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MBC in Press, published online ahead of print April 11, 2007
Mol. Biol. Cell 10.1091/mbc.E06-12-1084

A more recent version of this article appeared on June 1, 2007
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Submitted on December 9, 2006
Revised on March 22, 2007
Accepted on March 30, 2007

Fission Yeast Taz1 and RPA Are Synergistically Required to Prevent Rapid Telomere Loss

Tatsuya Kibe,*{dagger} Yuuki Ono,{dagger} Koichiro Sato,* and Masaru Ueno*{dagger}

*Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, 1-3-1 Kagamiyama, Higashi-Hiroshima 739-8530, Japan; {dagger}Department of Chemistry, Shizuoka University, 836 Oya, Shizuoka, 422-8529, Japan

Monitoring Editor: Orna Cohen-Fix

The telomere complex must allow nucleases and helicases to process chromosome ends to make them substrates for telomerase, while preventing these same activities from disrupting chromosome end-protection. Replication protein A (RPA) binds to single-stranded DNA and is required for DNA replication, recombination, repair, and telomere maintenance. In fission yeast, the telomere binding protein Taz1 protects telomeres ends and negatively regulates telomerase. Here we show that taz1-d rad11-D223Y double mutants lose their telomeric DNA, indicating that RPA (Rad11) and Taz1 are synergistically required to prevent telomere loss. Telomere loss in the taz1-d rad11-D223Y double mutants was suppressed by additional mutation of the helicase domain in a RecQ helicase (Rqh1), or by overexpression of Pot1, a single-strand telomere binding protein that is essential for protection of chromosome ends. From our results, we propose that in the absence of Taz1 and functional RPA, Pot1 cannot function properly and the helicase activity of Rqh1 promotes telomere loss. Our results suggest that controlling the activity of Rqh1 at telomeres is critical for the prevention of genomic instability.

Address correspondence to: Masaru Ueno (scmueno{at}hiroshima-u.ac.jp)




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