RNF219 attenuates global mRNA decay through inhibition of CCR4-NOT complex-mediated deadenylation
The CCR4-NOT complex acts as a central player in the control of mRNA turnover and mediates accelerated mRNA degradation upon HDAC inhibition. Here, we explored acetylation-induced changes in the composition of the CCR4-NOT complex by purification of the endogenously tagged scaffold subunit NOT1 and...
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| Hauptverfasser: | , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
09 December 2021
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| In: |
Nature Communications
Year: 2021, Jahrgang: 12, Pages: 1-19 |
| ISSN: | 2041-1723 |
| DOI: | 10.1038/s41467-021-27471-6 |
| Online-Zugang: | Resolving-System, kostenfrei, Volltext: https://doi.org/10.1038/s41467-021-27471-6 Verlag, kostenfrei, Volltext: https://www.nature.com/articles/s41467-021-27471-6 
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| Verfasserangaben: | Fabian Poetz, Joshua Corbo, Yevgen Levdansky, Alexander Spiegelhalter, Doris Lindner, Vera Magg, Svetlana Lebedeva, Jörg Schweiggert, Johanna Schott, Eugene Valkov & Georg Stoecklin |
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| 520 | |a The CCR4-NOT complex acts as a central player in the control of mRNA turnover and mediates accelerated mRNA degradation upon HDAC inhibition. Here, we explored acetylation-induced changes in the composition of the CCR4-NOT complex by purification of the endogenously tagged scaffold subunit NOT1 and identified RNF219 as an acetylation-regulated cofactor. We demonstrate that RNF219 is an active RING-type E3 ligase which stably associates with CCR4-NOT via NOT9 through a short linear motif (SLiM) embedded within the C-terminal low-complexity region of RNF219. By using a reconstituted six-subunit human CCR4-NOT complex, we demonstrate that RNF219 inhibits deadenylation through the direct interaction of the α-helical SLiM with the NOT9 module. Transcriptome-wide mRNA half-life measurements reveal that RNF219 attenuates global mRNA turnover in cells, with differential requirement of its RING domain. Our results establish RNF219 as an inhibitor of CCR4-NOT-mediated deadenylation, whose loss upon HDAC inhibition contributes to accelerated mRNA turnover. | ||
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