Sir3 heterochromatin protein promotes non‐homologous end joining by direct inhibition of Sae2 - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue EMBO Journal Année : 2021

Sir3 heterochromatin protein promotes non‐homologous end joining by direct inhibition of Sae2

Résumé

Heterochromatin is a conserved feature of eukaryotic chromosomes, with central roles in gene expression regulation and maintenance of genome stability. How heterochromatin proteins regulate DNA repair remains poorly described. In the yeast Saccharomyces cerevisiae, the silent information regulator (SIR) complex assembles heterochromatin‐like chromatin at sub‐telomeric chromosomal regions. SIR‐mediated repressive chromatin limits DNA double‐strand break (DSB) resection, thus protecting damaged chromosome ends during homologous recombination (HR). As resection initiation represents the crossroads between repair by non‐homologous end joining (NHEJ) or HR, we asked whether SIR‐mediated heterochromatin regulates NHEJ. We show that SIRs promote NHEJ through two pathways, one depending on repressive chromatin assembly, and the other relying on Sir3 in a manner that is independent of its heterochromatin‐promoting function. Via physical interaction with the Sae2 protein, Sir3 impairs Sae2‐dependent functions of the MRX (Mre11‐Rad50‐Xrs2) complex, thereby limiting Mre11‐mediated resection, delaying MRX removal from DSB ends, and promoting NHEJ.
Fichier principal
Vignette du fichier
2021.05.26.445723v2.full.pdf (19.73 Mo) Télécharger le fichier
Origine : Fichiers produits par l'(les) auteur(s)

Dates et versions

hal-04312115 , version 1 (19-01-2024)

Identifiants

Citer

Hélène Bordelet, Rafaël Costa, Clémentine Brocas, Jordane Dépagne, Xavier Veaute, et al.. Sir3 heterochromatin protein promotes non‐homologous end joining by direct inhibition of Sae2. EMBO Journal, 2021, 41, pp.e108813. ⟨10.15252/embj.2021108813⟩. ⟨hal-04312115⟩
48 Consultations
1 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More