ABSTRACT
The mitochondria of flowering plants have large and complex genomes whose structure and segregation are modulated by recombination activities. Among unresolved questions is what are the pathways responsible for the late steps of homologous recombination: while the loss of mitochondrial recombination is not viable, a deficiency in RECG1-dependent branch migration has little impact on plant development. Here we present an additional pathway required for the processing of organellar recombination intermediates, the one depending on RADA. RADA is similar in structure and activity to bacterial RadA/Sms, and in vitro it binds to ssDNA and accelerates strand-exchange reactions initiated by RecA. RADA-deficient plants are severely impacted in their development and fertility, correlating with increased mtDNA ectopic recombination and replication of recombination-generated subgenomes. The radA mutation is epistatic to recG1, indicating that RADA drives the main branch migration pathway of plant mitochondria. In contrast, the double mutation radA recA3 is lethal, revealing the importance of an alternative RECA3-dependent pathway. Interestingly, the radA developmental phenotypes could not be correlated with obvious defects in mitochondrial gene expression. Rather, it seems that it is the activation of genes that repress cell cycle progression that is partially the cause of the stunted growth of radA mutants.
SYNOPSIS Arabidopsis RADA is a main branch migration activity in plant mitochondria, whose deficiency leads to mtDNA instability by recombination, and suppression of plant growth by the activation of repressors of cell cycle progression.