PRJNA492503
Arabidopsis thaliana Uracil-DNA-Glycosylase mitochondrial mutation accumulation study
Substitution rates in plant mitochondrial genes are extremely low, indicating strong selective pressure as well as efficient repair. Plant mitochondria possess base excision repair pathways, however, many repair pathways such as nucleotide excision repair and mismatch repair appear to be absent. In the absence of specific pathways, many DNA lesions must be repaired by a different mechanism. To test the hypothesis that double-strand break repair (DSBR) is that mechanism, we assayed plants deficient in uracil-DNA-glycosylase (UNG) to determine the repair outcomes when that pathway is missing. In the absence of UNG, there is an increase in in double-strand breaks as assayed by recombination at repeated sequences. The resulting DSBR appears sufficient to prevent the fixation of SNPs in ung- lines and does not significantly alter the pattern of heteroplasmic SNP accumulation. These results indicate that double strand break repair is a general system of repair in plant mitochondria, and appears to be so efficient that base excision repair is nearly dispensable. The existence of this general system may explain the seemingly anomalous differences between genes and non-genes in plant mitochondria.