N-methylpurines are heterogeneously repaired in human mitochondria but not evidently repaired in yeast mitochondria.

摘要: Base excision repair (BER) of dimethyl sulfate induced N-methylpurines (NMPs) was measured at nucleotide resolution in the mitochondrial DNA (mtDNA) cultured human and yeast (Saccharomyces cerevisiae) cells. NMPs were repaired with heterogeneous rates mtDNA. The nearest-neighbor nucleotides significantly affected rates: between pyrimidines much faster than those purines, a purine pyrimidine intermediate rates. Repair intermediates can also be detected certain sites mtDNA, indicating an ineffectiveness processing these by BER machinery. In contrast to mtDNA did not show detectable any sites. Furthermore, high level spontaneous strand breaks exists exclusively Spontaneous or oxidative lesions unlikely major causes for breaks. Rather, depurination combined inefficient nicks single-nucleotide gaps machinery may result Our results unveil striking difference mitochondria.