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Chromatin dynamics mediated by histone modifiers and histone chaperones in postreplicative recombination
Author(s) -
Endo Hirohito,
Kawashima Satoshi,
Sato Lui,
Lai Mong Sing,
Enomoto Takemi,
Seki Masayuki,
Horikoshi Masami
Publication year - 2010
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2010.01435.x
Subject(s) - biology , histone methyltransferase , histone h2a , histone code , histone methylation , histone , histone h1 , chromatin , genetics , histone h3 , microbiology and biotechnology , dna , nucleosome , dna methylation , gene expression , gene
Eukaryotic chromatin is regulated by chromatin factors such as histone modification enzymes, chromatin remodeling complexes and histone chaperones in a variety of DNA‐dependent reactions. Among these reactions, transcription in the chromatin context is well studied. On the other hand, how other DNA‐dependent reactions, including postreplicative homologous recombination, are regulated in the chromatin context remains elusive. Here, histone H3 Lys56 acetylation, mediated by the histone acetyltransferase Rtt109 and the histone chaperone Cia1/Asf1, is shown to be required for postreplicative sister chromatid recombination. This recombination did not occur in the cia1/asf1‐V94R mutant, which lacks histone binding and histone chaperone activities and which cannot promote the histone acetyltransferase activity of Rtt109. A defect in another histone chaperone, CAF‐1, led to an increase in acetylated H3‐K56 (H3‐K56‐Ac)‐dependent postreplicative recombination. Some DNA lesions recognized by the putative ubiquitin ligase complex Rtt101‐Mms1‐Mms22, which is reported to act downstream of the H3‐K56‐Ac signaling pathway, seem to be increased in CAF‐1 defective cells. Taken together, these data provide the framework for a postreplicative recombination mechanism controlled by histone modifiers and histone chaperones in multiple ways.