title: How to restore chromatin structure and function in response to DNA damage--let the chaperones play: delivered on 9 July 2013 at the 38th FEBS Congress in St Petersburg, Russia.
abstract: Histone deposition onto DNA assisted by specific chaperones forms the chromatin basic unit and serves to package the genome within the cell nucleus. The resulting chromatin organization, often referred to as the epigenome, contributes to a unique transcriptional program that defines cell identity. Importantly, during cellular life, substantial alterations in chromatin structure may arise due to cell stress, including DNA damage, which not only challenges the integrity of the genome but also threatens the epigenome. Considerable efforts have been made to decipher chromatin dynamics in response to genotoxic stress, and to assess how it affects both genome and epigenome stability. Here, we review recent advances in understanding the mechanisms of DNA damage-induced chromatin plasticity in mammalian cells. We focus specifically on the dynamics of histone H3 variants in response to UV irradiation, and highlight the role of their dedicated chaperones in restoring both chromatin structure and function. Finally, we discuss how, in addition to restoring chromatin integrity, the cellular networks that signal and repair DNA damage may also provide a window of opportunity for modulating the information conveyed by chromatin.
authors.affiliation: Institut Curie, Centre de Recherche, Paris, France; Centre National de la Recherche Scientifique, UMR3664, Paris, France; Equipe Labellisée Ligue Contre le Cancer, Paris, France; Institut de Formation Doctorale, University Pierre & Marie Curie, Paris, France; Sorbonne University, PSL*, Paris, France; Epigenetics and Cell Fate Centre, UMR7216, Centre National de la Recherche Scientifique/Paris Diderot University, Paris, France.
authors.forename: Salomé
authors.initials: S
authors.lastname: Adam
authors.forename: Sophie E
authors.initials: SE
authors.lastname: Polo
authors.forename: Geneviève
authors.initials: G
authors.lastname: Almouzni
mesh_terms: D018797:Cell Cycle Proteins / Q000378:metabolism; D002843:Chromatin / Q000235:genetics* / Q000378:metabolism* / Q000528:radiation effects; D056504:Chromatin Assembly Factor-1 / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D044127:Epigenesis, Genetic; D042822:Genomic Instability; D056488:Histone Chaperones / Q000378:metabolism; D006657:Histones / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects; D006801:Humans; D018832:Molecular Chaperones / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism; D014158:Transcription, Genetic; D014466:Ultraviolet Rays / Q000009:adverse effects
chemical_list: C489780:CNOT8 protein, human; D018797:Cell Cycle Proteins; D002843:Chromatin; D056504:Chromatin Assembly Factor-1; C086057:HIRA protein, human; D056488:Histone Chaperones; D006657:Histones; D018832:Molecular Chaperones; D014157:Transcription Factors
keywords: CAF-1; DNA damage; DNA repair; H3.1; H3.3; HIRA; UV irradiation; chromatin assembly; histone chaperones; histone variants