Abstract
Heterochromatin maintains genomic stability by inhibiting aberrant recombination. DNA lesions, however, still occur at heterochromatic loci. Therefore, a cell must have ways to circumvent heterochromatin structure during repair of DNA damage. Prior work by our lab identified a role for the chromatin remodeling enzyme SWI/SNF in heterochromatic DNA repair. Here, we present biochemical studies that suggest two distinct mechanisms by which SWI/SNF remodels heterochromatin in an ATP‐dependent manner. The first remodeling mechanism uses a unique physical interaction, between the BAH domain of Sir3p and the ATPase domain of the SWI/SNF catalytic subunit Swi2p, to evict Sir3p from nucleosomal arrays. The second remodeling mechanism occurs between SWI/SNF complex and Sir2/3/4 complex; this reaction results in the eviction of both the histone octamer and bound Sir proteins. These findings establish SWI/SNF complex as a unique regulator of heterochromatin structure.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
