Woo-Jae Yoo

Gut bugs and systemic disease risk What people eat has an immediate selective effect on the microbial populations resident in the gut. A high-fat diet is associated with the occurrence of microbes that catabolize choline and the accumulation of trimethylamine N -oxide (TMAO) in the bloodstream, a contributing factor for heart disease. Yoo et al . explored the microbial organisms and pathways that convert choline into TMAO in mice. Although gene clusters for choline metabolism are found widely am

The mechanisms by which the early-life microbiota protects against environmental factors that promote childhood obesity remain largely unknown. Using a mouse model in which young mice are simultaneously exposed to antibiotics and a high-fat (HF) diet, we show that Lactobacillus species, predominant members of the small intestine (SI) microbiota, regulate intestinal epithelial cells (IECs) to limit diet-induced obesity during early life. A Lactobacillus-derived metabolite, phenyllactic acid (PLA)

The gut microbiota benefits the host by limiting enteric pathogen expansion (colonization resistance), partially via the production of inhibitory metabolites. Propionate, a short-chain fatty acid produced by microbiota members, is proposed to mediate colonization resistance against Salmonella enterica serovar Typhimurium (S. Tm). Here, we show that S. Tm overcomes the inhibitory effects of propionate by using it as a carbon source for anaerobic respiration. We determine that propionate metabolis

Inflammation boosts the availability of electron acceptors in the intestinal lumen, creating a favorable niche for pathogenic Enterobacteriaceae. However, the mechanisms linking intestinal inflammation-mediated changes in luminal metabolites and pathogen expansion remain unclear. Here, we show that mucosal inflammation induced by Salmonella enterica serovar Typhimurium (S. Tm) infection increases intestinal levels of the amino acid aspartate. S. Tm used aspartate-ammonia lyase (aspA)-dependent f

The nitrogen-metabolic phosphotransferase system, PTS(Ntr), consists of the enzymes I(Ntr), NPr and IIA(Ntr) that are encoded by ptsP, ptsO, and ptsN, respectively. Due to the proximity of ptsO and ptsN to rpoN, the PTS(Ntr) system has been postulated to be closely related with nitrogen metabolism. To define the correlation between PTS(Ntr) and nitrogen metabolism, we performed ligand fishing with EIIA(Ntr) as a bait and revealed that D-glucosamine-6-phosphate synthase (GlmS) directly interacted

Abstract Many Proteobacteria possess a nitrogen-metabolic phosphotransferase system (PTS Ntr ) consisting of EI Ntr , NPr, and EIIA Ntr (encoded by ptsP, ptsO , and ptsN , respectively). The PTS Ntr plays diverse regulatory roles, but the substrate phosphorylated by EIIA Ntr and its primary functions have not yet been identified. To comprehensively understand the roles of PTS Ntr in Salmonella Typhimurium, we compared the whole transcriptomes of wild-type and a Δ ptsN mutant. Genome-wide RNA seq

Colorectal cancer (CRC) is the second-highest cause of cancer-associated mortality among both men and women worldwide. One of the risk factors for CRC is obesity, which is correlated with a high-fat diet prevalent in Western dietary habits. The association between an obesogenic high-fat diet and CRC has been established for several decades; however, the mechanisms by which a high-fat diet increases the risk of CRC remain unclear. Recent studies indicate that gut microbiota strongly influence the

To accomplish successful infection, pathogens must operate their virulence programs in a precise, time-sensitive, and coordinated manner. A major question is how pathogens control the timing of virulence gene expression during infection. Here we report that the intracellular pathogen Salmonella controls the timing and level of virulence gene expression by using an inhibitory protein, EIIA Ntr . A DNA binding master virulence regulator, PhoP, controls various virulence genes inside acidic phagoso

Flagellar biogenesis is controlled by a negative feedback loop. When FliD was secreted at the late step of flagellar assembly, the FliD-FliT complex disassembled and free FliT bound to the FlhDC complex, a master regulator of flagellar biogenesis, subsequently inhibiting the overall expression of flagellar proteins. In this study, we analyzed the role of the FliD C-terminal domain in pentamer formation and interaction with FliT. Our study showed that the FliD L443R mutant exists as a monomer in

Microbes support their growth in vertebrate hosts by exploiting a large variety of dietary components as nutrients, which determines the composition of gut microbiota. A pathogen <i>Salmonella</i> expands by utilizing 1,2-propanediol, a microbiota-fermented product, during mucosal inflammation. However, it remains largely unknown how the pathogen decides which nutrient to consume from the complex mixture in the gut. Here, we show that <i>Salmonella enterica</i> serovar Typhimurium utilizes 1,2-p

SUMMARY Inflammation boosts the availability of electron acceptors in the intestinal lumen creating a favorable niche for pathogenic Enterobacteriaceae. However, the mechanisms linking intestinal inflammation-mediated changes in luminal metabolites and pathogen expansion remain unclear. Here, we show that mucosal inflammation induced by Salmonella enterica serovar Typhimurium ( S. Tm) infection and chemical colitis results in increased intestinal levels of the amino acid aspartate. The S. Tm and

SUMMARY The gut microbiota benefits the host by limiting enteric pathogen expansion (colonization resistance) partially via the production of inhibitory metabolites. Propionate, a short-chain fatty acid produced by microbiota members, is proposed to mediate colonization resistance against Salmonella enterica serovar Typhimurium ( S. Tm). Here, we show that S. Tm overcomes the inhibitory effects of propionate by using it as a carbon source for anaerobic respiration. We determined that propionate