pubmed-article:19197357 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C0235480 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C0012899 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C1519591 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C1158557 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C0032172 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C0279389 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C0936012 | lld:lifeskim |
pubmed-article:19197357 | lifeskim:mentions | umls-concept:C0392760 | lld:lifeskim |
pubmed-article:19197357 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:19197357 | pubmed:dateCreated | 2009-2-6 | lld:pubmed |
pubmed-article:19197357 | pubmed:abstractText | RNA polymerases frequently deal with a number of obstacles during transcription elongation that need to be removed for transcription resumption. One important type of hindrance consists of DNA lesions, which are removed by transcription-coupled repair (TC-NER), a specific sub-pathway of nucleotide excision repair. To improve our knowledge of transcription elongation and its coupling to TC-NER, we used the yeast library of non-essential knock-out mutations to screen for genes conferring resistance to the transcription-elongation inhibitor mycophenolic acid and the DNA-damaging agent 4-nitroquinoline-N-oxide. Our data provide evidence that subunits of the SAGA and Ccr4-Not complexes, Mediator, Bre1, Bur2, and Fun12 affect transcription elongation to different extents. Given the dependency of TC-NER on RNA Polymerase II transcription and the fact that the few proteins known to be involved in TC-NER are related to transcription, we performed an in-depth TC-NER analysis of a selection of mutants. We found that mutants of the PAF and Ccr4-Not complexes are impaired in TC-NER. This study provides evidence that PAF and Ccr4-Not are required for efficient TC-NER in yeast, unraveling a novel function for these transcription complexes and opening new perspectives for the understanding of TC-NER and its functional interconnection with transcription elongation. | lld:pubmed |
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pubmed-article:19197357 | pubmed:language | eng | lld:pubmed |
pubmed-article:19197357 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19197357 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19197357 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |