Journal
JOURNAL OF CELL SCIENCE
Volume 129, Issue 18, Pages 3412-3425Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.195867
Keywords
Actin; Nuclear actin filaments; Nucleus; RNA polymerase II; Transcription
Categories
Funding
- National Institutes of Health (NIH) [GM80587, GM076561, GM114666, GM076516, GM103540]
- Chicago Biomedical Consortium
- Searle Funds at the Chicago Community Trust
- Northwestern University Physical Sciences Oncology Center
- National Cancer Institute [U54CA143869, 13PRE17050060]
- Chicago Biomedical Consortium Scholar award
- University of Illinois at Chicago (UIC) Dean's Scholar and Chancellor's graduate research fellowship
- UIC CM Craig Fellowship
- American Heart Association (AHA) [13PRE17050060, 13IRG14780028]
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Actin is abundant in the nucleus and it is clear that nuclear actin has important functions. However, mystery surrounds the absence of classical actin filaments in the nucleus. To address this question, we investigated how polymerizing nuclear actin into persistent nuclear actin filaments affected transcription by RNA polymerase II. Nuclear filaments impaired nuclear actin dynamics by polymerizing and sequestering nuclear actin. Polymerizing actin into stable nuclear filaments disrupted the interaction of actin with RNA polymerase II and correlated with impaired RNA polymerase II localization, dynamics, gene recruitment, and reduced global transcription and cell proliferation. Polymerizing and crosslinking nuclear actin in vitro similarly disrupted the actin-RNA-polymerase-II interaction and inhibited transcription. These data rationalize the general absence of stable actin filaments in mammalian somatic nuclei. They also suggest a dynamic pool of nuclear actin is required for the proper localization and activity of RNA polymerase II.
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