Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes.

Autor: Rogers CM; Molecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA., Simmons Iii RH; Molecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA., Fluhler Thornburg GE; Molecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA., Buehler NJ; Molecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA., Bochman ML; Molecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA. Electronic address: bochman@indiana.edu.
Jazyk: angličtina
Zdroj: Progress in biophysics and molecular biology [Prog Biophys Mol Biol] 2020 Dec; Vol. 158, pp. 33-46. Date of Electronic Publication: 2020 Aug 30.
DOI: 10.1016/j.pbiomolbio.2020.08.005
Abstrakt: DNA inter-strand crosslinks (ICLs) are dangerous lesions that can be caused by a variety of endogenous and exogenous bifunctional compounds. Because covalently linking both strands of the double helix locally disrupts DNA replication and transcription, failure to remove even a single ICL can be fatal to the cell. Thus, multiple ICL repair pathways have evolved, with the best studied being the canonical Fanconi anemia (FA) pathway. However, recent research demonstrates that different types of ICLs (e.g., backbone distorting vs. non-distorting) can be discriminated by the cell, which then mounts a specific repair response using the FA pathway or one of a variety of FA-independent ICL repair pathways. This review focuses on the latter, covering current work on the transcription-coupled, base excision, acetaldehyde-induced, and SNM1A/RecQ4 ICL repair pathways and highlighting unanswered questions in the field. Answering these questions will provide mechanistic insight into the various pathways of ICL repair and enable ICL-inducing agents to be more effectively used as chemotherapeutics.
(Copyright © 2020 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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