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Fission Yeast Tup1-Like Repressors Repress Chromatin Remodeling at the fbp1+ Promoter and the ade6-M26 Recombination Hotspot
Kouji Hirotaa, Charles S. Hoffmanb, Takehiko Shibatac, and Kunihiro Ohtaa,ca Genetic Dynamics Research Unit-Laboratory, The Institute of Physical and Chemical Research (RIKEN), Wako-shi, Saitama 351-0198, Japan,
b Biology Department, Boston College, Chestnut Hill, Massachusetts 02467
c Cellular and Molecular Biology Laboratory, The Institute of Physical and Chemical Research (RIKEN)/CREST of Japan Science and Technology Corporation, Wako-shi, Saitama 351-0198, Japan
Corresponding author: Kunihiro Ohta, The Institute of Physical and Chemical Research (RIKEN), Wako-shi, Saitama 351-0198, Japan., kohta{at}postman.riken.go.jp (E-mail)
Communicating editor: P. RUSSELL
tup12
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 tup11
tup12
defects in chromatin regulation but not in transcription repression. The chromatin at the M26 site in mitotic cultures of a tup11
tup12
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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