Mitochondria Controlled mTORC1 Activation Compartmentalizes Translation Initiation Factor eIF4E to Augment Intracellular Trafficking and Extracellular Export of miRNA in Mammalian Cells
作者： Susanta Chatterjee , Yogaditya Chakrabarty , Saikat Banerjee , Souvik Ghosh , Suvendra N. Bhattacharyya
DOI: 10.1101/2020.05.20.105601
关键词:
摘要: Defective intracellular trafficking and export of miRNAs has been observed in senescent mammalian cells having impaired mitochondrial potential. Similar to what happens cells, Uncoupling Protein 2 mediated depolarization membrane results sequestration with polysomes restricts release through extracellular vesicles. Mitochondrial detethering endoplasmic reticulum mitochondria depolarized found be responsible for defective compartmentalization translation initiation factor eIF4E ER attached polysomes. It causes retarded process target mRNAs rER ensure reduced miRNAs. We have identified a activity mTORC1 complex cause phosphorylation eIF4E-BP1 eIF-4E targeting polysome active miRNA-repressed messages. Cumulatively, these data connects potential dynamics stability cells. Mitochondria,by complex-eIF4E axis, sub-cellular locations miRNPs regulates the protein translational machinery miRNA
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