[摘要]：Different DNA repair systems are known to cooperate to deal with DNA damage. However, the regulatory role of the cross-talk between these pathways is unclear. Here, we have shown that MutL, an essential component of mismatch repair, is a RecA-interacting protein, and that its highly conserved N-terminal domain is sufficient for this interaction. Surface plasmon resonance and capillary electrophoresis analyses revealed that MutL has little effect on RecA-ssDNA filament formation, but dose down-regulate the ATPase activity of RecA. Our findings identify a new role for MutL, and suggest its regulatory role in homologous recombination. (C) 2011 Published by Elsevier Inc.
