NDP52 activates nuclear myosin VI to enhance RNA polymerase II transcription.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 29187741.
- Also identified by DOI 10.1038/s41467-017-02050-w and PMC identifier 5707354.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Cell Nucleus
- DNA
- Myosin Heavy Chains
- Nuclear Proteins
- Protein Folding
- RNA Polymerase II