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XB-ART-52578
Cell 2016 Oct 06;1672:498-511.e14. doi: 10.1016/j.cell.2016.09.008.
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Replication-Dependent Unhooking of DNA Interstrand Cross-Links by the NEIL3 Glycosylase.

Semlow DR , Zhang J , Budzowska M , Drohat AC , Walter JC .


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During eukaryotic DNA interstrand cross-link (ICL) repair, cross-links are resolved ("unhooked") by nucleolytic incisions surrounding the lesion. In vertebrates, ICL repair is triggered when replication forks collide with the lesion, leading to FANCI-FANCD2-dependent unhooking and formation of a double-strand break (DSB) intermediate. Using Xenopus egg extracts, we describe here a replication-coupled ICL repair pathway that does not require incisions or FANCI-FANCD2. Instead, the ICL is unhooked when one of the two N-glycosyl bonds forming the cross-link is cleaved by the DNA glycosylase NEIL3. Cleavage by NEIL3 is the primary unhooking mechanism for psoralen and abasic site ICLs. When N-glycosyl bond cleavage is prevented, unhooking occurs via FANCI-FANCD2-dependent incisions. In summary, we identify an incision-independent unhooking mechanism that avoids DSB formation and represents the preferred pathway of ICL repair in a vertebrate cell-free system.

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Species referenced: Xenopus laevis
Genes referenced: fancd2 fanci neil3

References [+] :
Alt, Bypass of DNA lesions generated during anticancer treatment with cisplatin by DNA polymerase eta. 2007, Pubmed