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首页> 外文期刊>Cell Reports >Two Distinct Pathways Support Gene Correction by Single-Stranded Donors at DNA Nicks
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Two Distinct Pathways Support Gene Correction by Single-Stranded Donors at DNA Nicks

机译：DNA尼克斯的两条不同途径支持单链供体的基因校正

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Nicks are the most common form of DNA damage. The mechanisms of their repair are fundamental to genomic stability and of practical importance for genome engineering. We define two pathways that support homology-directed repair by single-stranded DNA donors. One depends upon annealing-driven strand synthesis and acts at both nicks and double-strand breaks. The other depends upon annealing-driven heteroduplex correction and acts at nicks. Homology-directed repair via these pathways, as well as mutagenic end joining, are inhibited by RAD51 at nicks but largely independent of RAD51 at double-strand breaks. Guidelines for coordinated design of targets and donors for gene correction emerge from definition of these pathways. This analysis further suggests that naturally occurring nicks may have significant recombinogenic and mutagenic potential that is normally inhibited by RAD51 loading onto DNA, thereby identifying a function for RAD51 in maintenance of genomic stability.
机译：缺损是最常见的DNA损伤形式。它们的修复机制是基因组稳定性的基础，对基因组工程具有实际意义。我们定义了两种途径，支持单链DNA供体的同源性定向修复。一种取决于退火驱动的链合成，并且在缺口和双链断裂处起作用。另一个依赖于退火驱动的异质双相校正，并在刻痕处起作用。通过这些途径进行的由同源性指导的修复以及诱变的末端连接，在切口处被RAD51抑制，但在双链断裂时很大程度上独立于RAD51。从这些途径的定义中出现了针对基因校正的靶标和供体的协调设计指南。该分析进一步表明，天然存在的切口可能具有显着的重组和诱变潜力，通常可通过RAD51加载到DNA上来抑制，从而确定RAD51在维持基因组稳定性方面的功能。

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