Fission Yeast Tup1-Like Repressors Repress Chromatin Remodeling at the fbp1+ Promoter and the ade6-M26 Recombination Hotspot
Author(s) -
Kouji Hirota,
Charles S. Hoffman,
Takehiko Shibata,
Kunihiro Ohta§
Publication year - 2003
Publication title -
genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.792
H-Index - 246
eISSN - 1943-2631
pISSN - 0016-6731
DOI - 10.1093/genetics/165.2.505
Subject(s) - biology , recombination , genetics , repressor , chromatin , chromatin remodeling , yeast , fission , microbiology and biotechnology , gene , transcription factor , physics , nuclear physics , neutron
Chromatin remodeling plays crucial roles in the regulation of gene expression and recombination. Transcription of the fission yeast fbp1+ gene and recombination at the meiotic recombination hotspot ade6-M26 (M26) are both regulated by cAMP responsive element (CRE)-like sequences and the CREB/ATF-type transcription factor Atf1•Pcr1. The Tup11 and Tup12 proteins, the fission yeast counterparts of the Saccharomyces cerevisiae Tup1 corepressor, are involved in glucose repression of the fbp1+ transcription. We have analyzed roles of the Tup1-like corepressors in chromatin regulation around the fbp1+ promoter and the M26 hotspot. We found that the chromatin structure around two regulatory elements for fbp1+ was remodeled under derepressed conditions in concert with the robust activation of fbp1+ transcription. Strains with tup11Δ tup12Δ double deletions grown in repressed conditions exhibited the chromatin state associated with wild-type cells grown in derepressed conditions. Interestingly, deletion of rst2+, encoding a transcription factor controlled by the cAMP-dependent kinase, alleviated the tup11Δ tup12Δ defects in chromatin regulation but not in transcription repression. The chromatin at the M26 site in mitotic cultures of a tup11Δ tup12Δ mutant resembled that of wild-type meiotic cells. These observations suggest that these fission yeast Tup1-like corepressors repress chromatin remodeling at CRE-related sequences and that Rst2 antagonizes this function.
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