A new varietal of DNA interstrand crosslink repair
Knipscheer, Patel, and colleagues have identified a new mechanism that repairs alcohol-induced DNA interstrand crosslinks with a minimum of collateral DNA damage.Our cells are under constant assault by endogenous and exogenous agents that damage DNA and thereby threaten genome integrity.One of the most pernicious forms of damage is a DNA interstrand crosslink (ICL), which covalently crosslinks the two strands of the double helix.ICLs block DNA replication and transcription, and in the absence of repair, a single ICL can kill a eukaryotic cell.Given their toxicity, ICL-inducing agents are widely used in cancer chemotherapy, as exemplified by cisplatin and nitrogen mustard.Importantly, the most essential cellular pathways of ICL repair are coupled to DNA replication, most likely because failure to resolve ICLs during this phase of the cell cycle causes lethality due to a failure to complete genome duplication.Until recently, only two mechanisms of S phase ICL repair were known, both of which involve DNA intermediates that could cause gross chromosomal rearrangements (GCRs).Now, a third pathway has been discovered that repairs alcohol-induced, endogenous ICLs without the possibility of major concomitant DNA damage.
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2020-08-05（万方平台首次上网日期，不代表论文的发表时间）
共2页
459-460
