PT  - JOURNAL ARTICLE
AU  - Lai, Xianning
AU  - Heierhorst, Jörg
TI  - Suppression of Chromosome Healing and Anticheckpoint Pathways in Yeast Postsenescence Survivors
AID  - 10.1534/genetics.113.150813
DP  - 2013 Jun 01
TA  - Genetics
PG  - 403--408
VI  - 194
IP  - 2
4099  - http://www.genetics.org/content/194/2/403.short
4100  - http://www.genetics.org/content/194/2/403.full
SO  - Genetics2013 Jun 01; 194
AB  - 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.