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Life sciences · Journal article
Gut Microbes · August 24, 2026
Raises a question worth testing. It does not answer one.
This study identifies a single nucleotide C-to-A substitution at position –34 of the gtrABC III promoter in Salmonella Pullorum that disrupts OxyR binding and constitutively expresses a variant O-antigen phenotype. The mutation confers short-term immune evasion but is outcompeted long-term by phase-variable strains, illustrating a trade-off between transient and sustained fitness.
Experimental bacterial genetics study. Salmonella Pullorum laboratory strains; no clinical isolates or in vivo infection model specified in the text excerpt.. Intervention: Single nucleotide polymorphism (C-to-A substitution at position –34 of gtrABC III promoter) introducing constitutive variant O-antigen expression.. Compared with: Wild-type phase-variable Salmonella Pullorum strains expressing standard (O12 3) and variable (O12 2) O-antigens.. China (Hubei Academy of Agricultural Sciences, Wuhan) and Canada (Dalhousie University, Halifax); conducted in laboratory settings..
A C-to-A point substitution at position –34 of the gtrABC III promoter disrupts OxyR binding and enhances intrinsic promoter activity, resulting in constitutive expression of the variant antigenic type (O12 2). Standard type strains exhibit O-antigen phase variation and produce the O12 2 variant type during subculture at a rate of around 5% compared to O12 3. The monophasic variant strain exhibits enhanced resistance to standard-type antibody-mediated killing, conferring a short-term immune evasion advantage.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
This is a mechanistic study identifying a single nucleotide polymorphism in a promoter region and demonstrating its effect on O-antigen expression in Salmonella through in vitro and bacterial culture work, without clinical outcome data or human studies.
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The O-antigen of Salmonella is a key virulence determinant and serotype-defining structure, yet the regulatory mechanisms underlying its dynamic modification and evolutionary trade-offs remain incompletely understood. Salmonella Pullorum is a pathogen that displays both O-antigen unstable phase variation and stable antigenic conversion between standard (O123) and variant (O122) antigenic types. In this study, we identified the glycosyltransferase encoded by gtrC III as responsible for the variant-specific glucosylation of the O-antigen. The expression of gtrC III is co-regulated by the transcriptional repressor OxyR and methyltransferase Dam, generating stochastic ON‒OFF switching of the O-antigen modification, which is a classic phase variation and promotes immune evasion. Remarkably, a single C-to-A point substitution at position -34 of the gtrABC III promoter disrupts OxyR binding and simultaneously enhances intrinsic promoter activity, resulting in constitutive expression of the variant antigenic type. This monophasic variant strain exhibits enhanced resistance to standard-type antibody-mediated killing, conferring a short-term immune evasion advantage. However, in long-term colonization, it is outcompeted by the phase-variable standard type strain, exemplifying "short-sighted evolution", where an adaptive mutation trades off persistence for transient immune escape. Our findings reveal how a single nucleotide change can subvert a complex epigenetic switch to drive sub-serotype conversion, and provide insights into the evolutionary constraints shaping O-antigen diversity.
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