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MHF 1 plays F anconi anaemia complementation group M protein ( FANCM )‐dependent and FANCM ‐independent roles in DNA repair and homologous recombination in plants
Author(s) -
Dangel Natalie J.,
Knoll Alexander,
Puchta Holger
Publication year - 2014
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12507
Subject(s) - complementation , chemistry , biochemistry , phenotype , gene
Summary Fanconi anaemia complementation group M protein ( FANCM ), a component of the human F anconi anemia pathway, acts as DNA translocase that is essential during the repair of DNA interstrand cross‐links. The DNA ‐damage‐binding function of FANCM is strongly enhanced by the histone fold‐containing FANCM ‐associated protein MHF 1. We identified a single homologue of MHF 1 in the genome of A rabidopsis thaliana . Similar to the loss of A t FANCM , the loss of A t MHF 1 leads to several meiotic defects, such as chromosome bridges between bivalents and an unequal distribution of chromosomes. Moreover, MHF 1, together with FANCM , is involved in interstrand cross‐link repair in plants. This phenotype is detectable only in double mutants of the R ec Q helicase and BLM homologue RECQ 4 A , which appears to function in a parallel pathway to the FANCM / MHF 1 complex. However, in somatic cells, FANCM has an MHF 1‐independent function in replicative repair in a parallel pathway to the endonuclease MUS 81. Furthermore, MHF 1 is required for efficient somatic homologous recombination ( HR ) – a role antagonistic to FANCM . FANCM and RECQ 4A define two parallel pathways of HR suppression in Arabidopsis. Hyperrecombination in the fancm but not the recq4A mutant can be abolished by MHF 1 mutations. This finding indicates that MHF 1 and FANCM act at different steps of a single, common, HR pathway.