Redefining LuxI as a metabolic gatekeeper in bacterial spoilage of refrigerated turbot by Hafnia alvei H4.

Abstract

Refrigerated seafood spoilage, a major threat to food safety and quality, is primarily driven by specific spoilage organisms whose molecular mechanisms remain insufficiently elucidated. Here, we demonstrate that Hafnia alvei H4, a dominant spoiler in turbot, accelerates spoilage by deploying a LuxI-mediated metabolic override to disrupt putrescine homeostasis. Genetic knockout studies showed that luxI deletion (ΔluxI), but not luxR, most effectively suppressed spoilage, reducing putrescine and total volatile basic nitrogen (TVB-N) by 58 % and 52 %, respectively, compared to the wild type. Regression analysis established putrescine and cadaverine as an indicator of spoilage in aquatic products, strongly correlated with TVB-N (R2 > 0.966, p < 0.05). Subsequent induction assays with ornithine/putrescine uncovered a >110 mg/L feedback inhibition threshold, while genomic analysis mapped PotE as the primary efflux transporter. Real-time transport monitoring revealed that LuxI sustains extracellular putrescine at levels exceeding 500 mg/L-far above the inhibition threshold-effectively activating proteolytic pathways. This work position LuxI as a metabolic gatekeeper and offer a mechanistic basis for novel quorum sensing-targeted strategies to mitigate seafood spoilage.