English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

MYC recruits SPT5 to RNA polymerase II to promote processive transcription elongation.

MPS-Authors
/persons/resource/persons196569

Vos,  S. M.
Department of Molecular Biology, MPI for Biophysical Chemistry, Max Planck Society;

/persons/resource/persons127020

Cramer,  P.
Department of Molecular Biology, MPI for Biophysical Chemistry, Max Planck Society;

Locator
There are no locators available
Fulltext (public)

3039175.pdf
(Publisher version), 7MB

Supplementary Material (public)

3039175_Suppl_1.pdf
(Supplementary material), 6MB

3039175_Suppl_2.xlsx
(Supplementary material), 105KB

3039175_Suppl_3.xlsx
(Supplementary material), 80KB

3039175_Suppl_4.pdf
(Supplementary material), 12MB

Citation

Baluapuri, A., Hofstetter, J., Dudvarski Stankovic, N., Endres, T., Bhandare, P., Vos, S. M., et al. (2019). MYC recruits SPT5 to RNA polymerase II to promote processive transcription elongation. Molecular Cell, 74(4), 674-687. doi:10.1016/j.molcel.2019.02.031.


Cite as: http://hdl.handle.net/21.11116/0000-0003-4A4F-3
Abstract
The MYC oncoprotein binds to promoter-proximal regions of virtually all transcribed genes and enhances RNA polymerase II (Pol II) function, but its precise mode of action is poorly understood. Using mass spectrometry of both MYC and Pol II complexes, we show here that MYC controls the assembly of Pol II with a small set of transcription elongation factors that includes SPT5, a subunit of the elongation factor DSIF. MYC directly binds SPT5, recruits SPT5 to promoters, and enables the CDK7-dependent transfer of SPT5 onto Pol II. Consistent with known functions of SPT5, MYC is required for fast and processive transcription elongation. Intriguingly, the high levels of MYC that are expressed in tumors sequester SPT5 into non-functional complexes, thereby decreasing the expression of growth-suppressive genes. Altogether, these results argue that MYC controls the productive assembly of processive Pol II elongation complexes and provide insight into how oncogenic levels of MYC permit uncontrolled cellular growth.