Effects of Tetracycline Susceptibility and Virulence in an acrR Mutant of Erwinia amylovora.
- 1Interdisciplinary Program in Smart Agriculture, Kangwon National University, Chuncheon 24341, Republic of Korea.
- 2Plant Medicine Program, Division of Bioresource Sciences, College of Agriculture and Life Sciences, Kangwon National University, Chuncheon 24341, Republic of Korea.
Abstract
This study investigated whether AcrR-mediated regulation of the acrAB efflux system is associated with tetracycline susceptibility in Erwinia amylovora. We compared tetracycline susceptibility, acrAB expression, intracellular tetracycline accumulation, intracellular pH, ATP-associated luminescence, envelope-associated phenotypes, virulence, and responses to exogenous acyl-homoserine lactones (AHLs) among the wild type (WT), an acrR mutant (ΔacrR), the same mutant after prior tetracycline exposure (ΔacrRTc), and an acrR-complemented mutant (ΔacrR(acrR)). Relative to WT, ΔacrR showed fourfold increases in tetracycline MIC and MBC, whereas ΔacrRTc showed 16- and 32-fold increases, respectively. ΔacrRTc also showed markedly increased acrA and acrB expression, reduced intracellular tetracycline accumulation, lower intracellular pH, and reduced ATP-associated luminescence, suggesting that prior tetracycline exposure was associated with an enhanced AcrAB response in the acrR-deficient background. ΔacrRTc further displayed altered cell-envelope ultrastructure, increased waaL expression and lipopolysaccharide (LPS)-associated band intensity, reduced biofilm formation, and a weaker cellulose-associated colony phenotype, whereas amylovoran production and levansucrase-associated activity remained unchanged. In the pathogenicity assay, ΔacrRTc produced weaker necrotic symptoms, lower bacterial populations, and reduced in planta dspE expression. Among the AHLs tested, OHHL produced a distinct virulence pattern, with ΔacrR showing reduced disease severity relative to WT and ΔacrR(acrR), whereas this separation was not observed with HHL or OOHL; ΔacrRTc remained less virulent under all AHL conditions. These findings support tetracycline as an AcrAB substrate and suggest that prior tetracycline exposure can strengthen the subsequent AcrAB-associated response. The OHHL-specific phenotype further raises the possibility that OHHL may also serve as a substrate of the AcrAB efflux system.
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BibTeX
@article{choi2026effects,
title = {{Effects of Tetracycline Susceptibility and Virulence in an acrR Mutant of Erwinia amylovora.}},
author = {Jeong Ho Choi and Yeon Ju Kim and Hyun Ju Choi and Duck Hwan Park},
journal = {Journal of microbiology and biotechnology},
year = {2026},
month = oct,
doi = {10.4014/jmb.2608.08022},
url = {https://europepmc.org/article/MED/42861460},
note = {CC BY},
}
RIS
TY - JOUR
TI - Effects of Tetracycline Susceptibility and Virulence in an acrR Mutant of Erwinia amylovora.
AU - Jeong Ho Choi
AU - Yeon Ju Kim
AU - Hyun Ju Choi
AU - Duck Hwan Park
PY - 2026
DA - 2026/10/07
JO - Journal of microbiology and biotechnology
DO - 10.4014/jmb.2608.08022
UR - https://europepmc.org/article/MED/42861460
AB - This study investigated whether AcrR-mediated regulation of the acrAB efflux system is associated with tetracycline susceptibility in Erwinia amylovora. We compared tetracycline susceptibility, acrAB expression, intracellular tetracycline accumulation, intracellular pH, ATP-associated luminescence, envelope-associated phenotypes, virulence, and responses to exogenous acyl-homoserine lactones (AHLs) among the wild type (WT), an acrR mutant (ΔacrR), the same mutant after prior tetracycline exposure (ΔacrRTc), and an acrR-complemented mutant (ΔacrR(acrR)). Relative to WT, ΔacrR showed fourfold increases in tetracycline MIC and MBC, whereas ΔacrRTc showed 16- and 32-fold increases, respectively. ΔacrRTc also showed markedly increased acrA and acrB expression, reduced intracellular tetracycline accumulation, lower intracellular pH, and reduced ATP-associated luminescence, suggesting that prior tetracycline exposure was associated with an enhanced AcrAB response in the acrR-deficient background. ΔacrRTc further displayed altered cell-envelope ultrastructure, increased waaL expression and lipopolysaccharide (LPS)-associated band intensity, reduced biofilm formation, and a weaker cellulose-associated colony phenotype, whereas amylovoran production and levansucrase-associated activity remained unchanged. In the pathogenicity assay, ΔacrRTc produced weaker necrotic symptoms, lower bacterial populations, and reduced in planta dspE expression. Among the AHLs tested, OHHL produced a distinct virulence pattern, with ΔacrR showing reduced disease severity relative to WT and ΔacrR(acrR), whereas this separation was not observed with HHL or OOHL; ΔacrRTc remained less virulent under all AHL conditions. These findings support tetracycline as an AcrAB substrate and suggest that prior tetracycline exposure can strengthen the subsequent AcrAB-associated response. The OHHL-specific phenotype further raises the possibility that OHHL may also serve as a substrate of the AcrAB efflux system.
SN - 1017-7825
SN - 1738-8872
ER -