Dissecting transcription-coupled and global genomic repair in the chromatin of yeast GAL1-10 genes

Shisheng Li; Michael J Smerdon

doi:10.1074/jbc.M312004200

Back

Dissecting transcription-coupled and global genomic repair in the chromatin of yeast GAL1-10 genes

Journal article

Open access

Peer reviewed

Dissecting transcription-coupled and global genomic repair in the chromatin of yeast GAL1-10 genes

Shisheng Li and Michael J Smerdon

The Journal of biological chemistry, Vol.279(14), pp.14418-14426

04/02/2004

DOI: https://doi.org/10.1074/jbc.M312004200

Handle:

https://hdl.handle.net/2376/110454

PMCID: PMC1343541

PMID: 14734564

Files and links (1)

url

https://doi.org/10.1074/jbc.M312004200View

Published (Version of record) Open

Abstract

Gene Expression Regulation, Fungal

Galactose - metabolism

Transcription, Genetic - physiology

Saccharomyces cerevisiae - genetics

Chromatin - physiology

DNA Repair - physiology

Saccharomyces cerevisiae Proteins - metabolism

Schizosaccharomyces pombe Proteins - metabolism

Adenosine Triphosphatases - metabolism

Genes, Fungal

Mutation

RNA Polymerase II - metabolism

Transcription-coupled repair (TCR) and global genomic repair (GGR) of UV-induced cyclobutane pyrimidine dimers were investigated in the yeast GAL1-10 genes. Both Rpb9- and Rad26-mediated TCR are confined to the transcribed strands, initiating at upstream sites approximately 100 nucleotides from the upstream activating sequence shared by the two genes. However, TCR initiation sites do not correlate with either transcription start sites or TATA boxes. Rad16-mediated GGR tightly correlates with nucleosome positioning when the genes are repressed and are slow in the nucleosome core and fast in linker DNA. Induction of transcription enhanced GGR in nucleosome core DNA, especially in the nucleosomes around and upstream of the transcription start sites. Furthermore, when the genes were induced, GGR was slower in the transcribed regions than in the upstream regions. Finally, simultaneous deletion of RAD16, RAD26, and RPB9 resulted in no detectable repair in all sites along the region analyzed. Our results suggest that (a). TCR may be initiated by a transcription activator, presumably through the loading of RNA polymerase II, rather than by transcription initiation or elongation per se; (b). TCR and nucleosome disruption-enhanced GGR are the major causes of rapid repair in regions around and upstream of transcription start sites; (c). transcription machinery may hinder access of NER factors to a DNA lesion in the absence of a transcription-repair coupling factor; and (d). other than GGR mediated by Rad16 and TCR mediated by Rad26 and Rpb9, no other nucleotide excision repair pathway exists in these RNA polymerase II-transcribed genes.

Metrics

10 Record Views

Details

Title: Dissecting transcription-coupled and global genomic repair in the chromatin of yeast GAL1-10 genes
Creators: Shisheng Li - Biochemistry and Biophysics, School of Molecular Biosciences, Washington State University, Pullman, Washington 99164-4660, USA
Michael J Smerdon
Publication Details: The Journal of biological chemistry, Vol.279(14), pp.14418-14426
Academic Unit: Molecular Biosciences, School of
Publisher: United States
Grant note: ES04106 / NIEHS NIH HHS R01 ES004106 / NIEHS NIH HHS R37 ES002614 / NIEHS NIH HHS R01 ES002614 / NIEHS NIH HHS ES02614 / NIEHS NIH HHS
Identifiers: 99900547296501842
Language: English
Resource Type: Journal article