NDP52 activates nuclear myosin VI to enhance RNA polymerase II transcription

Natalia Fili, Yukti Hari-Gupta, Ália dos Santos, Alexander Cook, Simon Poland, Simon M. Ameer-Beg, Maddy Parsons and Christopher P. Toseland ()
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Natalia Fili: University of Kent
Yukti Hari-Gupta: University of Kent
Ália dos Santos: University of Kent
Alexander Cook: University of Kent
Simon Poland: King’s College London
Simon M. Ameer-Beg: King’s College London
Maddy Parsons: King’s College London
Christopher P. Toseland: University of Kent

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Myosin VI (MVI) has been found to be overexpressed in ovarian, breast and prostate cancers. Moreover, it has been shown to play a role in regulating cell proliferation and migration, and to interact with RNA Polymerase II (RNAPII). Here, we find that backfolding of MVI regulates its ability to bind DNA and that a putative transcription co-activator NDP52 relieves the auto-inhibition of MVI to enable DNA binding. Additionally, we show that the MVI–NDP52 complex binds RNAPII, which is critical for transcription, and that depletion of NDP52 or MVI reduces steady-state mRNA levels. Lastly, we demonstrate that MVI directly interacts with nuclear receptors to drive expression of target genes, thereby suggesting a link to cell proliferation and migration. Overall, we suggest MVI may function as an auxiliary motor to drive transcription.

Date: 2017
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DOI: 10.1038/s41467-017-02050-w

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