VEGF amplifies transcription through ETS1 acetylation to enable angiogenesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Jiahuan Chen, Yi Fu, Daniel S. Day, Ye Sun, Shiyan Wang, Xiaodong Liang, Fei Gu, Fang Zhang, Sean M. Stevens, Pingzhu Zhou, Kai Li, Yan Zhang, Ruei-zeng Lin, Lois E. H. Smith, Jin Zhang, Kun Sun, Juan M. Melero-Martin, Zeguang Han, Peter J. Park, Bing Zhang, William T. Pu

ABSTRACT

Release of promoter-proximally paused RNA polymerase II (RNAPII) is a recently recognized transcriptional regulatory checkpoint. The biological roles of RNAPII pause release and the mechanisms by which extracellular signals control it are incompletely understood. Here we show that VEGF stimulates RNAPII pause release by stimulating acetylation of ETS1, a master endothelial cell transcriptional regulator. In endothelial cells, ETS1 binds transcribed gene promoters and stimulates their expression by broadly increasing RNAPII pause release. 34 VEGF enhances ETS1 chromatin occupancy and increases ETS1 acetylation, enhancing its binding to BRD4, which recruits the pause release machinery and increases RNAPII pause release. Endothelial cell angiogenic responses in vitro and in vivo require ETS1-mediated transduction of VEGF signaling to release paused RNAPII. Our results define an angiogenic pathway in which VEGF enhances ETS1-BRD4 interaction to broadly promote RNAPII pause release and drive angiogenesis.Promoter proximal RNAPII pausing is a rate-limiting transcriptional mechanism. Chen et al. show that this process is essential in angiogenesis by demonstrating that the endothelial master transcription factor ETS1 promotes global RNAPII pause release, and that this process is governed by VEGF. More... »

PAGES

383

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-017-00405-x

    DOI

    http://dx.doi.org/10.1038/s41467-017-00405-x

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1091331666

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28851877


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