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Repriming of DNA synthesis at stalled replication forks by human PrimPol

Nature structural & molecular biology, 2013-12, Vol.20 (12), p.1383-1389 [Peer Reviewed Journal]

COPYRIGHT 2013 Nature Publishing Group ;COPYRIGHT 2013 Nature Publishing Group ;Copyright Nature Publishing Group Dec 2013 ;Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2013. ;ISSN: 1545-9993 ;EISSN: 1545-9985 ;DOI: 10.1038/nsmb.2719 ;PMID: 24240614

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Title:
Repriming of DNA synthesis at stalled replication forks by human PrimPol
Author: Mourón, Silvana ; Rodriguez-Acebes, Sara ; Martínez-Jiménez, María I ; García-Gómez, Sara ; Chocrón, Sandra ; Blanco, Luis ; Méndez, Juan
Subjects: Chemical synthesis ; Collapse ; Damage tolerance ; Deoxyribonucleic acid ; Depletion ; DNA ; DNA biosynthesis ; DNA Breaks, Double-Stranded ; DNA Damage ; DNA polymerase ; DNA polymerases ; DNA Primase - chemistry ; DNA Primase - metabolism ; DNA Primase - physiology ; DNA replication ; DNA Replication - physiology ; DNA structure ; DNA-directed DNA polymerase ; DNA-Directed DNA Polymerase - chemistry ; DNA-Directed DNA Polymerase - metabolism ; DNA-Directed DNA Polymerase - physiology ; Enzymes ; Genomic Instability ; Genomics ; Humans ; Identification and classification ; Irradiation ; Multifunctional Enzymes - chemistry ; Multifunctional Enzymes - metabolism ; Multifunctional Enzymes - physiology ; Primase ; Priming ; Properties ; Replication ; Replication fork ; Replication forks ; RNA, Messenger - metabolism ; S Phase ; Ultraviolet radiation ; Ultraviolet Rays
Is Part Of: Nature structural & molecular biology, 2013-12, Vol.20 (12), p.1383-1389
Description: DNA replication forks that collapse during the process of genomic duplication lead to double-strand breaks and constitute a threat to genomic stability. The risk of fork collapse is higher in the presence of replication inhibitors or after UV irradiation, which introduces specific modifications in the structure of DNA. In these cases, fork progression may be facilitated by error-prone translesion synthesis (TLS) DNA polymerases. Alternatively, the replisome may skip the damaged DNA, leaving an unreplicated gap to be repaired after replication. This mechanism strictly requires a priming event downstream of the lesion. Here we show that PrimPol, a new human primase and TLS polymerase, uses its primase activity to mediate uninterrupted fork progression after UV irradiation and to reinitiate DNA synthesis after dNTP depletion. As an enzyme involved in tolerance to DNA damage, PrimPol might become a target for cancer therapy.
Publisher: United States: Nature Publishing Group
Language: English
Identifier: ISSN: 1545-9993
EISSN: 1545-9985
DOI: 10.1038/nsmb.2719
PMID: 24240614
Source: MEDLINE
ProQuest Central

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Repriming of DNA synthesis at stalled replication forks by human PrimPol

COPYRIGHT 2013 Nature Publishing Group ;COPYRIGHT 2013 Nature Publishing Group ;Copyright Nature Publishing Group Dec 2013 ;Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2013. ;ISSN: 1545-9993 ;EISSN: 1545-9985 ;DOI: 10.1038/nsmb.2719 ;PMID: 24240614

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