Functional Diversity of Mitochondrial Peptidyl-tRNA Hydrolase ICT1 in Human Cells.

I.V Chicherin,M.V Patrushev,M.V Baleva,P.V Sergiev,S.V Dukhalin,P Kamenski,R.A Khannanov,S.A Levitskii

doi:10.3389/fmolb.2021.716885

I.V Chicherin, M.V Patrushev + Show 6 more

Open Access

https://doi.org/10.3389/fmolb.2021.716885

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Abstract

Mitochondria are energy producing organelles of the eukaryotic cell, involved in the synthesis of key metabolites, calcium homeostasis and apoptosis. Protein biosynthesis in these organelles is a relic of its endosymbiotic origin. While mitochondrial translational factors have homologues among prokaryotes, they possess a number of unique traits. Remarkably as many as four mammalian mitochondrial proteins possess a clear similarity with translation termination factors. The review focuses on the ICT1, which combines several functions. It is a non-canonical termination factor for protein biosynthesis, a rescue factor for stalled mitochondrial ribosomes, a structural protein and a regulator of proliferation, cell cycle, and apoptosis. Such a diversity of roles demonstrates the high functionality of mitochondrial translation associated proteins and their relationship with numerous processes occurring in a living cell.

Highlights

Energy metabolism is one of the most important processes in living systems
Mitochondria are semi-autonomous two-membrane organelles whose evolutionary ancestors were alpha-proteobacteria. Their main role is the biosynthesis of ATP, which is produced by ATP synthase during the dissipation of the gradient of H+ ions generated in a complex chain of redox reactions on the inner membrane of organelles
This review focuses on the factor ICT1 in human mitochondria

Summary

INTRODUCTION

Energy metabolism is one of the most important processes in living systems. In eukaryotic cells, it is mainly realized in the mitochondria, which are often called the “power stations” of the cell. With a decrease in ICT1, overexpression of miR-205 and miR-1301-3p leads to phenotypic manifestations similar to those observed with depletion of ICT1, for example, suppression of proliferation and migration, arrest of the cell cycle and induction of apoptosis (Tao et al, 2017; Peng et al, 2018) These consequences can be prevented by artificially increasing the expression of ICT1, which indicates antagonistic interactions of the factor with microRNAs. well as PARP (Wang et al, 2015; Lao et al, 2016; Xie et al, 2017) and Bax (Wang et al, 2015; Lao et al, 2016; Chang et al, 2017; Xie et al, 2017) cleavage. The amounts of ICT1 correlate negatively with miR1301-3p in breast cancer cells (Peng et al, 2018), miR-134 in hepatocarcinoma cells (Chang et al, 2017), and miR-205 in

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