Large-Scale Comparison of Toxin and Antitoxins in Listeria monocytogenes.

José Antonio Agüero,Laurent Falquet,Hatice Akarsu,Lisandra Aguilar-Bultet,Anna Oevermann

doi:10.3390/toxins12010029

Abstract

Toxin–antitoxin systems (TASs) are widely distributed in prokaryotes and encode pairs of genes involved in many bacterial biological processes and mechanisms, including pathogenesis. The TASs have not been extensively studied in Listeria monocytogenes (Lm), a pathogenic bacterium of the Firmicutes phylum causing infections in animals and humans. Using our recently published TASmania database, we focused on the known and new putative TASs in 352 Listeria monocytogenes genomes and identified the putative core gene TASs (cgTASs) with the Pasteur BIGSdb-Lm database and, by complementarity, the putative accessory gene TAS (acTASs). We combined the cgTASs with those of an additional 227 L. monocytogenes isolates from our previous studies containing metadata information. We discovered that the differences in 14 cgTAS alleles are sufficient to separate the four main lineages of Listeria monocytogenes. Analyzing these differences in more details, we uncovered potentially co-evolving residues in some pairs of proteins in cgTASs, probably essential for protein–protein interactions within the TAS complex.

Highlights

Toxin–antitoxin systems (TASs) were discovered because of their involvement in a biological process called post-segregational killing (PSK), a plasmid maintenance mechanism based on two plasmid-encoded genes: a toxin gene (T) and its antagonistic antitoxin (A) [1,2,3]
By comparing with the TASmania hits we identified n = 14 core gene TASs (Table 1) and their respective alleles
The current knowledge on TASs in L. monocytogenes is rather scarce and our list included the two core gene TASs (cgTASs) already identified by TADB2

Summary

Introduction

Toxin–antitoxin systems (TASs) were discovered because of their involvement in a biological process called post-segregational killing (PSK), a plasmid maintenance mechanism based on two plasmid-encoded genes: a toxin gene (T) and its antagonistic antitoxin (A) [1,2,3]. In this context, the toxin and antitoxin are distributed in the two daughter cells; the instability of the antitoxin will lead to an active toxin killing the cell lacking the plasmid because the antitoxin cannot be replaced. TAS toxicity relies on various molecular mechanisms targeting diverse biological processes, e.g., cell membrane integrity, assembly of the translational machinery, tRNA and mRNA stability, Toxins 2020, 12, 29; doi:10.3390/toxins12010029 www.mdpi.com/journal/toxins

Methods

Results

Conclusion