ArticlePloS one2025
CRISPR/Cas9-targeted smpB mutation revealing roles in biofilm formation, motility, and antibiotic susceptibility in Acinetobacter baumannii.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- CRISPR-Cas systems as next-generation antimicrobials: a systemic review of mechanisms, delivery strategies, and translational challenges.Frontiers in microbiology · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcinetobacter baumannii is a multidrug-resistant pathogen and a major cause of hospital-acquired infections worldwide. Its ability to survive in harsh environments and evade antibiotic treatments underscores the urgent need for new therapeutic targets. Emerging evidence suggests that the small protein B (SmpB) may also play broader roles in bacterial virulence, including regulation of biofilm formation, motility, and stress adaptation. However, the specific contributions of SmpB to these pathogenic traits in A. baumannii remain poorly defined. Addressing this knowledge gap is essential for evaluating SmpB as a potential antimicrobial target and developing new strategies to combat multidrug-resistant infections.
methodsCRISPR/Cas9-mediated gene editing was used to generate a targeted smpB mutant in A. baumannii. The smpB mutant was assessed for growth, biofilm formation, motility, antibiotic susceptibility, and virulence. Biofilm was quantified via crystal violet staining and microscopy, while motility was examined using swimming, swarming, and twitching assays. Antibiotic susceptibility was evaluated using disk diffusion. Virulence was tested in the Galleria mellonella infection model. Proteomic analysis was performed to identify changes in protein expression associated with smpB disruption.
resultsCRISPR/Cas9-mediated editing successfully introduced a C212T nucleotide substitution in the smpB gene, resulting in an A89G amino acid change. Growth curve analysis showed no significant difference between the wild-type and smpB mutant strains under nutrient-rich conditions. However, the mutant exhibited a significant reduction in biofilm formation (p = 0.0079) and impaired twitching motility, while swimming and swarming motility remained unaffected. Antibiotic susceptibility testing revealed increased sensitivity to ceftizoxime, piperacillin/tazobactam, and gentamicin, alongside decreased susceptibility to cefepime, tetracycline, and spectinomycin. In the G. mellonella infection model, the smpB mutant showed reduced virulence, with 84% larval survival compared to 72% in the wild type (p = 0.4183). Proteomic analysis revealed downregulation of key stress response and virulence-associated proteins, including GroEL, DnaK, RecA, and PirA, while proteins involved in ribosome maturation and transcription, such as RimP and RpoA, were upregulated. STRING network analysis supported the broad regulatory role of SmpB in biofilm formation, motility, stress adaptation, and pathogenesis.
conclusionThis study demonstrates that SmpB is a key regulator of biofilm formation, twitching motility, antibiotic response, and virulence in A. baumannii. While not essential for growth under optimal conditions, smpB disruption impairs multiple pathogenic traits and alters stress-related proteomic pathways. These findings highlight the potential of SmpB as a novel antimicrobial target, offering a promising strategy to weaken bacterial virulence without promoting resistance. Targeting the trans-translation system may pave the way for innovative therapies against multidrug-resistant A. baumannii.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.