Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 23, Issue 7, Pages 2341-2350Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.23.7.2341-2350.2003
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Funding
- NCI NIH HHS [CA 39662, R01 CA039662, CA 77433] Funding Source: Medline
- NIGMS NIH HHS [GM 59170] Funding Source: Medline
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Topoisomerase I (Top I)-DNA covalent complexes represent a unique type of DNA lesion whose repair and processing remain unclear. In this study, we show that Top I-DNA covalent complexes transiently arrest RNA transcription in normal nontransformed cells. Arrest of RNA transcription is coupled to activation of proteasomal degradation of Top I and the large subunit of RNA polymerase II. Recovery of transcription occurs gradually and depends on both proteasomal degradation of Top I and functional transcription-coupled repair (TCR). These results suggest that arrest of the RNA polymerase elongation complex by the Top I-DNA covalent complex triggers a 26S proteasome-mediated signaling pathway(s) leading to degradation of both Top I and the large subunit of RNA polymerase II. We propose that proteasomal degradation of Top I and RNA polymerase II precedes repair of the exposed single-strand breaks by TCR.
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