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Título

Nucleosome assembly and genome integrity

AutorPrado, Félix ; Clemente-Ruiz, Marta
Palabras claveGCRs
gross chromosomal rearrangements
H3K56ac
acetylated lysine 56 of histone H3
HU
hydroxyurea
DSB
double-strand break
MMS
methyl methanesulfonate
CPT
camptothecin
BIR
break-induced replication
FEN-1
flap endonuclease 1
Fecha de publicación1-mar-2012
EditorLandes Bioscience
CitaciónBioArchitecture 2(1): 6-10 (2012)
ResumenMaintaining the stability of the replication forks is one of the main tasks of the DNA damage response. Specifically, checkpoint mechanisms detect stressed forks and prevent their collapse. In the published report reviewed here we have shown that defective chromatin assembly in cells lacking either H3K56 acetylation or the chromatin assembly factors CAF1 and Rtt106 affects the integrity of advancing replication forks, despite the presence of functional checkpoints. This loss of replication intermediates is exacerbated in the absence of Rad52, suggesting that collapsed forks are rescued by homologous recombination and providing an explanation for the accumulation of recombinogenic DNA damage displayed by these mutants. These phenotypes mimic those obtained by a partial reduction in the pool of available histones and are consistent with a model in which defective histone deposition uncouples DNA synthesis and nucleosome assembly, thus making the fork more susceptible to collapse. Here, we review these findings and discuss the possibility that defects in the lagging strand represent a major source of fork instability in chromatin assembly mutants.
Versión del editorhttp://dx.doi.org/10.4161/bioa.19737
URIhttp://hdl.handle.net/10261/121684
DOI10.4161/bioa.19737
ISSN1949-0992
E-ISSN1949-100X
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