A Histone-Fold Complex and FANCM Form a Conserved DNA-Remodeling Complex to Maintain Genome Stability

作者：Yan Zhijiang; Delannoy Mathieu; Ling Chen; Daee Danielle; Osman Fekret; Muniandy Parameswary A; Shen Xi; Oostra Anneke B; Du Hansen; Steltenpool Jurgen; Lin Ti; Schuster Beatrice; Decaillet Chantal; Stasiak Andrzej; Stasiak Alicja Z; Stone Stacie; Hoatlin Maureen E; Schindler Detlev; Woodcock Christopher L; Joenje Hans; Sen Ranjan; de Winter Johan P; Li Lei; Seidman Michael M; Whitby Matthew C; Myung Kyungjae; Constantinou Angelos^*; Wang Weidong

来源：Molecular Cell, 2010, 37(6): 865-878.

DOI：10.1016/j.molcel.2010.01.039

FANCM remodels branched DNA structures and plays essential roles in the cellular response to DNA replication stress. Here, we show that FANCM forms a conserved DNA-remodeling complex with a histone-fold heterodimer, MHF. We find that MHF stimulates DNA binding and replication fork remodeling by FANCM. In the cell, FANCM and MHF are rapidly recruited to forks stalled by DNA interstrand crosslinks, and both are required for cellular resistance to such lesions. In vertebrates, FANCM-MHF associates with the Fanconi anemia (FA) core complex, promotes FANCD2 monoubiquitination in response to DNA damage, and suppresses sister-chromatid exchanges. Yeast orthologs of these proteins function together to resist MMS-induced DNA damage and promote gene conversion at blocked replication forks. Thus, FANCM-MHF is an essential DNA-remodeling complex that protects replication forks from yeast to human.

• 出版日期2010-3-26