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Titolo:
UV light-induced degradation of RNA polymerase II is dependent on the Cockayne's syndrome A and B proteins but not p53 or MLH1
Autore:
McKay, BC; Chen, F; Clarke, ST; Wiggin, HE; Harley, LM; Ljungman, M;
Indirizzi:
Univ Michigan, Ctr Comprehens Canc, Div Canc Biol, Dept Radiat Oncol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 adiat Oncol, Ann Arbor, MI 48109 USA Univ Ottawa, Ottawa Reg Canc Ctr, Ctr Canc Therapeut, Dept Radiol, Ottawa,ON K1H 8L6, Canada Univ Ottawa Ottawa ON Canada K1H 8L6 pt Radiol, Ottawa,ON K1H 8L6, Canada Univ Michigan, Sch Med, Program Mol & Cellular Biol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 llular Biol, Ann Arbor, MI 48109 USA
Titolo Testata:
MUTATION RESEARCH-DNA REPAIR
fascicolo: 2, volume: 485, anno: 2001,
pagine: 93 - 105
SICI:
0921-8777(20010307)485:2<93:ULDORP>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSCRIPTION-COUPLED REPAIR; NUCLEOTIDE EXCISION-REPAIR; CARBOXYL-TERMINAL DOMAIN; DNA-REPAIR; SYNDROME CELLS; INDUCED UBIQUITINATION; XERODERMA-PIGMENTOSUM; PREFERENTIAL REPAIR; PYRIMIDINE DIMERS; HUMAN FIBROBLASTS;
Keywords:
Cockayne's syndrome; proteasome; transcription-coupled repair; mismatch repair; transcription;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Ljungman, M Univ Michigan, Ctr Comprehens Canc, Div Canc Biol, Dept RadiatOncol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 Ann Arbor, MI 48109 USA
Citazione:
B.C. McKay et al., "UV light-induced degradation of RNA polymerase II is dependent on the Cockayne's syndrome A and B proteins but not p53 or MLH1", MUT R-DNA R, 485(2), 2001, pp. 93-105

Abstract

It has been hypothesized that the degradation of the largest subunit of RNA polymerase II (polIILS) is required for transcription-coupled repair (TCR) of UV light-induced transcription-blocking lesions. In this study we further investigated the mechanism of UV-induced degradation of polIILS using cell lines with specific defects in TCR or in the recovery of RNA synthesis. It was found that the hypophosphorylated IIa form of polIILS rapidly decreased following UV-irradiation in all cell lines tested. Inhibition of proteasome activity resulted in an increase of the hyperphosphorylated IIo form of polIILS in UV-irradiated cells, while inhibition of CTD-kinases resultedin the retention of the IIa form. In UV-irradiated Cockayne's syndrome cells, which are defective in TCR, the levels of the IIo form increased in a similar manner as when proteasome inhibitors were added to UV-irradiated normal cells. In contrast, TCR-deficient HCT116 cells, which lack the mismatchrepair protein MLH1, showed proficient degradation of polIILS as did cellswith deficiencies in the recovery of RNA synthesis following UV-irradiation due to defective p53. Furthermore, we found that proteasome function was important for the recovery of mRNA synthesis even in TCR-deficient HCT116 cells. Our results suggest that proteasome-mediated degradation of polIILS is preceded by phosphorylation of the C-terminal domain of polIILS and requires the CS-A and CS-B but not MLH1 or p53 proteins. Furthermore, our results suggest that following UV-irradiation, the degradation of polIILS is required for the efficient recovery of mRNA synthesis but not for TCR per se. (C) 2001 Elsevier Science B.V. All rights reserved.

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Documento generato il 30/11/20 alle ore 07:11:53