Nucleic Acids Research Advance Access originally published online on January 30, 2007
Nucleic Acids Research 2007 35(4):1187-1197; doi:10.1093/nar/gkm015
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Nucleic Acids Research, 2007, Vol. 35, No. 4 1187-1197
© 2007 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
Caf1 regulates translocation of ribonucleotide reductase by releasing nucleoplasmic Spd1–Suc22 assembly
Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo 113-0033, Japan
*To Whom Correspondence should be addressed. Tel: +81-3-5841-4750; Fax: +81 3 5841 4751; E-mail: katada{at}mol.f.u-tokyo.ac.jp
Received October 5, 2006. Revised December 25, 2006. Accepted January 1, 2007.
Appropriate supply of deoxyribonucleotides by the ribonucleotide reductase (RNR) complex is essential for DNA replication and repair. One recent model for the RNR activation in Schizosaccharomyces pombe is translocation of the regulatory subunit Suc22 from the nucleoplasm to the cytoplasm. The RNR inhibitory protein Spd1, which retains Suc22 in the nucleoplasm, is rapidly degraded upon DNA-replication stress, resulting in release of Suc22 to form the active RNR complex in the cytoplasm. Here, we show that Caf1, a component of the Ccr4–Not complex, is responsible for resistance of the replication stress and control of the Suc22 translocation. Caf1 is required not only for the stress-induced translocation of Suc22 from nucleoplasm to cytoplasm but also for the degradation of nucleoplasmic Spd1. DNA-replication stress appears to allow Caf1 to interact with Suc22, resulting in release of the nucleoplasmic Spd1–Suc22 assembly. Taken together, these results suggest a novel function of Caf1 as a key regulator in the stress-induced RNR activation.
Present address: Yasuhiro Araki, Zentrum fur Molekulare Biologie der Universitat Heidelberg (ZMBH), Im Neuenheimer Feld 282, 69120 Heidelberg, Germany
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