This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Akamatsu, Y.
Right arrow Articles by Iwasaki, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Akamatsu, Y.
Right arrow Articles by Iwasaki, H.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, June 2008, p. 3639-3651, Vol. 28, No. 11
0270-7306/08/$08.00+0     doi:10.1128/MCB.01828-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Molecular Characterization of the Role of the Schizosaccharomyces pombe nip1+/ctp1+ Gene in DNA Double-Strand Break Repair in Association with the Mre11-Rad50-Nbs1 Complex{triangledown}

Yufuko Akamatsu ,1,{dagger},{ddagger} Yasuto Murayama,1,{dagger} Takatomi Yamada,2 Tomofumi Nakazaki,1 Yasuhiro Tsutsui,3 Kunihiro Ohta,2 and Hiroshi Iwasaki1*

Division of Molecular and Cellular Biology, International Graduate School of Arts and Sciences, Yokohama City University, Suehiro-cho, Tsurumi, Yokohama, Kanagawa 230-0045,1 Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Komaba, Meguro-ku, Tokyo 153-8902,2 Division of Mutagenesis, National Institute of Genetics, Yata, Mishima, Shizuoka 411-8540, Japan3

Received 8 October 2007/ Returned for modification 13 November 2007/ Accepted 17 March 2008

The Schizosaccharomyces pombe nip1+/ctp1+ gene was previously identified as an slr (synthetically lethal with rad2) mutant. Epistasis analysis indicated that Nip1/Ctp1 functions in Rhp51-dependent recombinational repair, together with the Rad32 (spMre11)-Rad50-Nbs1 complex, which plays important roles in the early steps of DNA double-strand break repair. Nip1/Ctp1 was phosphorylated in asynchronous, exponentially growing cells and further phosphorylated in response to bleomycin treatment. Overproduction of Nip1/Ctp1 suppressed the DNA repair defect of an nbs1-s10 mutant, which carries a mutation in the FHA phosphopeptide-binding domain of Nbs1, but not of an nbs1 null mutant. Meiotic DNA double-strand breaks accumulated in the nip1/ctp1 mutant. The DNA repair phenotypes and epistasis relationships of nip1/ctp1 are very similar to those of the Saccharomyces cerevisiae sae2/com1 mutant, suggesting that Nip1/Ctp1 is a functional homologue of Sae2/Com1, although the sequence similarity between the proteins is limited to the C-terminal region containing the RHR motif. We found that the RxxL and CxxC motifs are conserved in Schizosaccharomyces species and in vertebrate CtIP, originally identified as a cofactor of the transcriptional corepressor CtBP. However, these two motifs are not found in other fungi, including Saccharomyces and Aspergillus species. We propose that Nip1/Ctp1 is a functional counterpart of Sae2/Com1 and CtIP.

* Corresponding author. Mailing address: Division of Molecular and Cellular Biology, International Graduate School of Arts and Sciences, Yokohama City University, Suehiro-cho, Tsurumi, Yokohama, Kanagawa 230-0045, Japan. Phone: 81-45-508-7238. Fax: 81-45-508-7269. E-mail: iwasaki{at}tsurumi.yokohama-cu.ac.jp

{triangledown} Published ahead of print on 31 March 2008.

{dagger} These two authors contributed equally to this work.

{ddagger} Present address: Developmental Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021.

Molecular and Cellular Biology, June 2008, p. 3639-3651, Vol. 28, No. 11
0270-7306/08/$08.00+0     doi:10.1128/MCB.01828-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Milman, N., Higuchi, E., Smith, G. R. (2009). Meiotic DNA Double-Strand Break Repair Requires Two Nucleases, MRN and Ctp1, To Produce a Single Size Class of Rec12 (Spo11)-Oligonucleotide Complexes. Mol. Cell. Biol. 29: 5998-6005 [Abstract] [Full Text]  
  • Huertas, P., Jackson, S. P. (2009). Human CtIP Mediates Cell Cycle Control of DNA End Resection and Double Strand Break Repair. J. Biol. Chem. 284: 9558-9565 [Abstract] [Full Text]  
  • Hartsuiker, E., Mizuno, K., Molnar, M., Kohli, J., Ohta, K., Carr, A. M. (2009). Ctp1CtIP and Rad32Mre11 Nuclease Activity Are Required for Rec12Spo11 Removal, but Rec12Spo11 Removal Is Dispensable for Other MRN-Dependent Meiotic Functions. Mol. Cell. Biol. 29: 1671-1681 [Abstract] [Full Text]  
  • Porter-Goff, M. E., Rhind, N. (2009). The Role of MRN in the S-Phase DNA Damage Checkpoint Is Independent of Its Ctp1-dependent Roles in Double-Strand Break Repair and Checkpoint Signaling. Mol. Biol. Cell 20: 2096-2107 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»