Mind the gap: Keeping UV lesions in check

Daniele Novarina, Flavio Amara, Federico Lazzaro, Paolo Plevani*, Marco Muzi-Falconi

*Corresponding author voor dit werk

Onderzoeksoutputpeer review

35 Citaten (Scopus)

Samenvatting

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. (C) 2011 Elsevier B.V. All rights reserved.

Originele taal-2English
Pagina's (van-tot)751-759
Aantal pagina's9
TijdschriftDna repair
Volume10
Nummer van het tijdschrift7
DOI's
StatusPublished - 15-jul.-2011
Extern gepubliceerdJa

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