Project description:The aim was to study the transcriptional profiling of the tdc cluster delection mutant E. faecalis V583 Δtdc (non-tyramine producer) compared to the wild type strain E. faecalis V583 (tyramine producer). We compared the expression profile of the strains grown in M17 medium with glucose as carbon source and suplemented with tyrosine.
Project description:The aim was to study the transcriptional profiling of the tdc cluster delection mutant E. faecalis V583 Î?tdc (non-tyramine producer) compared to the wild type strain E. faecalis V583 (tyramine producer). We compared the expression profile of the strains grown in M17 medium with glucose as carbon source and suplemented with tyrosine. E. faecalis V583 Î?tdc cells (test) compared with E. faecalis V583 cells (reference). Both strains grown in GM17 medium suplemented 15 mM tyrosine.
Project description:The aim was to study the transcriptional profiling of the tdc and agdi clusters delection mutant E. faecalis V583 ΔtdcΔagdi (non-tyramine non-putrescine producer) compared to the wild type strain E. faecalis V583 (tyramine producer). We compared the expression profile of the strains grown in M17 medium with glucose as carbon source and suplemented with tyrosine.
Project description:Inflammatory bowel disease (IBD) is characterized by dysbiosis of the gut microbiota and dysfunction of in testinal stem cells (ISCs). However, the direct interactions between IBD microbial factors and ISCs are unde scribed. Here, we identify α2A-adrenergic receptor (ADRA2A) as a highly expressed GPCR in ISCs. Through PRESTO-Tango screening, we demonstrate that tyramine, primarily produced by Enterococcus via tyrosine decarboxylase (tyrDC), serves as a microbial ligand for ADRA2A. Using an engineered tyrDC deficient Enterococcus faecalis strain and intestinal epithelial cell-specific Adra2a knockout mice, we show that Enterococcus-derived tyramine suppresses ISC proliferation, thereby impairing epithelial regeneration and exacerbating DSS-induced colitis through ADRA2A. Importantly, blocking the axis with an ADRA2A antagonist, yohimbine, disrupts tyramine-mediated suppression on ISCs and alleviates colitis.Our findings highlight a microbial ligand-GPCR pair in ISCs, revealing a causal link between microbial regulation of ISCs and colitis exacerbation and yielding a targeted therapeutic approach to restore ISC function in colitis.
Project description:UPLC-MS/MS data used to confirm the retention times of bile acid conjugates to GABA and tyramine that were detected in microbial culture and human fecal samples. Synthesized conjugates included here are GABA-deoxycholic acid, tyramine-deoxycholic acid, GABA-cholic acid, tyramine-cholic acid, GABA-chenodeoxycholic acid, and tyramine-chenodeoxycholic acid. Data of biological samples (B. fragilis P207 spiked with DCA, healthy human donor 11 feces, patient 207 v12 feces) from the same UPLCMS/MS sequence is included for comparison and validation. All using positive ionization.
Project description:The goal of this study is to compare the RNA expression profile of wild-type C. elegans nematodes to mutants defective in the synthesis of the biogenic amine neurotransmitters dopamine, serotonin, tyramine, and octopamine in day 2 adults.
Project description:Previously we reported that Salmonella can proliferate by deriving energy from two metabolites that naturally occur in the host as gut microbial metabolic byproducts, namely, tyramine (TYR, an aromatic amine) and D-glucuronic acid (DGA, a hexuronic acid). Salmonella Pathogenicity Island 13 (SPI-13) plays a critical role in the ability of Salmonella to derive energy from TYR and DGA, however the catabolism of these two micronutrients in Salmonella are poorly defined. The objective of this study was to identify the specific genetic components and the regulatory circuits for the construction of the TYR and DGA catabolic pathways in Salmonella. To accomplish this, we employed TYR and DGA-induced global transcriptional profiling and gene functional network analysis.
