Characterization of a Novel Quorum Quencher Acinetobacter schindleri Strain XJ-10: AHL Degradation Capability, Metabolic Pathways and Its Role in Soft Rot Disease Biocontrol
Quorum sensing (QS) is critically involved in mediating microbial interactions and serves as a central regulatory mechanism in bacterial pathogenesis. As an emerging countermeasure, quorum quenching (QQ) suppresses QS-regulated virulence through enzymatic or chemical disruption of signal systems. N-acyl homoserine lactone (AHL), an evolutionarily conserved QS signal, coordinates the pathogenicity of multiple plant pathogens, particularly Dickeya zeae, which causes soft rot disease in various crops and leads to substantial agricultural losses. In this study, the QQ strain Acinetobacter schindleri XJ-10 was evaluated for its capacity to degrade AHL and attenuate the pathogenicity of D. zeae EC1 in host plants. Notably, strain XJ-10 exhibited efficient AHL degradation at 0.2 mmol/L within 24 h, achieving a degradation efficiency of 98.80%. Subsequently, gas chromatography–mass spectrometry (GC-MS) analysis identified N-hexanoyl-L-homoserine lactone and propanamide as key intermediates during AHL degradation, confirming complete mineralization to CO2 and H2O. Based on the structural characterization of AHL and its intermediates, the metabolic pathway within strain XJ-10 was proposed. The degradation pathway initiates with the hydrolysis of the ester ring of N-hexanoyl-L-homoserine lactone, generating N-hexanoyl-L-homoserine. Subsequent carbon–nitrogen bond scission is predicted to yield N-cyclohexyl-propanamide, which is further catabolized to produce hexanamide and propanamide. Furthermore, strain XJ-10 exhibited biocontrol activity against soft rot disease affecting potato (Solanum tuberosum), radish (Raphanus sativus), and Chinese cabbage (Brassica rapa subsp. pekinensis), as its crude enzyme extract effectively reduced disease incidence and severity in planta. While strain XJ-10 showed no detectable acylase activity, it exhibited significant degradation activity against AHL, suggesting a distinct QQ mechanism. Collectively, these findings broaden the scope of QQ-based biocontrol strategies and enhance mechanistic insights into managing bacterial diseases through QS modulation.