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Activation of a novel ubiquitin-independent proteasome pathway when RNA polymerase II encounters a protein roadblock. | LitMetric

Activation of a novel ubiquitin-independent proteasome pathway when RNA polymerase II encounters a protein roadblock.

Mol Cell Biol

Department of Pharmacology, Robert Wood Johnson Medical School, Rutgers University, Piscataway, New Jersey, USA.

Published: October 2013

AI Article Synopsis

Article Abstract

Topoisomerase IIβ (Top2β)-DNA cleavage complexes are known to arrest elongating RNA polymerase II (RNAPII), triggering a proteasomal degradation of the RNAPII large subunit (RNAPII LS) and Top2β itself as a prelude to DNA repair. Here, we demonstrate that the degradation of Top2β occurs through a novel ubiquitin-independent mechanism that requires only 19S AAA ATPases and 20S proteasome. Our results suggest that 19S AAA ATPases play a dual role in sensing the Top2β cleavage complex and coordinating its degradation by 20S proteasome when RNAPII is persistently stalled by the Top2β protein roadblock. Clarification of this transcription-associated proteasome pathway could shed light on a general role of 19S AAA ATPases in processing tight protein-DNA complexes during transcription elongation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3811683PMC
http://dx.doi.org/10.1128/MCB.00403-13DOI Listing

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