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. 2014 Dec 22;207(6):717–733. doi: 10.1083/jcb.201405077

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© 2014 Klement et al.

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Figure 10. — Model for heterochromatin nucleosome relaxation and Artemis-dependent DSB repair. (1) Artemis-dependent DSB repair stalls within the KAP-1– and CHD3.1-rich heterochromatin of nondividing cells. (2) During DNA replication, the heterochromatic superstructure is perturbed, and newly synthesized strands remain in an open configuration, bypassing the need for additional chromatin relaxation during repair of DSBs incurred during S phase. (3) ATM protein kinase activity triggers two signaling axes. The first (3A) enables the dispersal of class II CHD chromatin remodeling activity (CHD3.1) via the IRIF mediator proteins (such as 53BP1) and densely localized pKAP-1. The other (3B) promotes the gain of ISWI-class chromatin remodeling activity via RNF20-RNF40 activation and the recruitment/activation of ACF1–SNF2H, which we propose occupies PHD finger binding sites vacated by CHD3.1. (4) These mechanisms converge to enable heterochromatin relaxation, which is favorable for the repair of DSBs via Artemis. P, phosphorylation.