1. DNA Mismatch Repair: Dr. Jekyll and Mr. Hyde?
Peggy Hsieh 
Molecular Cell 
Volume 47, Issue 5, Pages (September 2012)
DOI: /j.molcel
Copyright © 2012 Elsevier Inc. Terms and Conditions

2. Figure 1 Mutagenic and Nonmutagenic Outcomes of DNA Mismatch Repair
(A) General scheme for replication-linked MMR in which recognition of a mismatch by a MutSα-MutLα complex modulated by interaction with PCNA and ATP/ADP binding by MMR proteins licenses excision of the newly synthesized strand by EXO1 and an endonuclease function in the PMS2 subunit of MutLα. The resulting RPA-coated single-strand gap is a substrate for resynthesis by high-fidelity Pol-δ.
(B) In activated B cells, AID creates G/U mispairs that are substrates for MutSα-MutLα. An ncMMR pathway is utilized in which mUbPCNA recruits Pol-η to carry out error-prone gap filling to achieve somatic hypermutation at variable regions of Ig genes.
(C) A scenario for a ncMMR pathway operating in nonlymphoid cells that responds to a variety of DNA lesions that are substrates for MutSα including uracil, alkylated bases, and distorted DNA structures that impede replication. Recruitment of Pol-η by monoubiquitinated PCNA leads to error-prone gap filling.
Molecular Cell  , DOI: ( /j.molcel )
Copyright © 2012 Elsevier Inc. Terms and Conditions