Proteomics

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The 3’-UTR of MYC couples RNA polymerase II function to ribonucleotide levels


ABSTRACT: Deregulated expression of MYC enhances glutamine utilization and renders cell survival dependent on glutamine, inducing “glutamine addiction”. Surprisingly, colon cancer cells that express high levels of MYC due to WNT pathway mutations, are not glutamine-addicted but undergo a reversible cell cycle arrest upon glutamine deprivation. We show here that glutamine deprivation suppresses translation of endogenous MYC via the 3’-UTR of the MYC mRNA, enabling escape from apoptosis. This regulation is mediated by glutamine-dependent changes in adenosine nucleotide levels. Glutamine deprivation causes a global reduction in promoter association of RNA Polymerase II (RNAPII) and slows transcriptional elongation. While activation of MYC restores binding of MYC and RNAPII function on most promoters, restoration of elongation is imperfect and activation of MYC in the absence of glutamine causes stalling of RNAPII on multiple genes, correlating with R-loop formation. Stalling of RNAPII and R-loop formation can cause DNA damage, arguing that the MYC 3’-UTR is critical for maintaining genome stability when ribonucleotide levels are low.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Colon

DISEASE(S): Colon Cancer

SUBMITTER: Jens Vanselow  

LAB HEAD: Andreas Schlosser

PROVIDER: PXD005829 | Pride | 2022-02-28

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
2017-01-24-velos_16641.raw Raw
2017-01-24-velos_16642.raw Raw
2017-01-24-velos_16643.raw Raw
2017-01-24-velos_16644.raw Raw
2017-01-24-velos_16645.raw Raw
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