Cited by 113DNA Repair MechanismsGenetic factors in colorectal cancerNuclear Structure and Function

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Replication of damaged DNA: molecular defect in Xeroderma pigmentosum variant cells

Cordonnier, Agnes M, Fuchs, Robert P.P·1999·Mutation Research/DNA Repair

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Abstract

Individuals with Xeroderma pigmentosum (XP) syndrome have a genetic predisposition to sunlight-induced skin cancer. Genetically different forms of XP have been identified by cell fusion. Cells of individuals expressing the classical form of XP (complementation groups A through G) are deficient in the nucleotide excision repair (NER) pathway. In contrast, the cells belonging to the variant class of XP (XPV) are NER-proficient and are only slightly more sensitive than normal cells to the killing action of UV light radiation. The XPV fibroblasts replicate damaged DNA generating abnormally short fragments either in vivo [A.R. Lehmann, The relationship between pyramidine dimers and replicating DNA in UV-irradiated human fibroblasts, Nucleic Acids Res. 7 (1979) 1901-1912; S.D. Park, J.E. Cleaver, Postreplication repair: question of its definition and possible alteration in Xeroderma pigmentosum cell strains, Proc. Natl. Acad. Sci. U.S.A. 76 (1979) 3927-3931.] or in vitro [S.M. Cordeiro, L.S. Zaritskaya, L.K. Price, W.K. Kaufmann, Replication fork bypass of a pyramidine dimer blocking leading strand DNA synthesis, J. Biol. Chem. 272 (1997) 13945-13954; D.L. Svoboda, L.P. Briley, J.M. Vos, Defective bypass replication of a leading strand cyclobutane thymine dimer in Xeroderma pigmentosum variant cell extracts, Cancer Res. 58 (1998) 2445-2448; I. Ensch-Simon, P.M. Burgers, J.S. Taylor, Bypass of a site-specific cis-syn thymine dimer in an SV40 vector during in vitro replication by HeLa and XPV cell-free extracts, Biochemistry 37 (1998) 8218-8226.], suggesting that in XPV cells, replication has an increased probability of being blocked at a lesion. Furthermore, extracts from XPV cells were found to be defective in translesion synthesis [A. Cordonnier, A.R. Lehmann, R.P.P. Fuchs, Impaired translesion synthesis in Xeroderma pigmentosum variant extracts, Mol. Cell. Biol. 19 (1999) 2206-2211.]. Recently, Masutani et al. [C. Masutani, M. Araki, A. Yamada, R. Kusomoto, T. Nogimori, T. Maekawa, S. Iwai, F. Hanaoka, Xeroderma pigmentosum variant (XP-V) correcting protein from HeLa cells has a thymine dimer bypass DNA polymerase activity, EMBO J. 18 (1999) 3491-3501.] have shown that the XPV defect can be corrected by a novel human DNA polymerase, homologue to the yeast DNA polymerase eta, which is able to replicate past cyclobutane pyrimidine dimers in DNA templates. This review focuses on our current understanding of translesion synthesis in mammalian cells whose defect, unexpectedly, is responsible for the hypermutability of XPV cells and for the XPV pathology.

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Authors: Cordonnier, A. M., & Fuchs, R. P. P.
Affiliations: Centre National de la Recherche Scientifique (FR)
Corresponding author: Fuchs, Robert P.P
ORCID: Cordonnier, Agnes M
Fuchs, Robert P.P
Venue: Mutation Research/DNA Repair
Publisher: Elsevier BV
Published: 1999-10
Volume: 435
Issue: 2
Pages: 111-119
ISSN: 0921-8777 (ISSN-L)
DOI: 10.1016/s0921-8777(99)00047-6
OpenAlex: W2014999904
Cited by: 113
References: 67
Citations by year: 2026: 1 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 1 · 2018: 6 · 2017: 2 · 2016: 5 · 2015: 2 · 2014: 2 · 2013: 5 · 2012: 10
FWCI: 3.68
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Mutation Research/DNA Repair (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
Keywords: DNA replication, DNA damage, thymine dimers, cyclobutane thymine dimers, postreplication repair, translesion synthesis, nucleotide excision repair, replication fork stalling, DNA polymerase, UV-induced DNA damage, skin cancer predisposition
MeSH terms: Animals, DNA Damage, DNA Replication, Humans, Xeroderma Pigmentosum

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Replication of damaged DNA: molecular defect in Xeroderma pigmentosum variant cells

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