Type VI secretion system completeness shapes evolutionary trade-offs in the Acinetobacter baumannii resistome
Meng Zhang1, Shuang Wang1, Jinying Gao1
1State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Department of Respiratory Medicine, Center of Pathogen Biology and Infectious Diseases, The First Hospital of Jilin University, Changchun, China.
The Type VI Secretion System (T6SS) influences how multidrug-resistant Acinetobacter baumannii acquires resistance genes. T6SS-complete bacteria utilize chromosomal resistance, while T6SS-incomplete ones acquire external potent genes.
Area of Science:
- Microbiology
- Genomics
- Evolutionary Biology
Background:
- Multidrug-resistant Acinetobacter baumannii is a global public health threat.
- The Type VI Secretion System (T6SS) is an interbacterial weapon, but its role in antimicrobial resistance is unclear.
Purpose of the Study:
- To investigate the association between T6SS completeness and the organization of antimicrobial resistance genes (ARGs) in A. baumannii.
- To understand the distinct resistance acquisition strategies employed by T6SS-complete and T6SS-incomplete strains.
Main Methods:
- Integrated clinical metagenomics and large-scale comparative genomics.
- Analyzed the association between T6SS status and ARG burden, diversity, and composition.
- Performed experimental validation of T6SS-dependent killing.
Main Results:
- T6SS completeness was not linked to overall ARG burden but was associated with distinct resistome composition.
- T6SS-complete genomes showed enrichment in chromosomal resistance determinants and tighter ARG-mobile genetic element (MGE) co-localization.
- TSS-incomplete genomes were enriched in potent exogenously acquired ARGs, often with uncoupled MGEs.
Conclusions:
- A. baumannii populations exhibit distinct resistance acquisition strategies based on T6SS status.
- An evolutionary trade-off model explains divergent resistome organization and horizontal gene transfer contexts.
- Findings highlight the complex interplay between T6SS and the genomic landscape of antimicrobial resistance.
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