Minh Viet, Tomoaki Mizuno, Yasuyuki Suda, Kenji Irie

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Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
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3 · Its place in the literature

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4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Pham Thi Kim LienDepartment of Molecular Cell Biology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Nguyen Thi Minh VietDepartment of Molecular Cell Biology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Tomoaki MizunoDepartment of Molecular Cell Biology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Yasuyuki SudaDepartment of Molecular Cell Biology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Kenji IrieDepartment of Molecular Cell Biology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.ORCID 0000-0001-6364-1487

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The S. cerevisiae Pop2 protein is an exonuclease in the Ccr4-Not complex that is a conserved regulator of gene expression. Pop2 regulates gene expression post-transcriptionally by shortening the poly(A) tail of mRNA. A previous study has shown that Pop2 is phosphorylated at threonine 97 (T97) by Yak1 protein kinase in response to glucose limitation. However, the physiological importance of Pop2 phosphorylation remains unknown. In this study, we found that Pop2 is phosphorylated at serine 39 (S39) under unstressed conditions. The dephosphorylation of S39 was occurred rapidly after glucose depletion, and the addition of glucose to the glucose-deprived culture recovered this phosphorylation, suggesting that Pop2 phosphorylation at S39 is regulated by glucose. This glucose-regulated phosphorylation of Pop2 at S39 is dependent on Pho85 kinase. We previously reported that Pop2 takes a part in the cell wall integrity pathway by regulating LRG1 mRNA; however, S39 phosphorylation of Pop2 is not involved in LRG1 expression. On the other hand, Pop2 phosphorylation at S39 is involved in the expression of HSP12 and HSP26, which encode a small heat shock protein. In the medium supplemented with glucose, Pop2 might be phosphorylated at S39 by Pho85 kinase, and this phosphorylation contributes to repress the expression of HSP12 and HSP26. Glucose starvation inactivated Pho85, which resulted in the derepression of HSP12 and HSP26, together with other glucose sensing mechanisms. Our results suggest that Pho85-dependent phosphorylation of Pop2 is a part of the glucose sensing system in yeast.

Indexed as

Catabolite RepressionGene Expression Regulation, FungalGlucoseGlycoproteinsGTPase-Activating ProteinsHeat-Shock ProteinsPhosphorylationRibonucleasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSerineGlucoseGlycoproteinsGTPase-Activating ProteinsHeat-Shock ProteinsHSP12 protein, S cerevisiaeHSP26 protein, S cerevisiaeLRG1 protein, S cerevisiaePir3 protein, S cerevisiaePOP2 protein, S cerevisiaeRibonucleasesSaccharomyces cerevisiae ProteinsSerine

Identifiers

PMID30973945
PMCPMC6459547

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.