Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1288138 | ENA |
REPOSITORIES: ENA
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Project description:In the brain, tryptophan byproducts are involved in the biosynthesis of proteins, energy-rich molecules (e.g., NAD+), and neurotransmitters (serotonin and melatonin). Impaired tryptophan catabolism, seen in aging, neurodegeneration and psychiatric diseases affects mood, learning, and sleep; however, the reasons for those impairments in elder and these ailments remain unknown. Our results from cellular, Drosophila melanogaster, and mouse models indicate that SIRT6 regulates tryptophan catabolism by balancing its usage. Mechanistically, SIRT6 regulates tryptophan and sleep quality through changes in gene expression of key genes (e.g., TDO2, AANAT), which results in elevated concentration of neurotoxic metabolites from the kynurenic pathway at the expense of serotonin and melatonin production. Such neurotoxic metabolites can affect various processes in the brain. However, by redirecting tryptophan through TDO2 inhibition in our new SIRT6-KO Drosophila model, the impairments in neuromotor behavior and vacuolar formation a parameters of neurodegeneration could be significantly reversed.
2025-10-01 | GSE309387 | GEO
Project description:Here, we employed L-tryptophan metabolomics and iTRAQ based proteomic profiling of strain JA2 to decipher the molecular response. Wherein, L-tryptophan catabolism and molecular response of strain JA2 unexpected under chemotrophic conditions. Molecular response of L-tryptophan is essential to our understanding of L-tryptophan catabolism and can be demonstrated the physiological condition of microorganisms, when organisms was exposed with aromatic compounds ever changing the environment conditions. Cellular response such as membrane protein, RND and ABC pumps implicate to efflux of aromatic compounds metabolism of tryptophan by strain JA2. Furthermore, strain JA2 feed with tryptophan 210 differentially regulated proteins related signaling, transcription couple translation, stress, membrane transport and aromatic compounds metabolism highly upregulated. L-tryptophan metabolomics and global proteomic approaches rewiring the amino acid, fatty acid, lipid and energy of cells fed with tryptophan. Aromatic amino acid metabolism proteins upregulated and sulpher containing amino acid were down regulated leading toward the adaptation of L-tryptophan feed by strain JA2.
2024-11-27 | PXD055514 | Pride
Project description:Gene arrays were used to characterize the global transcriptional alterations in skin biopsy samples of EM lesions in comparison to controls. The transcriptional pattern in EM biopsies consisted of 254 differentially regulated genes (180 induced and 74 repressed) characterized by the induction of chemokines, cytokines, Toll-like receptors, antimicrobial peptides, monocytoid cell activation markers, and numerous genes annotated as interferon (IFN)-inducible. The IFN-inducible genes included 3 transcripts involved in tryptophan catabolism (IDO1, KMO, KYNU) that play a pivotal role in immune evasion by certain other microbial pathogens by driving the differentiation of regulatory T cells. PMCID: PMC5853807
2020-07-23 | GSE154916 | GEO
Project description:Altered tryptophan catabolism has been identified in inflammatory diseases like rheumatoid arthritis (RA) and spondyloarthritis (SpA), but the causal mechanisms linking tryptophan metabolites to disease are unknown. Using the collagen-induced arthritis (CIA) model we identify alterations in tryptophan metabolism, and specifically indole, that correlate with disease. We demonstrate that both bacteria and dietary tryptophan are required for disease, and indole supplementation is sufficient to induce disease in their absence. When mice with CIA on a low-tryptophan diet were supplemented with indole, we observed significant increases in serum IL-6, TNF, and IL-1β; splenic RORγt+CD4+ T cells and ex vivo collagen-stimulated IL-17 production; and a pattern of anti-collagen antibody isotype switching and glycosylation that corresponded with increased complement fixation. IL-23 neutralization reduced disease severity in indole-induced CIA. Finally, exposure of human colon lymphocytes to indole increased expression of genes involved in IL-17 signaling and plasma cell activation. Altogether, we propose a mechanism by which intestinal dysbiosis during inflammatory arthritis results in altered tryptophan catabolism, leading to indole stimulation of arthritis development. Blockade of indole generation may present a novel therapeutic pathway for RA and SpA.
2023-11-13 | GSE241655 | GEO
Project description:SIRT6 regulates Tryptophan catabolism preventing metabolite imbalance and neurodegeneration
| PRJNA1335944 | ENA
Project description:For the establishment of synthetic microbial communities comprising complementary auxotrophic strains, transport processes for common goods are extremely important. Most auxotrophic strains reach wild type level growth with external supplementation of the required metabolite. One exception was the tryptophan auxotrophic strain Corynebacterium glutamicum ΔTRP ΔtrpP, which grew about 35% slower than the wild type in supplemented minimal medium. Corynebacterium glutamicum ΔTRP ΔtrpP lacks the whole tryptophan biosynthesis cluster (TRP) as well as the putative tryptophan transporter TrpP. We wanted to explore the role of TrpP in tryptophan transport or synthesis and to unravel the cause for the growth limitation of the auxotrophic strain.
2025-03-24 | GSE272128 | GEO
Project description:Tryptophan metabolite analysis of mouse serum by targeted LCMS.
Data are associated with publication in prep "Christensenella minuta boosts gut microbial biomass and voluntary physical activity in mice"
2023-10-10 | MSV000093077 | MassIVE
Project description:DimKYNU-1: Genetic Polymorphism and differential expression of the integral tryptophan catabolism component kynureninase
| PRJNA910938 | ENA