Abstract

DNA double strand break (DSB) is a kind of highly toxic damage, causing genomic instability, chromatin aberration and cancer. A number of conserved DSB damage repair pathways have been found in eukaryotes, most notably classical non-homologous end joining (cNHEJ) and homologous recombination (HR). These two repair pathways resolve most DSBs in cells. For different types of DSBs, cells could wittily choose the optimal approach with the lowest risk for genomic instability. Relying on the developing cell imaging techniques and molecular biological methods, sophisticated mechanism of DSB repair pathway choice has been revealed. The regulation mechanism of pathway choice is complex and precise. In this review, the effect factors such as the structures of the broken terminals, the degree of DNA end resection, cell cycle, chromatin environment, histone modification and RNA metabolism on the DSB repair pathway choice are discussed, showing the diversity and flexibility of DSB repair pathway choice.

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