Literature DB >> 7563073

Characteristics of UV-induced mutation spectra in human XP-D/ERCC2 gene-mutated xeroderma pigmentosum and trichothiodystrophy cells.

C Marionnet1, A Benoit, S Benhamou, A Sarasin, A Stary.   

Abstract

To study the relationships between mutagenesis and carcinogenesis, we compared the mutations and their frequency induced by ultraviolet irradiation at 254 nm (UV-C) in XP-D (GM-08207B/XP6BE), TTD/XP-D (TTD1VI-LAS-KMT11) and wild-type (MRC-5V1) human cells. XP-D and TTD/XP-D cells, mutated in the same XP-D/ERCC2 gene, are deficient in nucleotide excision repair. Whereas XP-D patients develop early skin tumors, TTD patients do not exhibit abnormal levels of cancers. After verification of UV hypersensitivity and DNA repair defect of the immortalized cell lines XP-D and TTD compared with a wild-type cell line, UV-induced mutagenesis was studied with a new shuttle vector pR2, carrying the target lacZ' gene. The UV-mutation frequencies in XP-D and TTD cells were similar and significantly increased compared with normal cells. Sequence analysis of 312 independent mutant plasmids revealed that more rearrangements were induced in TTD cells (16%) than in XP-D (5%) and normal cells (1%), while XP-D cells exhibited a twofold higher rate of tandem mutations compared with TTD and normal cells. In the three cell lines, a predominance of G:C to A:T transitions was found, especially in chiefly on the cytosine at 5'-TC-3' sites. The types of UV-induced point mutations in TTD cells were, however, more similar to those in normal cells than those found in XP-D cells. XP-D mutations were preferentially located in 5'-TCPur-3' sites, while mutations in normal and TTD cells were mostly at 5'-TCC-3' sites. Analysis of mutation spectra revealed differences in the location of the mutational hotspots between the three lines. Although the mutation frequency of the UV-irradiated pR2 vector is much higher in TTD and XP-D cells than in normal cells, the mutation spectrum is closer between TTD and normal cells as compared with XP-D cells. These dissimilarities could contribute to an explanation of some of the differences between the two syndromes.

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Year:  1995        PMID: 7563073     DOI: 10.1006/jmbi.1995.0519

Source DB:  PubMed          Journal:  J Mol Biol        ISSN: 0022-2836            Impact factor:   5.469


  7 in total

1.  Persistence of repair proteins at unrepaired DNA damage distinguishes diseases with ERCC2 (XPD) mutations: cancer-prone xeroderma pigmentosum vs. non-cancer-prone trichothiodystrophy.

Authors:  Jennifer Boyle; Takahiro Ueda; Kyu-Seon Oh; Kyoko Imoto; Deborah Tamura; Jared Jagdeo; Sikandar G Khan; Carine Nadem; John J Digiovanna; Kenneth H Kraemer
Journal:  Hum Mutat       Date:  2008-10       Impact factor: 4.878

2.  Photocarcinogenesis and inhibition of intercellular adhesion molecule 1 expression in cells of DNA-repair-defective individuals.

Authors:  C Ahrens; M Grewe; M Berneburg; S Grether-Beck; X Quilliet; M Mezzina; A Sarasin; A R Lehmann; C F Arlett; J Krutmann
Journal:  Proc Natl Acad Sci U S A       Date:  1997-06-24       Impact factor: 11.205

3.  Evidence for recent, population-specific evolution of the human mutation rate.

Authors:  Kelley Harris
Journal:  Proc Natl Acad Sci U S A       Date:  2015-03-02       Impact factor: 11.205

4.  The impact of genetic modifiers on variation in germline mutation rates within and among human populations.

Authors:  William R Milligan; Guy Amster; Guy Sella
Journal:  Genetics       Date:  2022-07-30       Impact factor: 4.402

5.  Genomic analysis identifies new drivers and progression pathways in skin basal cell carcinoma.

Authors:  Ximena Bonilla; Laurent Parmentier; Bryan King; Fedor Bezrukov; Gürkan Kaya; Vincent Zoete; Vladimir B Seplyarskiy; Hayley J Sharpe; Thomas McKee; Audrey Letourneau; Pascale G Ribaux; Konstantin Popadin; Nicole Basset-Seguin; Rouaa Ben Chaabene; Federico A Santoni; Maria A Andrianova; Michel Guipponi; Marco Garieri; Carole Verdan; Kerstin Grosdemange; Olga Sumara; Martin Eilers; Iannis Aifantis; Olivier Michielin; Frederic J de Sauvage; Stylianos E Antonarakis; Sergey I Nikolaev
Journal:  Nat Genet       Date:  2016-03-07       Impact factor: 38.330

Review 6.  The involvement of DNA-damage and -repair defects in neurological dysfunction.

Authors:  Avanti Kulkarni; David M Wilson
Journal:  Am J Hum Genet       Date:  2008-03       Impact factor: 11.025

7.  The absence of Mth1 inactivation and DNA polymerase kappa overexpression in rat mammary carcinomas with frequent A:T to C:G transversions.

Authors:  Eriko Okochi; Shizue Ichimura; Takashi Sugimura; Toshikazu Ushijima
Journal:  Jpn J Cancer Res       Date:  2002-05
  7 in total

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