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Moriel-Carretero M and Aguilera A  (2010) A Postincision-Deficient TFIIH Causes Replication Fork Breakage and Uncovers Alternative Rad51- or Pol32-Mediated Restart Mechanisms. Mol Cell 37(5):690-701

Abstract: Homologous recombination is a major double-strand break (DSB) repair mechanism that acts during the S and G2 phases. In contrast, nucleotide excision repair (NER) is a major pathway for the repair of DNA bulky adducts that is unrelated to replication. We show that replication can be strongly disturbed in a specific type of rad3/XPD NER mutant of TFIIH, causing replication fork breakage. In contrast to classical NER-deficient mutations, the S. cerevisiae rad3-102 allele, which has a minimal impact on UV resistance, channels bulky adducts into DSBs. rad3-102 allows Rad1/XPF- and Rad2/XPG-catalyzed DNA incisions but fails to perform postincision steps retaining TFIIH at the damaged site. Broken forks are rescued by MRX-Rad52-Rfc1-dependent recombination via two types of replication restart mechanisms, one being Rad51 dependent and the other Pol32 dependent. Our results define the genetic and molecular hallmarks of replication fork breakage and restart and bring insights to understand specific NER-related human syndromes.CI - Copyright (c) 2010 Elsevier Inc. All rights reserved.

Status: Published Type: Journal Article PubMed ID: 20227372

Topics addressed in this paper

Number of different genes curated to this paper: 27

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Topics Genes linked to topics (#1 - 10 )
ARS305 ASF1 CSM3 CTF18 ELG1 MUS81 PIF1 POL3 POL32 RAD1
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Topics Genes linked to topics (#11 - 20 )
RAD2 RAD3 RAD50 RAD51 RAD52 RAD54 RAD59 RAD9 RFC1 RNH1
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Topics Genes linked to topics (#21 - 27 )
RRM3 SAE2 SGS1 SRS2 TFB4 TOF1 TOP3
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