Stabilization of Reversed Replication Forks by Telomerase Drives Telomere Catastrophe.
Margalef, Pol; Kotsantis, Panagiotis; Borel, Valerie; Bellelli, Roberto; Panier, Stephanie; Boulton, Simon J.
; 172(3): 439-453.e14, 2018 01 25.
Artigo em Inglês | MEDLINE | ID: mdl-29290468
A Distinct Class of Genome Rearrangements Driven by Heterologous Recombination.
Sgs1 helicase and two nucleases Dna2 and Exo1 resect DNA double-strand break ends.
The RAD6 DNA damage tolerance pathway operates uncoupled from the replication fork and is functional beyond S phase.
Top3-Rmi1 dissolve Rad51-mediated D loops by a topoisomerase-based mechanism.
The <i>Saccharomyces cerevisiae</i> Hrq1 and Pif1 DNA helicases synergistically modulate telomerase activity <i>in vitro</i>.
BLM prevents instability of structure-forming DNA sequences at common fragile sites.
BOD1L Is Required to Suppress Deleterious Resection of Stressed Replication Forks.
The motor activity of DNA2 functions as an ssDNA translocase to promote DNA end resection.
HELB Is a Feedback Inhibitor of DNA End Resection.
The 9-1-1 checkpoint clamp stimulates DNA resection by Dna2-Sgs1 and Exo1.