Cargando…
Rev1 promotes replication through UV lesions in conjunction with DNA polymerases η, ι, and κ but not DNA polymerase ζ
Translesion synthesis (TLS) DNA polymerases (Pols) promote replication through DNA lesions; however, little is known about the protein factors that affect their function in human cells. In yeast, Rev1 plays a noncatalytic role as an indispensable component of Polζ, and Polζ together with Rev1 mediat...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cold Spring Harbor Laboratory Press
2015
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4699387/ https://www.ncbi.nlm.nih.gov/pubmed/26680302 http://dx.doi.org/10.1101/gad.272229.115 |
_version_ | 1782408182068412416 |
---|---|
author | Yoon, Jung-Hoon Park, Jeseong Conde, Juan Wakamiya, Maki Prakash, Louise Prakash, Satya |
author_facet | Yoon, Jung-Hoon Park, Jeseong Conde, Juan Wakamiya, Maki Prakash, Louise Prakash, Satya |
author_sort | Yoon, Jung-Hoon |
collection | PubMed |
description | Translesion synthesis (TLS) DNA polymerases (Pols) promote replication through DNA lesions; however, little is known about the protein factors that affect their function in human cells. In yeast, Rev1 plays a noncatalytic role as an indispensable component of Polζ, and Polζ together with Rev1 mediates a highly mutagenic mode of TLS. However, how Rev1 functions in TLS and mutagenesis in human cells has remained unclear. Here we determined the role of Rev1 in TLS opposite UV lesions in human and mouse fibroblasts and showed that Rev1 is indispensable for TLS mediated by Polη, Polι, and Polκ but is not required for TLS by Polζ. In contrast to its role in mutagenic TLS in yeast, Rev1 promotes predominantly error-free TLS opposite UV lesions in humans. The identification of Rev1 as an indispensable scaffolding component for Polη, Polι, and Polκ, which function in TLS in highly specialized ways opposite a diverse array of DNA lesions and act in a predominantly error-free manner, implicates a crucial role for Rev1 in the maintenance of genome stability in humans. |
format | Online Article Text |
id | pubmed-4699387 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Cold Spring Harbor Laboratory Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-46993872016-06-15 Rev1 promotes replication through UV lesions in conjunction with DNA polymerases η, ι, and κ but not DNA polymerase ζ Yoon, Jung-Hoon Park, Jeseong Conde, Juan Wakamiya, Maki Prakash, Louise Prakash, Satya Genes Dev Research Paper Translesion synthesis (TLS) DNA polymerases (Pols) promote replication through DNA lesions; however, little is known about the protein factors that affect their function in human cells. In yeast, Rev1 plays a noncatalytic role as an indispensable component of Polζ, and Polζ together with Rev1 mediates a highly mutagenic mode of TLS. However, how Rev1 functions in TLS and mutagenesis in human cells has remained unclear. Here we determined the role of Rev1 in TLS opposite UV lesions in human and mouse fibroblasts and showed that Rev1 is indispensable for TLS mediated by Polη, Polι, and Polκ but is not required for TLS by Polζ. In contrast to its role in mutagenic TLS in yeast, Rev1 promotes predominantly error-free TLS opposite UV lesions in humans. The identification of Rev1 as an indispensable scaffolding component for Polη, Polι, and Polκ, which function in TLS in highly specialized ways opposite a diverse array of DNA lesions and act in a predominantly error-free manner, implicates a crucial role for Rev1 in the maintenance of genome stability in humans. Cold Spring Harbor Laboratory Press 2015-12-15 /pmc/articles/PMC4699387/ /pubmed/26680302 http://dx.doi.org/10.1101/gad.272229.115 Text en © 2015 Yoon et al.; Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/. |
spellingShingle | Research Paper Yoon, Jung-Hoon Park, Jeseong Conde, Juan Wakamiya, Maki Prakash, Louise Prakash, Satya Rev1 promotes replication through UV lesions in conjunction with DNA polymerases η, ι, and κ but not DNA polymerase ζ |
title | Rev1 promotes replication through UV lesions in conjunction with DNA polymerases η, ι, and κ but not DNA polymerase ζ |
title_full | Rev1 promotes replication through UV lesions in conjunction with DNA polymerases η, ι, and κ but not DNA polymerase ζ |
title_fullStr | Rev1 promotes replication through UV lesions in conjunction with DNA polymerases η, ι, and κ but not DNA polymerase ζ |
title_full_unstemmed | Rev1 promotes replication through UV lesions in conjunction with DNA polymerases η, ι, and κ but not DNA polymerase ζ |
title_short | Rev1 promotes replication through UV lesions in conjunction with DNA polymerases η, ι, and κ but not DNA polymerase ζ |
title_sort | rev1 promotes replication through uv lesions in conjunction with dna polymerases η, ι, and κ but not dna polymerase ζ |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4699387/ https://www.ncbi.nlm.nih.gov/pubmed/26680302 http://dx.doi.org/10.1101/gad.272229.115 |
work_keys_str_mv | AT yoonjunghoon rev1promotesreplicationthroughuvlesionsinconjunctionwithdnapolymerasesēiandkbutnotdnapolymerasez AT parkjeseong rev1promotesreplicationthroughuvlesionsinconjunctionwithdnapolymerasesēiandkbutnotdnapolymerasez AT condejuan rev1promotesreplicationthroughuvlesionsinconjunctionwithdnapolymerasesēiandkbutnotdnapolymerasez AT wakamiyamaki rev1promotesreplicationthroughuvlesionsinconjunctionwithdnapolymerasesēiandkbutnotdnapolymerasez AT prakashlouise rev1promotesreplicationthroughuvlesionsinconjunctionwithdnapolymerasesēiandkbutnotdnapolymerasez AT prakashsatya rev1promotesreplicationthroughuvlesionsinconjunctionwithdnapolymerasesēiandkbutnotdnapolymerasez |