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. Author manuscript; available in PMC: 2014 Feb 21.
Published in final edited form as: Mol Cell. 2012 Dec 27;49(4):657–667. doi: 10.1016/j.molcel.2012.11.020

Figure 5.

Figure 5

Model for resection of neat DSBs in LSS and HSS. In LSS, resection can be initiated by Exo1, in an ATM-independent manner (a), or by CtIP-MRN in an ATM-dependent manner (b). In HSS, Exo1 is not active and resection is initiated by CtIP-MRN in an ATM-dependent manner (b). Initiation by either pathway allows clipping of DSBs to provide sufficient RPA-ssDNA to locally activate ATR (c). ATR then phosphorylates CtIP on T818, which is essential for stable CtIP chromatin-binding, and downstream extension of resection tracts by a DNA2-dependent mechanism.