期刊
NATURE REVIEWS MOLECULAR CELL BIOLOGY
卷 15, 期 7, 页码 465-481出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nrm3822
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资金
- European commission [FP7-Health-2008-200880, HEALTH-F2-2010-259893]
- US National Institutes of Health and National Institute on Ageing [1PO1 AG-17242-02]
- US National Institute of Environmental Health Sciences (NIEHS) [1UO1 ES011044]
- Royal Academy of Arts and Sciences of the Netherlands
- European Research Council Advanced Grants
- Dutch Cancer Society
- National Genomics Initiative
- Earth and Life Sciences TOP grant
- Medical Sciences TOP grant
- Dutch Science Organization (NWO)
- Erasmus MC fellowship
Nucleotide excision repair (NER) eliminates various structurally unrelated DNA lesions by a multiwise 'cut and patch'-type reaction. The global genome NER (GG-NER) subpathway prevents mutagenesis by probing the genome for helix-distorting lesions, whereas transcription-coupled NER (TC-NER) removes transcription-blocking lesions to permit unperturbed gene expression, thereby preventing cell death. Consequently, defects in GG-NER result in cancer predisposition, whereas defects in TC-NER cause a variety of diseases ranging from ultraviolet radiation-sensitive syndrome to severe premature ageing conditions such as Cockayne syndrome. Recent studies have uncovered new aspects of DNA-damage detection by NER, how NER is regulated by extensive post-translational modifications, and the dynamic chromatin interactions that control its efficiency. Based on these findings, a mechanistic model is proposed that explains the complex genotype-phenotype correlations of transcription-coupled repair disorders.
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