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Molecular and Cellular Biology, August 2002, p. 5679-5687, Vol. 22, No. 16
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.16.5679-5687.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Involvement of Replicative Polymerases, Tel1p, Mec1p, Cdc13p, and the Ku Complex in Telomere-Telomere Recombination

Yun-Luen Tsai, Shun-Fu Tseng, Shih-Husan Chang, Chuan-Chuan Lin, and Shu-Chun Teng*

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

Received 14 December 2001/ Returned for modification 12 February 2002/ Accepted 15 May 2002

Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of the reverse transcriptase telomerase. In both tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. Genetic studies have led to the identification of DNA polymerases, cell cycle checkpoint proteins, and telomere binding proteins involved in the telomerase pathway. However, how these proteins affect telomere-telomere recombination has not been identified to date. Using an assay to trace the in vivo recombinational products throughout the course of survivor development, we show here that three major replicative polymerases, {alpha}, {delta}, and {varepsilon}, play roles in telomere-telomere recombination and that each causes different effects and phenotypes when they as well as the telomerase are defective. Polymerase {delta} appears to be the main activity for telomere extension, since neither type I nor type II survivors arising via telomere-telomere recombination were seen in its absence. The frequency of type I versus type II is altered in the polymerase {alpha} and {varepsilon} mutants relative to the wild type. Each prefers to develop a particular type of survivor. Moreover, type II recombination is mediated by the cell cycle checkpoint proteins Tel1 and Mec1, and telomere-telomere recombination is regulated by telomere binding protein Cdc13 and the Ku complex. Together, our results suggest that coordination between DNA replication machinery, DNA damage signaling, DNA recombination machinery, and the telomere protein-DNA complex allows telomere recombination to repair telomeric ends in the absence of telomerase.

* Corresponding author. Mailing address: Department of Microbiology, National Taiwan University College of Medicine, No. 1, Sec. 1, Jen-Ai Road, Taipei, 10018, Taiwan, ROC. Phone: (886) 2-2312-3456, ext. 8711. Fax: (886) 2-23915293. E-mail: scteng{at}ha.mc.ntu.edu.tw.

Molecular and Cellular Biology, August 2002, p. 5679-5687, Vol. 22, No. 16
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.16.5679-5687.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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