Author: ["Ruben C. Petreaca","Huan-Chih Chiu","Holly A. Eckelhoefer","Charles Chuang","Ling Xu","Constance I. Nugent"]
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Abstract
Genome stability necessitates a mechanism to protect the termini of linear chromosomes from inappropriate degradation or recombination1,2. In many species this protection depends on 'capping' proteins that bind telomeric DNA3,4. The budding yeast Cdc13p binds single-stranded telomeric sequences5,6, prevents lethal degradation of chromosome ends7,8 and regulates telomere extension by telomerase5,9. Two Cdc13-interacting proteins, Stn1p and Ten1p, are also required for viability and telomere length regulation10,11. It has been proposed that Cdc13p DNA binding directs a Cdc13p–Stn1p–Ten1p complex to telomeres to mediate end protection12. However, the functional significance of these protein interactions, and their respective roles in maintaining telomere integrity, remain undefined. Here, we show that co-overexpressing TEN1 with a truncated form of STN1 efficiently bypasses the essential role of CDC13. We further show that this truncated Stn1p binds directly to Pol12p, a polymerase α-primase regulatory subunit, and that Pol12 activity is required for CDC13 bypass. Thus, Stn1p and Ten1p control a Cdc13p-independent telomere capping mechanism that is coupled to the conventional DNA replication machinery.Cite this article
Petreaca, R., Chiu, HC., Eckelhoefer, H. et al. Chromosome end protection plasticity revealed by Stn1p and Ten1p bypass of Cdc13p. Nat Cell Biol 8, 748–755 (2006). https://doi.org/10.1038/ncb1430 