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bioRxiv · 10.1101/834283

RNF219 regulates CCR4-NOT function in mRNA translation and deadenylation

Guenole, A.·Velilla, F.·Chartier, A.·Sardet, C.·Simonelig, M.·Sobhian, B.
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Abstract

Post-transcriptional regulatory mechanisms play a role in many biological contexts through the control of mRNA degradation, translation and localization. Here, we show that the uncharacterized RING finger protein RNF219 co-purifies and strongly associates with the CCR4-NOT complex, the major mRNA deadenylase in eukaryotes, that mediates translational repression in a deadenylase activity-dependent and -independent manner. Strikingly, although RNF219, inhibits the deadenylase activity of CCR4-NOT, it enhances its capacity to repress translation of a targeted mRNA, an effect of RNF219 that requires its interaction with CCR4-NOT. We propose that RNF219 is an interacting partner of the CCR4-NOT complex that switches the translational repressive activity of CCR4-NOT from a deadenylation-dependent to a deadenylation-independent mechanism.

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Guenole, A., Velilla, F., Chartier, A., Sardet, C., Simonelig, M., Sobhian, B.. 2019-11-08. RNF219 regulates CCR4-NOT function in mRNA translation and deadenylation. https://doi.org/10.1101/834283

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