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Harvesting Venom Toxins from Assassin Bugs and Other Heteropteran Insects
Published on: April 21, 2018
Toxins of toxin/antitoxin systems are inactivated primarily through promoter mutations
L Fernandez-Garcia1,2, J-S Kim3, M Tomas3
1Department of Chemical Engineering, Pennsylvania State University, University Park, PA, USA.
Aims:
Given the extreme toxicity of some of the toxins of toxin-antitoxin (TA) systems, we were curious how the cell silences toxins, if the antitoxin is inactivated or independent toxins are obtained via horizontal gene transfer.
Methods And Results:
Growth curves of Escherichia coli K12 BW25113 harbouring plasmid pCA24N to produce RalR, MqsR, GhoT or Hha toxins, showed toxin inactivation after 3 h. Sequencing plasmids from these cultures revealed toxin inactivation occurred primarily due to consistent deletions in the promoter. The lack of mutation in the structural genes was corroborated by a bioinformatics analysis of 1000 E. coli genomes which showed both conservation and little variability in the four toxin genes. For those strains that lacked a mutation in the plasmid, single nucleotide polymorphism analysis was performed to identify that chromosomal mutations iraM and mhpR inactivate the toxins GhoT and MqsR/GhoT respectively.
Conclusion:
We find that the RalR (type I), MqsR (type II), GhoT (type V) and Hha (type VII) toxins are inactivated primarily by a mutation that inactivates the toxin promoter or via the chromosomal mutations iraM and mhpR.
Significance And Impact Of The Study:
This study demonstrates toxins of TA systems may be inactivated by mutations that primarily affect the toxin gene promoter instead of the toxin structural gene.
Insights
Toxin-antitoxin (TA) systems in bacteria silence toxic proteins primarily through mutations in the toxin gene promoter, not the structural gene. This mechanism prevents cellular damage from highly toxic TA system components.
Area of Science:
- Molecular Biology
- Bacterial Genetics
- Microbial Pathogenesis
Background:
- Toxin-antitoxin (TA) systems are crucial for bacterial survival and plasmid maintenance.
- Some TA system toxins exhibit extreme toxicity, necessitating cellular control mechanisms.
- Understanding toxin inactivation is key to controlling bacterial virulence and antibiotic resistance.
Purpose of the Study:
- To investigate how bacterial cells silence highly toxic components of toxin-antitoxin (TA) systems.
- To determine if toxin inactivation involves antitoxin modification or independent toxin regulation.
- To explore the role of horizontal gene transfer in acquiring independent toxins.
Main Methods:
- Growth curve analysis of Escherichia coli strains expressing RalR, MqsR, GhoT, and Hha toxins.
- Plasmid sequencing to identify genetic alterations leading to toxin inactivation.
- Bioinformatic analysis of 1000 E. coli genomes for toxin gene conservation.
- Single nucleotide polymorphism (SNP) analysis to identify chromosomal mutations affecting toxin activity.
Main Results:
- Toxin inactivation was observed within 3 hours in E. coli expressing four different TA toxins.
- Sequencing revealed primary inactivation occurred due to deletions in the toxin gene promoter.
- Bioinformatic analysis confirmed high conservation and low variability in the toxin structural genes.
- Chromosomal mutations (iraM and mhpR) were identified as inactivating GhoT and MqsR/GhoT toxins, respectively.
Conclusions:
- RalR, MqsR, GhoT, and Hha toxins are primarily inactivated by mutations affecting their promoter regions.
- Alternatively, chromosomal mutations iraM and mhpR can inactivate specific toxins.
- This study highlights promoter mutation as a key mechanism for silencing toxic TA system components, rather than structural gene alteration.
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