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Arabidopsis thaliana MRE 11 is essential for activation of cell cycle arrest, transcriptional regulation and DNA repair upon the induction of double‐stranded DNA breaks
Author(s) -
Šamanić I.,
Cvitanić R.,
Simunić J.,
Puizina J.
Publication year - 2016
Publication title -
plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.871
H-Index - 87
eISSN - 1438-8677
pISSN - 1435-8603
DOI - 10.1111/plb.12453
Subject(s) - biology , microbiology and biotechnology , arabidopsis thaliana , dna , cell cycle , cell cycle checkpoint , genetics , cell , gene , mutant
Given the fundamental role of MRE 11 in many aspects of DNA metabolism and signalling in eukaryotes, we analysed the impact of several MRE 11 mutations on DNA damage response ( DDR ) and DNA repair in Arabidopsis thaliana . Three different atmre11 and an atatm‐2 mutant lines, together with the wild type ( WT ), were compared using a new Arabidopsis genotoxic assay for in situ evaluation of genome integrity and DNA damage repair efficiency after double strand break ( DSB ) induction. The results showed that, despite the phenotypic differences and different lengths of the putative truncated At MRE 11 proteins, all three atmre11 and the atatm‐2 mutant lines exhibited common hypersensitivity to bleomycin treatment, where they only slightly reduced mitotic activity, indicating a G2/M checkpoint abrogation. In contrast to the WT , which reduced the frequency of chromosomal aberrations throughout the recovery period after treatment, none of the three atmre11 and atatm‐2 mutants recovered. Moreover, atmre11‐3 mutants, similarly to atatm‐2 mutants, failed to transcriptionally induce several DDR genes and had altered expression of the CYCB 1;1:: GUS protein. Nevertheless, numerous chromosomal fusions in the atmre11 mutants, observed after DNA damage induction, suggest intensive DNA repair activity. These results indicate that functional and full‐length At MRE 11 is essential for activation of the cell cycle arrest, transcriptional regulation and DNA repair upon induction of DSB .