Author
Listed:
- Dhvani Parikh
(University of Pittsburgh)
- Elise Fouquerel
(University of Pittsburgh
University of Pittsburgh Cancer Institute)
- Connor T. Murphy
(University of Pittsburgh
Center for Nucleic Acids Science and Technology, Carnegie Mellon University)
- Hong Wang
(North Carolina State University)
- Patricia L. Opresko
(University of Pittsburgh
University of Pittsburgh Cancer Institute
Center for Nucleic Acids Science and Technology, Carnegie Mellon University
North Carolina State University)
Abstract
Ultraviolet light induces cyclobutane pyrimidine dimers (CPD) and pyrimidine(6–4)pyrimidone photoproducts, which interfere with DNA replication and transcription. Nucleotide excision repair (NER) removes these photoproducts, but whether NER functions at telomeres is unresolved. Here we use immunospot blotting to examine the efficiency of photoproduct formation and removal at telomeres purified from UVC irradiated cells at various recovery times. Telomeres exhibit approximately twofold fewer photoproducts compared with the bulk genome in cells, and telomere-binding protein TRF1 significantly reduces photoproduct formation in telomeric fragments in vitro. CPD removal from telomeres occurs 1.5-fold faster than the bulk genome, and is completed by 48 h. 6–4PP removal is rapidly completed by 6 h in both telomeres and the overall genome. A requirement for XPA protein indicates the mechanism of telomeric photoproduct removal is NER. These data provide new evidence that telomeres are partially protected from ultraviolet irradiation and that NER preserves telomere integrity.
Suggested Citation
Dhvani Parikh & Elise Fouquerel & Connor T. Murphy & Hong Wang & Patricia L. Opresko, 2015.
"Telomeres are partly shielded from ultraviolet-induced damage and proficient for nucleotide excision repair of photoproducts,"
Nature Communications, Nature, vol. 6(1), pages 1-10, November.
Handle:
RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9214
DOI: 10.1038/ncomms9214
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