ArticleCommunications biology2025
Cas3 of type I-Fa CRISPR-Cas system upregulates bacterial biofilm formation and virulence in Acinetobacter baumannii.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Beyond adaptive immunity: Functional diversity of the type III-A CRISPR-Cas system inCell insight · 2026Review
- Green synthesis of ZnO/FeRSC advances · 2026Article
- AbCro, a novel transcription factor, promotes biofilm formation and virulence in Acinetobacter baumannii.BMC microbiology · 2026Article
- Comprehensive in silico analysis of Acinetobacter isolates from South Korea reveals genomic diversity, antimicrobial resistance, virulence factors, and evolutionary dynamics.Genes & genomics · 2026Article
- Emerging Multimodal Strategies for Bacterial Biofilm Eradication: A Comprehensive Review.Microorganisms · 2025Review
- Article
- Bioinformatic Identification of CRISPR-Cas Systems inPathogens (Basel, Switzerland) · 2025Article
- Exploring the additive antibacterial potential ofFrontiers in microbiology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Acinetobacter baumannii (A. baumannii) is an important pathogen causing various nosocomial infections. CRISPR-Cas system is the adaptive immune system of bacteria, which is also closely related to the drug resistance and virulence of bacteria. However, the effect and mechanism of cas3 (type I-Fa) in A. baumannii is still unclear. In this study, we successfully constructed a cas3 deletion mutant (19606Δcas3) and complemented strain (19606Δcas3/pcas3) to study the regulatory mechanism of type I-Fa cas3 on bacterial virulence. Our results showed that deletion of cas3(type I-Fa) significantly reduced the biofilm formation, virulence and pathogenicity to mice. The organ bacterial load of mice infected with cas3 deletion strain was significantly reduced, the lung inflammation was slightly changed, and the serum cytokine level was also decreased. All results demonstrated that cas3 enhanced the virulence and pathogenicity of A. baumannii. Mechanism analysis showed that deletion of cas3 can lead to the down-regulation of virulence factors such as biofilm formation related factors and outer membrane protein A(ompA). In addition, cas3 was also involved in the regulation of carbon metabolism and oxidative phosphorylation pathway of A. baumannii. Altogether, our study may provide cas3 as a therapeutic target in the future because of the close link to the virulence of A. baumannii.
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