Mind the gap: Keeping UV lesions in check

Cells respond to genotoxic insults by triggering a DNA damage checkpoint surveillance mechanism and by activating repair pathways. Recent findings indicate that the two processes are more related than originally thought. Here we discuss the mechanisms involved in responding to UV-induced lesions in...

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Main Authors:	Novarina, Daniele, Amara, Flavio, Lazzaro, Federico, Plevani, Paolo, Muzi-Falconi, Marco
Format:	Online
Language:	English
Published:	Elsevier 2011
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171152/

id	pubmed-3171152
recordtype	oai_dc
spelling	pubmed-31711522011-11-03 Mind the gap: Keeping UV lesions in check Novarina, Daniele Amara, Flavio Lazzaro, Federico Plevani, Paolo Muzi-Falconi, Marco Mini Review Cells respond to genotoxic insults by triggering a DNA damage checkpoint surveillance mechanism and by activating repair pathways. Recent findings indicate that the two processes are more related than originally thought. Here we discuss the mechanisms involved in responding to UV-induced lesions in different phases of the cell cycle and summarize the most recent data in a model where Nucleotide Excision Repair (NER) and exonucleolytic activities act in sequence leading to checkpoint activation in non replicating cells. The critical trigger is likely represented by problematic intermediates that cannot be completely or efficiently repaired by NER. In S phase cells, on the other hand, the replicative polymerases, blocked by bulky UV lesions, re-initiate DNA synthesis downstream of the lesions, leaving behind a ssDNA tract. If these gaps are not rapidly refilled, checkpoint kinases will be activated. Elsevier 2011-07-15 /pmc/articles/PMC3171152/ /pubmed/21602108 http://dx.doi.org/10.1016/j.dnarep.2011.04.030 Text en © 2011 Elsevier B.V. This document may be redistributed and reused, subject to certain conditions (http://www.elsevier.com/wps/find/authorsview.authors/supplementalterms1.0) .
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Novarina, Daniele Amara, Flavio Lazzaro, Federico Plevani, Paolo Muzi-Falconi, Marco
spellingShingle	Novarina, Daniele Amara, Flavio Lazzaro, Federico Plevani, Paolo Muzi-Falconi, Marco Mind the gap: Keeping UV lesions in check
author_facet	Novarina, Daniele Amara, Flavio Lazzaro, Federico Plevani, Paolo Muzi-Falconi, Marco
author_sort	Novarina, Daniele
title	Mind the gap: Keeping UV lesions in check
title_short	Mind the gap: Keeping UV lesions in check
title_full	Mind the gap: Keeping UV lesions in check
title_fullStr	Mind the gap: Keeping UV lesions in check
title_full_unstemmed	Mind the gap: Keeping UV lesions in check
title_sort	mind the gap: keeping uv lesions in check
description	Cells respond to genotoxic insults by triggering a DNA damage checkpoint surveillance mechanism and by activating repair pathways. Recent findings indicate that the two processes are more related than originally thought. Here we discuss the mechanisms involved in responding to UV-induced lesions in different phases of the cell cycle and summarize the most recent data in a model where Nucleotide Excision Repair (NER) and exonucleolytic activities act in sequence leading to checkpoint activation in non replicating cells. The critical trigger is likely represented by problematic intermediates that cannot be completely or efficiently repaired by NER. In S phase cells, on the other hand, the replicative polymerases, blocked by bulky UV lesions, re-initiate DNA synthesis downstream of the lesions, leaving behind a ssDNA tract. If these gaps are not rapidly refilled, checkpoint kinases will be activated.
publisher	Elsevier
publishDate	2011
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171152/
_version_	1611475081648668672

Mind the gap: Keeping UV lesions in check

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