Translesion DNA Synthesis and Damage Tolerance Pathways View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2016-01-23

AUTHORS

Yuji Masuda , Fumio Hanaoka , Chikahide Masutani

ABSTRACT

One of the critical cellular effects of DNA damage is the impediment of the activity of high-fidelity DNA polymerases for replication. Although DNA repair mechanisms physically remove DNA damage before the initiation of DNA replication, remaining damage DNA can still persist in S phase and inhibit replicative DNA polymerases. To deal with this, cells have developed mechanisms to copy chromosomes with unrepaired DNA damage, known as DNA damage tolerance (DDT) mechanisms. As a consequence of DDT, cells can complete chromosomal duplication even in the presence of low levels of DNA damage. DDT mechanisms have been classified into two pathways: translesion DNA synthesis (TLS) and homology-directed repair. In TLS, specialized TLS DNA polymerases utilize damaged DNA as the template and extend the 3′ end of the stalled primer beyond the damage. In homology-directed repair, the stalled primer anneals with the newly synthesized daughter strand and transiently utilizes the undamaged complementary sequence as a template for DNA synthesis. In this article, we summarize and discuss the molecular mechanisms of the DDT pathways of well-analyzed organisms: Escherichia coli, the budding yeast Saccharomyces cerevisiae, and mammalians. More... »

PAGES

249-304

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-4-431-55873-6_11

DOI

http://dx.doi.org/10.1007/978-4-431-55873-6_11

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041067481


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