Sodium L-Glutamate-Induced Physiological Changes in Lactobacillus Brevis NCL912 During GABA Production Under Acidic Conditions

Previous studies showed that γ-Aminobutyric Acid (GABA) can protect some GABA-producing bacteria against acid stress through glutamate decarboxylation. However, the acid stress mechanism is a comprehensive network related to numerous genes and proteins. Other than the Glutamate Decarboxylase (GAD)/GABA antiporter system, limited information is available about the physiological modifications that occur in Lactobacillus brevis during GABA production under acidic conditions. Therefore, this study aims to investigate the physiological modifications that occur in a GABA-producing L. brevis NCL912 during GABA production under acidic conditions. The differential protein expression of L. brevis NCL912 under different culture conditions was determined by using proteome analysis. Eleven of the protein spots were identified by mass spectrometry. Among the 11 proteins, 10 were upregulated, whereas one was downregulated. The function of downregulated protein was unknown. The upregulated proteins were involved in stress response, protein synthesis, quorum sensing, glycolysis and membrane lipid synthesis. Stress response, protein synthesis, glycolysis-related proteins are general acid stress proteins, while LuxS-dependent quorum sensing system and membrane lipid synthesis-related proteins might be induced by sodium L-glutamate during GABA production under acid stress. In conclusion, sodium L-glutamate might trigger other acid-tolerance responses, except the GAD/GABA system in L. brevis NCL912 during GABA production under acidic conditions.