Abstract
BackgroundThe RAD21 cohesin plays, besides its well-recognised role in chromatid cohesion, a role in DNA double strand break (dsb) repair. In Arabidopsis there are three RAD21 paralog genes (AtRAD21.1, AtRAD21.2 and AtRAD21.3), yet only AtRAD21.1 has been shown to be required for DNA dsb damage repair. Further investigation of the role of cohesins in DNA dsb repair was carried out and is here reported.ResultsWe show for the first time that not only AtRAD21.1 but also AtRAD21.3 play a role in somatic DNA dsb repair. Comet data shows that the lack of either cohesins induces a similar high basal level of DNA dsb in the nuclei and a slower DNA dsb repair kinetics in both cohesin mutants. The observed AtRAD21.3 transcriptional response to DNA dsb induction reinforces further the role of this cohesin in DNA dsb repair. The importance of AtRAD21.3 in DNA dsb damage repair, after exposure to DNA dsb damage inducing agents, is notorious and recognisably evident at the phenotypical level, particularly when the AtRAD21.1 gene is also disrupted.Data on the kinetics of DNA dsb damage repair and DNA damage sensitivity assays, of single and double atrad21 mutants, as well as the transcription dynamics of the AtRAD21 cohesins over a period of 48 hours after the induction of DNA dsb damage is also shown.ConclusionsOur data demonstrates that both Arabidopsis cohesin (AtRAD21.1 and AtRAD21.3) play a role in somatic DNA dsb repair. Furthermore, the phenotypical data from the atrad21.1 atrad21.3 double mutant indicates that these two cohesins function synergistically in DNA dsb repair. The implications of this data are discussed.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-014-0353-9) contains supplementary material, which is available to authorized users.
Highlights
The RAD21 cohesin plays, besides its well-recognised role in chromatid cohesion, a role in DNA double strand break repair
To establish that the described phenotype is caused by the atrad21.1 mutation alone, and not derived from chromosomal rearrangement or the disruption of another gene not physically linked to the T-DNA insertion [38], atrad21.1 mutant plants were transformed with the complementation construct
AtRAD21.3, in association with AtRAD21.1, confers resistance to ionising radiation-induced damage Because quantitative real-time PCR (qRT-PCR) data shows that the induction of DNA dsb induces the doubling of the AtRAD21.3 steady-state transcript content, we investigated further if AtRAD21.3 does play a role in DNA dsb repair
Summary
The RAD21 cohesin plays, besides its well-recognised role in chromatid cohesion, a role in DNA double strand break (dsb) repair. Sister chromatid cohesion is established de novo during the G2/M diploid phases when DNA dsb are formed [5,7]. This de novo cohesion induced by DNA dsb occurs in budding yeast. DNA dsb can be repaired via different DNA repair pathways such as the error-free homologous recombination (HR) pathway, which requires a homologous DNA strand template for repair, or via other alternative DNA dsb repair pathways that do not require a homologous template. Mutations that affect either HR or C-NHEJ have been reported to cause loss of viability, or developmental delay, in seedlings germinated from imbibed mutants seeds of Arabidopsis thaliana ( Arabidopsis) and maize exposed to DNA dsb damage inducing agents [13,14,15,16]
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