Testicular nuclear receptor 4 (TR4) regulates UV light-induced responses via cockayne syndrome B protein-mediated transcription-coupled DNA repair

Su Liu, Shian-Jang Yan, Yi Fen Lee, Ning Chun Liu, Huei Ju Ting, Gonghui Li, Qiao Wu, Lu Min Chen, Chawnshang Chang

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

UV irradiation is one of the major external insults to cells and can cause skin aging and cancer. In response to UV light-induced DNA damage, the nucleotide excision repair (NER) pathways are activated to remove DNA lesions. We report here that testicular nuclear receptor 4 (TR4), a member of the nuclear receptor family, modulates DNA repair specifically through the transcription-coupled (TC) NER pathway but not the global genomic NER pathway. The level of Cockayne syndrome B protein (CSB), a member of the TC-NER pathway, is 10-fold reduced in TR4-deficient mouse tissues, and TR4 directly regulates CSB at the transcriptional level. Moreover, restored CSB expression rescues UV hypersensitivity of TR4-deficient cells. Together, these results indicate that TR4 modulates UV sensitivity by promoting the TC-NER DNA repair pathway through transcriptional regulation of CSB. These results may lead to the development of new treatments for UV light-sensitive syndromes, skin cancer, and aging.

Original languageEnglish
Pages (from-to)38103-38108
Number of pages6
JournalJournal of Biological Chemistry
Volume286
Issue number44
DOIs
Publication statusPublished - 2011 Nov 4

Fingerprint

Nuclear Receptor Subfamily 2, Group C, Member 2
Cockayne Syndrome
Transcription
Ultraviolet Rays
Cytoplasmic and Nuclear Receptors
DNA Repair
Ultraviolet radiation
Repair
DNA
Nucleotides
Skin Aging
Skin Neoplasms
Skin
Aging of materials
IgA receptor
Nuclear Family
DNA Damage
Hypersensitivity
Irradiation
Tissue

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Liu, Su ; Yan, Shian-Jang ; Lee, Yi Fen ; Liu, Ning Chun ; Ting, Huei Ju ; Li, Gonghui ; Wu, Qiao ; Chen, Lu Min ; Chang, Chawnshang. / Testicular nuclear receptor 4 (TR4) regulates UV light-induced responses via cockayne syndrome B protein-mediated transcription-coupled DNA repair. In: Journal of Biological Chemistry. 2011 ; Vol. 286, No. 44. pp. 38103-38108.
@article{80344b41cca740a1abec08930a8b4cbc,
title = "Testicular nuclear receptor 4 (TR4) regulates UV light-induced responses via cockayne syndrome B protein-mediated transcription-coupled DNA repair",
abstract = "UV irradiation is one of the major external insults to cells and can cause skin aging and cancer. In response to UV light-induced DNA damage, the nucleotide excision repair (NER) pathways are activated to remove DNA lesions. We report here that testicular nuclear receptor 4 (TR4), a member of the nuclear receptor family, modulates DNA repair specifically through the transcription-coupled (TC) NER pathway but not the global genomic NER pathway. The level of Cockayne syndrome B protein (CSB), a member of the TC-NER pathway, is 10-fold reduced in TR4-deficient mouse tissues, and TR4 directly regulates CSB at the transcriptional level. Moreover, restored CSB expression rescues UV hypersensitivity of TR4-deficient cells. Together, these results indicate that TR4 modulates UV sensitivity by promoting the TC-NER DNA repair pathway through transcriptional regulation of CSB. These results may lead to the development of new treatments for UV light-sensitive syndromes, skin cancer, and aging.",
author = "Su Liu and Shian-Jang Yan and Lee, {Yi Fen} and Liu, {Ning Chun} and Ting, {Huei Ju} and Gonghui Li and Qiao Wu and Chen, {Lu Min} and Chawnshang Chang",
year = "2011",
month = "11",
day = "4",
doi = "10.1074/jbc.M111.259523",
language = "English",
volume = "286",
pages = "38103--38108",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "44",

}

Testicular nuclear receptor 4 (TR4) regulates UV light-induced responses via cockayne syndrome B protein-mediated transcription-coupled DNA repair. / Liu, Su; Yan, Shian-Jang; Lee, Yi Fen; Liu, Ning Chun; Ting, Huei Ju; Li, Gonghui; Wu, Qiao; Chen, Lu Min; Chang, Chawnshang.

In: Journal of Biological Chemistry, Vol. 286, No. 44, 04.11.2011, p. 38103-38108.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Testicular nuclear receptor 4 (TR4) regulates UV light-induced responses via cockayne syndrome B protein-mediated transcription-coupled DNA repair

AU - Liu, Su

AU - Yan, Shian-Jang

AU - Lee, Yi Fen

AU - Liu, Ning Chun

AU - Ting, Huei Ju

AU - Li, Gonghui

AU - Wu, Qiao

AU - Chen, Lu Min

AU - Chang, Chawnshang

PY - 2011/11/4

Y1 - 2011/11/4

N2 - UV irradiation is one of the major external insults to cells and can cause skin aging and cancer. In response to UV light-induced DNA damage, the nucleotide excision repair (NER) pathways are activated to remove DNA lesions. We report here that testicular nuclear receptor 4 (TR4), a member of the nuclear receptor family, modulates DNA repair specifically through the transcription-coupled (TC) NER pathway but not the global genomic NER pathway. The level of Cockayne syndrome B protein (CSB), a member of the TC-NER pathway, is 10-fold reduced in TR4-deficient mouse tissues, and TR4 directly regulates CSB at the transcriptional level. Moreover, restored CSB expression rescues UV hypersensitivity of TR4-deficient cells. Together, these results indicate that TR4 modulates UV sensitivity by promoting the TC-NER DNA repair pathway through transcriptional regulation of CSB. These results may lead to the development of new treatments for UV light-sensitive syndromes, skin cancer, and aging.

AB - UV irradiation is one of the major external insults to cells and can cause skin aging and cancer. In response to UV light-induced DNA damage, the nucleotide excision repair (NER) pathways are activated to remove DNA lesions. We report here that testicular nuclear receptor 4 (TR4), a member of the nuclear receptor family, modulates DNA repair specifically through the transcription-coupled (TC) NER pathway but not the global genomic NER pathway. The level of Cockayne syndrome B protein (CSB), a member of the TC-NER pathway, is 10-fold reduced in TR4-deficient mouse tissues, and TR4 directly regulates CSB at the transcriptional level. Moreover, restored CSB expression rescues UV hypersensitivity of TR4-deficient cells. Together, these results indicate that TR4 modulates UV sensitivity by promoting the TC-NER DNA repair pathway through transcriptional regulation of CSB. These results may lead to the development of new treatments for UV light-sensitive syndromes, skin cancer, and aging.

UR - http://www.scopus.com/inward/record.url?scp=80055069189&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80055069189&partnerID=8YFLogxK

U2 - 10.1074/jbc.M111.259523

DO - 10.1074/jbc.M111.259523

M3 - Article

C2 - 21918225

AN - SCOPUS:80055069189

VL - 286

SP - 38103

EP - 38108

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 44

ER -