Acquisition and erosion of toxin-antitoxin systems in bacterial chromosomes
Abstract
Toxin-antitoxin systems (TAs) are widespread in bacterial genomes. Yet, their integration, persistence, and impact in chromosome dynamics remain unclear. Here, we identified 80 type II TAs in the single chromosome of Photorhabdus laumondii TT01, 50 of which were experimentally validated. Comparative analysis across the Photorhabdus genus revealed a highly heterogeneous distribution, with TAs frequently clustering within discrete genomic regions, either alone or associated with cointegrate-forming transposases and integrases. TAs rarely clustered with other putative defense systems and are preferentially associated with different types of recombinases, suggesting distinct pathways of acquisition for the two types of functions. Functional analyses showed that most validated TAs display addictive properties and stabilize plasmids. These addictive TAs are preferentially located in genomic regions characterized by high gene turnover, consistent with recent acquisition events. Despite their plasmid-stabilizing capacity, TAs do not promote long-term conservation of their immediate chromosomal neighborhoods. Instead, we observed frequent TA loss, either through complete deletion or toxin pseudogenization, indicating relaxed selection for their persistence in bacterial lineages. We propose a stepwise model for TA evolution in bacterial chromosomes: initial acquisition mediated by mobile genetic elements, preferential integration into permissive genomic regions, subsequent genetic streamlining of linked loci, and progressive gene loss. The short-lasting linkage between TAs and their genomic neighborhoods is consistent with the view that TA modules can behave as autonomous, selfish genetic elements.
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BibTeX
@article{belot2026acquisition,
title = {{Acquisition and erosion of toxin-antitoxin systems in bacterial chromosomes}},
author = {Ludovic Belot and Amaury Payelleville and Dukas Jurėnas and Eduardo P C Rocha and Laurence van Melderen},
journal = {Molecular Biology and Evolution},
year = {2026},
month = sep,
doi = {10.1093/molbev/msag230},
url = {https://hal.science/hal-05764875v1},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Acquisition and erosion of toxin-antitoxin systems in bacterial chromosomes
AU - Ludovic Belot
AU - Amaury Payelleville
AU - Dukas Jurėnas
AU - Eduardo P C Rocha
AU - Laurence van Melderen
PY - 2026
DA - 2026/09/09
JO - Molecular Biology and Evolution
DO - 10.1093/molbev/msag230
UR - https://hal.science/hal-05764875v1
AB - Toxin-antitoxin systems (TAs) are widespread in bacterial genomes. Yet, their integration, persistence, and impact in chromosome dynamics remain unclear. Here, we identified 80 type II TAs in the single chromosome of Photorhabdus laumondii TT01, 50 of which were experimentally validated. Comparative analysis across the Photorhabdus genus revealed a highly heterogeneous distribution, with TAs frequently clustering within discrete genomic regions, either alone or associated with cointegrate-forming transposases and integrases. TAs rarely clustered with other putative defense systems and are preferentially associated with different types of recombinases, suggesting distinct pathways of acquisition for the two types of functions. Functional analyses showed that most validated TAs display addictive properties and stabilize plasmids. These addictive TAs are preferentially located in genomic regions characterized by high gene turnover, consistent with recent acquisition events. Despite their plasmid-stabilizing capacity, TAs do not promote long-term conservation of their immediate chromosomal neighborhoods. Instead, we observed frequent TA loss, either through complete deletion or toxin pseudogenization, indicating relaxed selection for their persistence in bacterial lineages. We propose a stepwise model for TA evolution in bacterial chromosomes: initial acquisition mediated by mobile genetic elements, preferential integration into permissive genomic regions, subsequent genetic streamlining of linked loci, and progressive gene loss. The short-lasting linkage between TAs and their genomic neighborhoods is consistent with the view that TA modules can behave as autonomous, selfish genetic elements.
SN - 0737-4038
SN - 1537-1719
ER -