Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Jun 4;8:372. doi: 10.3389/fcell.2020.00372

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2020 Ravanidis and Doxakis.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Mitochondrial perturbations induced by PUM2. PUM2 reduces cytochrome c oxidase complex (Complex IV) activity, leading to impaired respiration and deformed cristae. Interestingly, the long non-coding RNA NORAD inhibits PUM2 function by sequestering PUM2 from binding to mitochondrial mRNA targets. Further, PINK1 in association with Tom20 promote the expression of nuclear-encoding mitochondrial (nRCC) mRNAs in the outer mitochondrial membrane by competing with PUM and other translation repressors. PINK1 competes with PUM for mRNA-binding, while PRKN mono-ubiquitinates PUM and HNRNPF lowering their affinity for nRCC mRNAs and possibly leading to their proteasomal degradation. However, when PUM is in excess, it binds to the nRCC mRNAs and represses their translation. Finally, PUM2 binds to MFF mRNA and represses its translation, leading to reduced fission and mitophagy.