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Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.

ABSTRACT: Interstrand crosslinks (ICLs) are a highly toxic form of DNA damage. ICLs can interfere with vital biological processes requiring separation of the two DNA strands, such as replication and transcription. If ICLs are left unrepaired, it can lead to mutations, chromosome breakage and mitotic catastrophe. The Fanconi anemia (FA) pathway can repair this type of DNA lesion, ensuring genomic stability. In this review, we will provide an overview of the cellular response to ICLs. First, we will discuss the origin of ICLs, comparing various endogenous and exogenous sources. Second, we will describe FA proteins as well as FA-related proteins involved in ICL repair, and the post-translational modifications that regulate these proteins. Finally, we will review the process of how ICLs are repaired by both replication-dependent and replication-independent mechanisms.

SUBMITTER: Lopez-Martinez D

PROVIDER: S-EPMC4951507 | biostudies-literature | 2016 Aug

REPOSITORIES: biostudies-literature

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Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.

Lopez-Martinez David D Liang Chih-Chao CC Cohn Martin A MA

Cellular and molecular life sciences : CMLS 20160419 16

Interstrand crosslinks (ICLs) are a highly toxic form of DNA damage. ICLs can interfere with vital biological processes requiring separation of the two DNA strands, such as replication and transcription. If ICLs are left unrepaired, it can lead to mutations, chromosome breakage and mitotic catastrophe. The Fanconi anemia (FA) pathway can repair this type of DNA lesion, ensuring genomic stability. In this review, we will provide an overview of the cellular response to ICLs. First, we will discuss ...[more]

PMID: 27094386

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Project description:Abstract is in manuscript file

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SCAI promotes error-free repair of DNA interstrand crosslinks via the Fanconi anemia pathway.

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