RT Journal Article
SR Electronic
T1 <em>YGR042W/MTE1</em> Functions in Double-Strand Break Repair with <em>MPH1</em>
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 032581
DO 10.1101/032581
A1 Askar Yimit
A1 TaeHyung Kim
A1 Ranjith P. Anand
A1 Sarah Meister
A1 Jiongwen Ou
A1 James E. Haber
A1 Zhaolei Zhang
A1 Grant W. Brown
YR 2015
UL http://biorxiv.org/content/early/2015/11/23/032581.abstract
AB Double-strand DNA breaks occur upon exposure of cells to agents such as ionizing radiation and ultraviolet light or indirectly through replication fork collapse at DNA damage sites. If left unrepaired double-strand breaks can cause genome instability and cell death. In response to DNA damage, proteins involved in double-strand break repair by homologous recombination re-localize into discrete nuclear foci. We identified 29 proteins that co-localize with the recombination repair protein Rad52 in response to DNA damage. Of particular interest, Ygr042w/Mte1, a protein of unknown function, showed robust colocalization with Rad52. Mte1 foci fail to form when the DNA helicase Mph1 is absent. Mte1 and Mph1 form a complex, and are recruited to double-strand breaks in vivo in a mutually dependent manner. Mte1 is important for resolution of Rad52 foci during double-strand break repair, and for suppressing break-induced replication. Together our data indicate that Mte1 functions with Mph1 in double-strand break repair.