Salt Stress Accelerates Tyrosine Depletion by Enterococcus lactis KUST2812: Multi-Omics Insights into Metabolic Remodeling
TL;DR
E evaluation in BBP fermentation suggested that E. lactis KUST2812 may reduce tyrosine accumulation without causing a significant increase in tyramine, and coordinated responses involving the Na+/H+ antiporter system, compatible solute transporters, and oxidative stress markers contributed to the metabolic basis for salt adaptation of this strain.
Abstract
Enterococcus lactis KUST2812 is a halotolerant strain isolated from broad bean paste (BBP). It shows strong potential as a safe fermentation starter due to its high survival rate (98.32% in 18% NaCl), absence of hemolytic activity, and susceptibility to clinically relevant antibiotics, with resistance limited to intrinsic traits. Growth and metabolic dynamics suggest that salt stress decouples growth from tyrosine catabolism: while 6% NaCl significantly inhibited bacterial cell growth, tyrosine depletion occurred within 12 h under 6% NaCl, compared with the 96 h required under non-saline conditions. Multi-omics analyses suggest a molecular network associated with this tyrosine conversion under salt stress. Two tyrosine decarboxylase genes (tdc) were upregulated by 1.85- and 6.50-fold, respectively. The tyrosine-specific transporter gene tyrP was upregulated 4.99-fold, and the protein synthesis-associated gene tyrS was upregulated 4.93-fold. These changes collectively support a diversified tyrosine utilization strategy of E. lactis KUST2812. Moreover, coordinated responses involving the Na+/H+ antiporter system, compatible solute transporters, and oxidative stress markers contributed to the metabolic basis for salt adaptation of this strain. Evaluation in BBP fermentation suggested that E. lactis KUST2812 may reduce tyrosine accumulation without causing a significant increase in tyramine. These findings offer a potential microbial resource and a theoretical basis for managing tyrosine-related quality issues in fermented foods.
