DNA Damage Bypass

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Competition, collaboration and coordination--determining how cells bypass DNA damage.

Cells must overcome replication blocks that might otherwise lead to genomic instability or cell death. Classical genetic experiments have identified a series of mechanisms that cells use to replicate damaged DNA: translesion synthesis, template switching and homologous recombination. In translesion synthesis, DNA lesions are replicated directly by specialised DNA polymerases, a potentially erro...

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Monoubiquitylation of histone H2B contributes to the bypass of DNA damage during and after DNA replication.

DNA lesion bypass is mediated by DNA damage tolerance (DDT) pathways and homologous recombination (HR). The DDT pathways, which involve translesion synthesis and template switching (TS), are activated by the ubiquitylation (ub) of PCNA through components of the RAD6-RAD18 pathway, whereas the HR pathway is independent of RAD18 However, it is unclear how these processes are coordinated within th...

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DNA repair mechanisms and the bypass of DNA damage in Saccharomyces cerevisiae.

DNA repair mechanisms are critical for maintaining the integrity of genomic DNA, and their loss is associated with cancer predisposition syndromes. Studies in Saccharomyces cerevisiae have played a central role in elucidating the highly conserved mechanisms that promote eukaryotic genome stability. This review will focus on repair mechanisms that involve excision of a single strand from duplex ...

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Evidence for lesion bypass by yeast replicative DNA polymerases during DNA damage

The enzyme ribonucleotide reductase, responsible for the synthesis of deoxyribonucleotides (dNTP), is upregulated in response to DNA damage in all organisms. In Saccharomyces cerevisiae, dNTP concentration increases approximately 6- to 8-fold in response to DNA damage. This concentration increase is associated with improved tolerance of DNA damage, suggesting that translesion DNA synthesis is m...

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ژورنال

عنوان ژورنال: Reactome - a curated knowledgebase of biological pathways

سال: 2004

ISSN: 1934-1792

DOI: 10.3180/react_2174.1