Functional Interactions of Human Rad54 with the Rad51 Recombinase
Abstract
Unrepaired or incorrectly repaired double strand breaks (DSBs) produced by ionizing radiation, exogenous DNA damaging chemicals, free oxygen radicals or programmed cellular mechanisms, can lead to deletions or mutations in the coding sequence of a gene, translocations, inversions, chromosome loss during or cell death. Accurate repair of DSBs is performed by a group of highly conserved genes termed the RAD54 epistatis group consisting of RAD51, RAD52, RAD54, RAD55, RAD57, RAD59, and RDH54/TIDl. A key intermediate in recombinational repair involves single-strands of the broken DNA invading and displacing DNA from an intact homologous duplex joint forming a heteroduplex DNA joint to be utilized as a template to replace lost or damaged DNA. In mammals, human genes central to homologous recombination interact with and their biochemical efficiency is governed by the tumor suppressors BRCA1 and BRCA2 indicating a role of recombinational repair in the suppression of cancer formation. The human Rad51 recombinase protein DNA pairing and strand exchange yielding heteroduplex DNA joints between ssDNA and dsDNA. Our biochemical studies address the manner in which hRad54 and hRad5l functionally interact to promote hRad5l-mediated D-loop formation and hRad54 catalyzed DNA supercoiling and transient DNA strand opening.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 2002
- Accession Number
- ADA407443
Entities
People
- Stephen J. Van Komen
Organizations
- University of Texas Health Science Center at San Antonio