Significance The mechanism of eukaryotic transcription-coupled nucleotide excision repair (TC-NER) is poorly understood. Here, we studied the genome-wide role of yeast Rad26, a homolog of the human Cockayne syndrome group B (CSB) protein, in the repair of UV-induced DNA damage. We found that Rad26 is not uniformly required for TC-NER in transcribed chromatin. Instead, nucleosome organization and the distribution of transcription regulators such as TFIIH and Spt4/Spt5 significantly modulate the requirement for Rad26 in TC-NER. Importantly, TC-NER is conserved from yeast to humans. Our data provide insights into the mechanism of TC-NER in eukaryotes.
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Duan et al. (2020) studied this question.
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