BLM helicase stimulates the ATPase and chromatin-remodeling activities of RAD54.

ABSTRACT: Mutation of BLM helicase results in the autosomal recessive disorder Bloom syndrome (BS). Patients with BS exhibit hyper-recombination and are prone to almost all forms of cancer. BLM can exhibit its anti-recombinogenic function either by dissolution of double Holliday junctions or by disruption of RAD51 nucleofilaments. We have now found that BLM can interact with the pro-recombinogenic protein RAD54 through an internal ten-residue polypeptide stretch in the N-terminal region of the helicase. The N-terminal region of BLM prevented the formation of RAD51-RAD54 complex, both in vitro and in vivo. Using the fluorescence recovery after photobleaching (FRAP) technique, we found that RAD54 and BLM rapidly and concurrently, yet transiently, bound to the chromatinized foci. Presence of BLM enhanc

SUBMITTER: Srivastava V 

PROVIDER: S-EPMC2729260 | biostudies-literature | 2009 Sep

REPOSITORIES: biostudies-literature