hBRCA1 and hBARD1 are tumor suppressor proteins that are involved as heterodimer via ubiquitinylation in many cellular processes, such as DNA repair. Loss of BRCA1 or BARD1 results in early embryonic lethality and chromosomal instability. The Arabidopsis genome carries a BRCA1 homologue, and we were able to identify a BARD1 homologue. AtBRCA1 and the putative AtBARD1 protein are able to interact with each other as indicated by in vitro and in planta experiments. We have identified T-DNA insertion mutants for both genes, which show no visible phenotype under standard growth conditions and are fully fertile. Thus, in contrast to animals, both genes have no indispensable role during development and meiosis in plants. The two single as well as the double mutant are to a similar extent sensitive to mitomycin C, indicating an epistatic interaction in DNA crosslink repair. We could further demonstrate that in Arabidopsis BARD1 plays a prominent role in the regulation of homologous DNA repair in somatic cells.

BRCA1 is a well-known tumor suppressor protein in mammals, involved in multiple cellular processes such as DNA repair, chromosome segregation and chromatin remodeling. Interestingly, homologs of BRCA1 and several of its complex partners are also found in plants. As the respective mutants are viable, in contrast to mammalian mutants, detailed analyses of their biological role is possible. Here we demonstrate that the model plant Arabidopsis thaliana harbors two homologs of the mammalian BRCA1 interaction partner BRCC36, AtBRCC36A and AtBRCC36B. Mutants of both genes as well as the double mutants are fully fertile and show no defects in development. We were able to show that mutation of one of the homologs, AtBRCC36A, leads to a severe defect in intra- and interchromosomal homologous recombination (HR). A HR defect is also apparent in Atbrca1 mutants. As the Atbrcc36a/Atbrca1 double mutant behaves like the single mutants of AtBRCA1 and AtBRCC36A both proteins seem to be involved in a common pathway in the regulation of HR. AtBRCC36 is also epistatic to AtBRCA1 in DNA crosslink repair. Upon genotoxic stress, AtBRCC36A is transferred into the nucleus.

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