Regions of genomic DNA containing repetitive nucleotide sequences can adopt a number of different structures in addition to the canonical B-DNA form: many of these non-B DNA structures are causative factors in genetic instability and human disease. Although chromosomal DNA replication through such repetitive sequences has been considered a major cause of non-B form DNA structure-induced genetic instability, it is also observed in non-proliferative tissues. In this review, we discuss putative mechanisms responsible for the mutagenesis induced by non-B DNA structures in the absence of chromosomal DNA replication.
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Wang et al. (2009) studied this question.
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