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Genetics. 2013 Jun;194(2):403-8. doi: 10.1534/genetics.113.150813. Epub 2013 Mar 27.

Suppression of chromosome healing and anticheckpoint pathways in yeast postsenescence survivors.

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  • 1St. Vincent's Institute of Medical Research, Fitzroy, Victoria 3065, Australia.

Abstract

Telomere repeat-like sequences at DNA double-strand breaks (DSBs) inhibit DNA damage signaling and serve as seeds to convert DSBs to new telomeres in mutagenic chromosome healing pathways. We find here that the response to seed-containing DSBs differs fundamentally between budding yeast (Saccharomyces cerevisiae) cells that maintain their telomeres via telomerase and so-called postsenescence survivors that use recombination-based alternative lengthening of telomere (ALT) mechanisms. Whereas telomere seeds are efficiently elongated by telomerase, they remain remarkably stable without de novo telomerization or extensive end resection in telomerase-deficient (est2Δ, tlc1Δ) postsenescence survivors. This telomere seed hyper-stability in ALT cells is associated with, but not caused by, prolonged DNA damage checkpoint activity (RAD9, RAD53) compared to telomerase-positive cells or presenescent telomerase-negative cells. The results indicate that both chromosome healing and anticheckpoint activity of telomere seeds are suppressed in yeast models of ALT pathways.

KEYWORDS:

ALT; Est2; Rad53; Rad9; TLC1

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