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Nucleic Acids Research Advance Access originally published online on April 9, 2009
Nucleic Acids Research 2009 37(11):3602-3611; doi:10.1093/nar/gkp235
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Nucleic Acids Research, 2009, Vol. 37, No. 11 3602-3611
© 2009 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

Rapid Cdc13 turnover and telomere length homeostasis are controlled by Cdk1-mediated phosphorylation of Cdc13

Shun-Fu Tseng, Zih-Jie Shen, Hung-Ji Tsai, Yi-Hsuan Lin and Shu-Chun Teng*

Department of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan

*To whom correspondence should be addressed. Tel: +886 2 23123456 (ext. 88294); Fax: +886 2 23915293; E-mail: shuchunteng{at}ntu.edu.tw

Received January 15, 2009. Revised March 13, 2009. Accepted March 30, 2009.

Budding yeast telomerase is mainly activated by Tel1/Mec1 (yeast ATM/ATR) on Cdc13 from late S to G2 phase of the cell cycle. Here, we demonstrated that the telomerase-recruitment domain of Cdc13 is also phosphorylated by Cdk1 at the same cell cycle stage as the Tel1/Mec1-dependent regulation. Phosphor-specific gel analysis demonstrated that Cdk1 phosphorylates residues 308 and 336 of Cdc13. The residue T308 of Cdc13 is critical for efficient Mec1-mediated S306 phosphorylation in vitro. Phenotypic analysis in vivo revealed that the mutations in the Cdc13 S/TP motifs phosphorylated by Cdk1 caused cell cycle delay and telomere shortening and these phenotypes could be partially restored by the replacement with a negative charge residue. In the absence of Ku or Tel1, Cdk1-mediated phosphorylation of Cdc13 showed no effect on telomere length maintenance. Moreover, this Cdk1-mediated phosphorylation was required to promote the regular turnover of Cdc13. Together these results demonstrate that Cdk1 phosphorylates the telomerase recruitment domain of Cdc13, thereby preserves optimal function and expression level of Cdc13 for precise telomere replication and cell cycle progression.

Present address: Hung-Ji Tsai, Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, MN 55455, USA


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