Genetics, Vol. 159, 1467-1478, December 2001, Copyright © 2001

Counteracting Regulation of Chromatin Remodeling at a Fission Yeast cAMP Responsive Element-Related Recombination Hotspot by Stress-Activated Protein Kinase, cAMP-Dependent Kinase and Meiosis Regulators

Ken-ichi Mizunoa,b, Tomoko Hasemib,c, Toshiharu Ubukatab,c, Takatomi Yamadaa,d, Elisabeth Lehmanne, Jürg Kohlie, Yoshinori Watanabed, Yuichi Iinod, Masayuki Yamamotod, Mary E. Foxf, Gerald R. Smithf, Hiromu Murofushid, Takehiko Shibatab,c, and Kunihiro Ohtaa,b
a Genetic Dynamics Research Unit-Laboratory, RIKEN (The Institute of Physical and Chemical Research), Wako, Saitama 351-0198, Japan,
b Cellular and Molecular Biology Laboratory, RIKEN (The Institute of Physical and Chemical Research)/CREST of the JST, Wako, Saitama 351-0198, Japan,
c The Graduate School of Science and Engineering, Saitama University, Saitamashi, Saitama 338-8570, Japan,
d Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0032, Japan,
e Institute of Cell Biology, University of Bern, Bern CH-3012, Switzerland
f Fred Hutchinson Cancer Research Center, Seattle, Washington 98109

Corresponding author: Kunihiro Ohta, Genetic Dynamics Research Unit-Laboratory, RIKEN (The Institute of Physical and Chemical Research), Hirosawa 2-1, Wako, Saitama 351-0198, Japan., kohta{at}postman.riken.go.jp (E-mail)

Communicating editor: M. LICHTEN

In fission yeast, an ATF/CREB-family transcription factor Atf1-Pcr1 plays important roles in the activation of early meiotic processes via the stress-activated protein kinase (SAPK) and the cAMP-dependent protein kinase (PKA) pathways. In addition, Atf1-Pcr1 binds to a cAMP responsive element (CRE)-like sequence at the site of the ade6-M26 mutation, which results in local enhancement of meiotic recombination and chromatin remodeling. Here we studied the roles of meiosis-inducing signal transduction pathways in M26 chromatin remodeling. Chromatin analysis revealed that persistent activation of PKA in meiosis inhibited M26 chromatin remodeling, suggesting that the PKA pathway represses M26 chromatin remodeling. The SAPK pathway activated M26 chromatin remodeling, since mutants lacking a component of this pathway, the Wis1 or Spc1/Sty1 kinases, had no M26 chromatin remodeling. M26 chromatin remodeling also required the meiosis regulators Mei2 and Mei3 but not the subsequently acting regulators Sme2 and Mei4, suggesting that induction of M26 chromatin remodeling needs meiosis-inducing signals before premeiotic DNA replication. Similar meiotic chromatin remodeling occurred meiotically around natural M26 heptamer sequences. These results demonstrate the coordinated action of genetic and physiological factors required to remodel chromatin in preparation for high levels of meiotic recombination and eukaryotic cellular differentiation.





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