The Structural and Molecular Mechanisms of Mycobacterium tuberculosis Translational Elongation Factor Proteins

TL;DR

This paper reviews how specific proteins in tuberculosis bacteria help with protein production and could be targets for new drugs.

Contribution

The paper provides a detailed review of the structural and molecular mechanisms of Mtb translation elongation factors as potential drug targets.

Findings

Translation elongation factors EF-Tu, EF-Ts, and EF-G are essential for Mtb's ribosome rescue mechanisms.

These proteins are absent in eukaryotes, making them promising targets for anti-tuberculosis drugs.

Structure-based computational methods are being used to study potential drugs targeting these proteins.

Abstract

Targeting translation factor proteins holds promise for developing innovative anti-tuberculosis drugs. During protein translation, many factors cause ribosomes to stall at messenger RNA (mRNA). To maintain protein homeostasis, bacteria have evolved various ribosome rescue mechanisms, including the predominant trans-translation process, to release stalled ribosomes and remove aberrant mRNAs. The rescue systems require the participation of translation elongation factor proteins (EFs) and are essential for bacterial physiology and reproduction. However, they disappear during eukaryotic evolution, which makes the essential proteins and translation elongation factors promising antimicrobial drug targets. Here, we review the structural and molecular mechanisms of the translation elongation factors EF-Tu, EF-Ts, and EF-G, which play essential roles in the normal translation and ribosome rescue mechanisms of Mycobacterium tuberculosis (Mtb). We also briefly describe the structure-based, computer-assisted study of anti-tuberculosis drugs.

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