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Pbp1 mediates the aberrant expression of genes involved in growth defect of ccr4 ∆ and pop2 ∆ mutants in yeast Saccharomyces cerevisiae
Author(s) -
Valderrama Arvin Lapiz,
Fujii Shiori,
Duy Duong Long,
Irie Kaoru,
Mizuno Tomoaki,
Suda Yasuyuki,
Irie Kenji
Publication year - 2021
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/gtc.12846
Subject(s) - mutant , saccharomyces cerevisiae , biology , gene , phenotype , gene expression , genetics , mutation , microbiology and biotechnology
Abstract CCR4 and POP2 genes encode the catalytic subunit of the Ccr4‐Not complex involved in shortening mRNA poly(A) tail in Saccharomyces cerevisiae . The ccr4 Δ and pop2∆ mutants exhibit pleiotropic phenotypes such as slow and temperature‐sensitive growth, aberrant expression of glucose repression genes and abnormal cell wall synthesis. We previously found that the growth defect of the ccr4 Δ and pop2∆ mutants is suppressed by deletion of the PBP1 gene, which encodes poly(A)‐binding protein (Pab1)‐binding protein 1. In this study, we investigated the functional relationship between Ccr4/Pop2 and Pbp1 by measuring changes in gene expression in ccr4 Δ and pop2∆ single mutants and ccr4 Δ pbp1∆ and pop2∆ pbp1∆ double mutants. We found that expression of HSP12, HSP26 , PIR3 , FUS1 and GPH1 was increased in ccr4 Δ and pop2∆ single mutants. The pbp1∆ mutation not only restored the growth defect but also reduced the increased expression of those genes found in the ccr4 Δ and pop2∆ mutants. Over‐expression of PBP1 in the ccr4 Δ mutant further increased the expression of HSP12, HSP26 , PIR3 and FUS1 and exacerbated the cell growth. These results suggest that the aberrant expression of a subset of genes, which is facilitated by Pbp1, contributes to the pleiotropic phenotypes of the ccr4 Δ and pop2∆ mutants.