ArticlePloS one2022
Knockout of mlaA increases Escherichia coli virulence in a silkworm infection model.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Symbiotic bacteria produce non-lytic vesicles with nucleic acid cargo.Nature communications · 2026Article
- Overexpression of Escherichia coli yaiX Confers Multidrug Resistance and Enhances Virulence in the Silkworm Infection Model.Microbiology and immunology · 2026Article
- Dual deletion of ugd and phoB Attenuates virulence and enhances vaccine potential in Aeromonas dhakensis.BMC veterinary research · 2026Article
- Virulence regulation in the fish pathogenFrontiers in cellular and infection microbiology · 2026Review
- Curli-independent defense againstMicrobiology spectrum · 2025Article
- Article
- Exploring roles of the chitinase ChiC in modulatingMicrobiology spectrum · 2024Article
- Effects of pleiotropicJournal of bacteriology · 2024Article
- Maintenance of bacterial outer membrane lipid asymmetry: insight into MlaA.BMC microbiology · 2024Review
- Genetic synergy betweenmBio · 2024Article
- Knockout ofJournal of bacteriology · 2022Article
- Experimental evolution ofFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mlaA gene encodes a lipoprotein to maintain an outer membrane lipid asymmetry in gram-negative bacteria. Although the role of mlaA in bacterial virulence has been studied in several bacterial species, there are no reports of its role in E. coli virulence. In this study, we found that knockout of mlaA in E. coli increased its virulence against silkworms. The mlaA-knockout mutant was sensitive to several antibiotics and detergents, but resistant to vancomycin and chlorhexidine. The mlaA-knockout mutant grew faster than the parent strain in the presence of silkworm hemolymph. The mlaA-knockout mutant also produced a larger amount of outer membrane vesicles than the parent strain. These findings suggest that mlaA knockout causes E. coli resistance to specific antimicrobial substances and increases outer membrane vesicle production, thereby enhancing E. coli virulence properties in the silkworm infection model.
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Registered trials
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