Inefficient Double-Strand DNA Break Repair is Associated with Increased Fasciation in Arabidopsis brca2 mutants

Abstract

Brca2 is a breast tumor susceptibility factor with functions in maintaining genome stability through ensuring efficient double-strand DNA break (DSB) repair via homologous recombination. To investigate the role of Arabidopsis BRCA2 genes in DNA repair in somatic cells, we identified and characterized transposon insertion mutants of the AtBRCA2a and AtBRCA2b genes. atbrca2a-1 and atbrca2b-1 single mutant, and atbrca2a-1/atbrca2b-1 double mutant showed hypersensitivity to genotoxic stresses compared to wild-type. Interestingly, approximately 13% of double mutant plants showed stem fasciation. In addition, the frequency of the fasciation phenotype in the double mutant increased by up to 46% following g-irradiation. Moreover, we established atbrca2 double mutant line carrying a CYCB1-GUS reporter construct. The GUS fusion gene was expressed in shoot and root apical meristems of the double mutant. These data suggest that inefficient DSB repair in the atbrca2 double mutant leads to disorganization of the programmed cell cycle of apical meristems.