Recovery of RNA synthesis after TC-NER

Stable Identifier
R-HSA-6782234
Type
Reaction [omitted]
Species
Homo sapiens
Compartment
nucleoplasm
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Recovery of RNA synthesis after TC-NER
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After DNA repair synthesis is completed at transcription-coupled nucleotide excision repair (TC-NER) sites, transcription resumes. A number of factors have been implicated in this process. ERCC6 (CSB) contains an ubiquitin-binding domain that is indispensable for its function in TC-NER and the restoration of damage-inhibited RNA synthesis (Anindya et al. 2010). The ubiquitin ligase activity of the ERCC8:DDB1:CUL4:RBX1 complex plays an important role in termination of TC-NER, possibly by targeting ERCC6 or its ubiquitinated partner for degradation and promoting dissociation of repair factors from the RNA polymerase II complex (Groisman et al. 2006, Vermeulen and Fousteri 2013). The ubiquitin protease complex composed of UVSSA and USP7 is also implicated in the recovery of RNA synthesis (RRS) (Nakazawa et al. 2012, Scwertman et al. 2012, Zhang et al. 2012, Fei and Chen 2012). ELL protein, recruited to the TFIIH complex, possibly as a component of the little elongation complex, is needed for RRS (Mourgues et al. 2013). Furthermore, histone chaperone FACT promotes accelerated histone exchange at TC-NER sites, allowing efficient progression of TC-NER and restoration of RNA synthesis after the repair of transcription blocking damages is completed (Dinant et al. 2013).

Literature References
PubMed ID Title Journal Year
16751180 CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome

Groisman, R, Kuraoka, I, Chevallier, O, Gaye, N, Magnaldo, T, Tanaka, K, Kisselev, AF, Harel-Bellan, A, Nakatani, Y

Genes Dev. 2006
24127601 ELL, a novel TFIIH partner, is involved in transcription restart after DNA repair

Mourgues, S, Gautier, V, Lagarou, A, Bordier, C, Mourcet, A, Slingerland, J, Kaddoum, L, Coin, F, Vermeulen, W, Gonzales de Peredo, A, Monsarrat, B, Mari, PO, Giglia-Mari, G

Proc. Natl. Acad. Sci. U.S.A. 2013
22466611 UV-sensitive syndrome protein UVSSA recruits USP7 to regulate transcription-coupled repair

Schwertman, P, Lagarou, A, Dekkers, DH, Raams, A, van der Hoek, AC, Laffeber, C, Hoeijmakers, JH, Demmers, JA, Fousteri, M, Vermeulen, W, Marteijn, JA

Nat. Genet. 2012
23906714 Mammalian transcription-coupled excision repair

Vermeulen, W, Fousteri, M

Cold Spring Harb Perspect Biol 2013
22466612 Mutations in UVSSA cause UV-sensitive syndrome and destabilize ERCC6 in transcription-coupled DNA repair

Zhang, X, Horibata, K, Saijo, M, Ishigami, C, Ukai, A, Kanno, S, Tahara, H, Neilan, EG, Honma, M, Nohmi, T, Yasui, A, Tanaka, K

Nat. Genet. 2012
22902626 KIAA1530 protein is recruited by Cockayne syndrome complementation group protein A (CSA) to participate in transcription-coupled repair (TCR)

Fei, J, Chen, J

J. Biol. Chem. 2012
22466610 Mutations in UVSSA cause UV-sensitive syndrome and impair RNA polymerase IIo processing in transcription-coupled nucleotide-excision repair

Nakazawa, Y, Sasaki, K, Mitsutake, N, Matsuse, M, Shimada, M, Nardo, T, Takahashi, Y, Ohyama, K, Ito, K, Mishima, H, Nomura, M, Kinoshita, A, Ono, S, Takenaka, K, Masuyama, R, Kudo, T, Slor, H, Utani, A, Tateishi, S, Yamashita, S, Stefanini, M, Lehmann, AR, Yoshiura, K, Ogi, T

Nat. Genet. 2012
20541997 A ubiquitin-binding domain in Cockayne syndrome B required for transcription-coupled nucleotide excision repair

Anindya, R, Mari, PO, Kristensen, U, Kool, H, Giglia-Mari, G, Mullenders, LH, Fousteri, M, Vermeulen, W, Egly, JM, Svejstrup, JQ

Mol. Cell 2010
23973375 Enhanced chromatin dynamics by FACT promotes transcriptional restart after UV-induced DNA damage

Dinant, C, Ampatziadis-Michailidis, G, Lans, H, Tresini, M, Lagarou, A, Grosbart, M, Theil, AF, van Cappellen, WA, Kimura, H, Bartek, J, Fousteri, M, Houtsmuller, AB, Vermeulen, W, Marteijn, JA

Mol. Cell 2013
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Authored
Hoeijmakers, JH  (2004-01-29)
Orlic-Milacic, M  (2015-06-16)
Reviewed
Fousteri, M  (2015-08-03)
Created
Orlic-Milacic, M  (2015-06-05)