RNF219 regulates CCR4-NOT function in mRNA translation and deadenylation

被引:4
作者
Guenole, Aude [1 ]
Velilla, Fabien [1 ]
Chartier, Aymeric [2 ]
Rich, April [3 ]
Carvunis, Anne-Ruxandra [3 ]
Sardet, Claude [1 ]
Simonelig, Martine [2 ]
Sobhian, Bijan [1 ,2 ]
机构
[1] Univ Montpellier, Inst Reg Canc Montpellier ICM, INSERM, Inst Rech Cancerol Montpellier IRCM, F-34298 Montpellier, France
[2] Univ Montpellier, Inst Genet Humaine, CNRS, F-34396 Montpellier, France
[3] Univ Pittsburgh, Sch Med, Pittsburgh Ctr Evolutionary Biol & Med, Dept Computat & Syst Biol, Pittsburgh, PA 15213 USA
关键词
GERM-CELLS; COMPLEX; REVEALS; REPRESSION; PROTEINS; CAF1; DEGRADATION; MICRORNA; INITIATION; INSIGHTS;
D O I
10.1038/s41598-022-13309-8
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 RING finger protein RNF219 co-purifies with the CCR4-NOT complex, the major mRNA deadenylase in eukaryotes, which mediates translational repression in both a deadenylase activity-dependent and -independent manner. Strikingly, RNF219 both inhibits the deadenylase activity of CCR4-NOT and enhances its capacity to repress translation of a target mRNA. We propose that the interaction of RNF219 with the CCR4-NOT complex directs the translational repressive activity of CCR4-NOT to a deadenylation-independent mechanism.
引用
收藏
页数:17
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