Journal of applied microbiology · 2026
RatA regulates growth, biofilm formation, motility, and virulence in avian pathogenic Escherichia coli.
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Yu Fangheng, Wang Mengdi, Hu Jiangang, Zuo Jiakun, Jiang Wei, Bao Yinli, Yin Huifang, Zhang Jinqiu, Xu Fazhi, Han Xiangan
Аннотация
AIMS: Avian pathogenic Escherichia coli (APEC) causes colibacillosis, incurring significant economic losses. Toxin-antitoxin (TA) systems regulate bacterial virulence, biofilm formation, and antibiotic resistance. This study focuses on RatA, a toxin characterized as a ribosomal large subunit from our Tn5 transposon mutant library biofilm screen. In the clinical isolate APEC81, ratA is co-transcribed with its putative antitoxin gene, ratB, in the ratAB operon. This study aims to characterize the function of ratA in APEC and determine if ratB affects its regulation.
METHODS AND RESULTS: We found that deletion of ratA (ΔratA and ΔratAB) significantly impaired bacterial growth, biofilm formation, and motility, while deletion of the antitoxin gene ratB had no observable effect, indicating that RatA acts independently of RatB in modulating these traits. Further analysis identified four key active sites (V34, W103, F117, F147) essential for RatA binding to coenzyme Q. Mutating these sites recapitulated the ΔratA phenotype, confirming their functional importance.In host-pathogen interactions assays, the ΔratA mutant exhibited markedly reduced adhesion and invasion in HD-11 macrophages, diminished colonization in murine tissues, and a weakened capacity to provoke host inflammatory responses.
CONCLUSION: Studies demonstrate RatA as a central virulence factor in APEC, governing multiple pathogenic traits-from bacterial fitness to host interaction. These results underscore the potential of ratA as a target for anti-virulence strategies against APEC infections.
METHODS AND RESULTS: We found that deletion of ratA (ΔratA and ΔratAB) significantly impaired bacterial growth, biofilm formation, and motility, while deletion of the antitoxin gene ratB had no observable effect, indicating that RatA acts independently of RatB in modulating these traits. Further analysis identified four key active sites (V34, W103, F117, F147) essential for RatA binding to coenzyme Q. Mutating these sites recapitulated the ΔratA phenotype, confirming their functional importance.In host-pathogen interactions assays, the ΔratA mutant exhibited markedly reduced adhesion and invasion in HD-11 macrophages, diminished colonization in murine tissues, and a weakened capacity to provoke host inflammatory responses.
CONCLUSION: Studies demonstrate RatA as a central virulence factor in APEC, governing multiple pathogenic traits-from bacterial fitness to host interaction. These results underscore the potential of ratA as a target for anti-virulence strategies against APEC infections.