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Trimethylamine oxide is a new plant signaling molecule that mediates abiotic stress tolerance

ABSTRACT: Trimethylamine oxide is a new plant signaling molecule that mediates abiotic stress tolerance

PROVIDER: PRJNA603806 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10987231.fastq.gz	Fastqsanger.gz
	SRR10987232.fastq.gz	Fastqsanger.gz

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Similar Datasets

Trimethylamine oxide is a new plant signaling molecule that mediates abiotic stress tolerance

Project description:We report the identification of RCI5, an Arabidopsis cold inducible gene encoding a FMO. RCI5 seems to participate in the biosynthesis of TMAO, a new plant methabolite. We also demonstrate that TMAO positevely controls Arabidopsis tolerance to low temperature, high salt in the soil and drough stress, by promoting a wide transcriptomic reprograming of stress-relate genes. Finally, we found that diferent crops also contain TMAO in their tissues, and that exogenous applications of TMAO also increases tomato tolerance to abiotic stress.

2021-05-26 | GSE144502 | GEO

Trimethylamine N-oxide impairs β-cell function and glucose tolerance

Project description:Trimethylamine N-oxide impairs β-cell function and glucose tolerance

| PRJNA1016338 | ENA

Trimethylamine N-oxide impairs β-cell function and glucose tolerance

Project description:β-Cell dysfunction, manifested as impaired glucose-stimulated insulin secretion (GSIS), and β-cell loss, which presents as dedifferentiation, inhibited transcriptional identity and death, are the hallmarks of type 2 diabetes. Trimethylamine N-oxide (TMAO), a gut microbiota metabolite, has been shown to play a role in cardiovascular disease. Here, we found that plasma TMAO levels are elevated in both diabetic mice and human subjects and that TMAO at a similar concentration to that found in diabetes could directly decrease β-cell GSIS in both MIN6 cells and primary islets from mice or humans. Elevation of TMAO levels through choline diet feeding impairs GSIS, the β-cell proportion, and glucose tolerance. TMAO inhibits calcium transients through NLRP3 inflammasome-related inflammatory cytokines and induced Serca2 loss, and a Serca2 agonist reversed the effect of TMAO on β-cell function in vitro and in vivo. Additionally, long-term TMAO exposure promotes β-cell ER stress, dedifferentiation, and apoptosis and inhibits β-cell transcriptional identity. Inhibition of TMAO production through either genetic knockdown or antisense oligomers of Fmo3, the TMAO-producing enzyme, improves β-cell GSIS, the β-cell proportion, and glucose tolerance in both db/db and choline diet-fed mice. These observations elucidate a novel role for TMAO in β-cell dysfunction and maintenance, and inhibition of TMAO could be a new approach for the treatment of type 2 diabetes.

2024-02-23 | GSE243083 | GEO

Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

Project description:Trimethylamine N-oxide (TMAO), a metabolite derived from intestine microbial flora, enhances vascular inflammation in a variety of cardiovascular disease, and the bacterial communities associated with trimethylamine N-oxide (TMAO) metabolism is higher in pulmonary hypertension (PH) patients. The effects of TMAO on PH, however, has not been elucidated. In the present study, we found that circulating TMAO is elevated in intermediate to high-risk PH patients when compared to healthy control or low-risk PH patients. In monocrotaline-induced rat PH models, circulating TMAO is elevated; and reduction of TMAO using 3,3-dimethyl-1-butanol (DMB) significantly decreased right ventricle systolic pressure, pulmonary vascular muscularization in both monocrotaline-induced rat PH and hypoxia induced mice PH models. RNA sequencing of rat lungs on DMB revealed significant suppression of pathways involved in cytokine-cytokine receptor interaction, and cytokine and chemokine signaling. Protein-protein interaction analysis of the differentially expressed transcripts regulated by DMB showed 5 hub genes with a strong connectivity of proinflammatory cytokines and chemokines including Kng1, Cxcl1, Cxcl2, CxcL6 and Il6. In vivo, TMAO significantly increased the expression of Kng1, Cxcl1, Cxcl2, CxcL6 and Il6 in bone marrow derived macrophage. And TMAO-treated conditioned medium from macrophage increased the proliferation and migration of pulmonary artery smooth muscle cells; but TMAO treatment did not change the proliferation or migration of pulmonary artery smooth muscle cells. In conclusion, our study demonstrates that TMAO is increased in severe PH, and the reduction of TMAO using DMB reduces pulmonary vascular muscularization and alleviates PH via suppressing the macrophage production of chemokines and cytokines.

2022-06-07 | GSE190203 | GEO

Time-dependent specific molecular signatures of inflammation and remodelling are associated with Trimethylamine-N-oxide (TMAO)-induced endothelial cell dysfunction

Project description:Cardiovascular diseases (CVDs) are leading causes of death worldwide. Endothelial dysfunction is a critical initiating factor contributing to CVDs, which progression involves the gut microbiome-derived metabolite Trimethylamine N-oxide (TMAO). Here, we aim to clarify the time-dependent pathways by which TMAO mediates endothelial dysfunction.

2023-11-23 | GSE235204 | GEO

Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

Project description:Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

| PRJNA786337 | ENA

Trimethylamine <i>N</i>-oxide is a new plant molecule that promotes abiotic stress tolerance.

Project description:Trimethylamine N-oxide (TMAO) is a well-known naturally occurring osmolyte in animals that counteracts the effect of different denaturants related to environmental stress and has recently been associated with severe human chronic diseases. In plants, however, the presence of TMAO has not yet been reported. In this study, we demonstrate that plants contain endogenous levels of TMAO, that it is synthesized by flavin-containing monooxygenases, and that its levels increase in response to abiotic stress conditions. In addition, our results reveal that TMAO operates as a protective osmolyte in plants, promoting appropriate protein folding and as an activator of abiotic stress-induced gene expression. Consistent with these functions, we show that TMAO enhances plant adaptation to low temperatures, drought, and high salt. We have thus uncovered a previously unidentified plant molecule that positively regulates abiotic stress tolerance.

| S-EPMC8133759 | biostudies-literature

Next Generation Sequencing of TMAO (Trimethylamine N-oxide)-treated Cardiac Transcriptomes

Project description:Next Generation Sequencing of TMAO (Trimethylamine N-oxide)-treated Cardiac Transcriptomes

| PRJNA532642 | ENA

RNA-seq of mouse brain tissue to investigate the integrity of the blood brain barrier to trimethylamine N-oxide

Project description:In vivo work done to determine how trimethylamine N-oxide (TMAO) affects integrity of the blood-brain barrier. Wild-type male C57Bl/6 mice were injected with saline or TMAO (1.8 mg/kg in saline), and killed 2 h after injection. Mice were transcardially perfused with 0.9% saline at 4 °C to remove circulating blood, and brains were removed and collected into RNAlater. Whole brain total RNA was extracted using a PureLink RNA Mini Kit. RNA samples (n=3 TMAO, n=3 control) were sent to Macrogen Inc. (Republic of Korea) where they were subject to quality checks (RIN analysis), library prep and sequencing [TruSeq Stranded mRNA LT Sample Prep Kit; paired-end (2x 100 nt) sequencing; Illumina HiSeq 4000].

2020-12-19 | E-MTAB-9869 | biostudies-arrayexpress

Gut-Derived Metabolite Trimethylamine N-Oxide Promotes Inflammation and Fibrosis Following Ischemia/Reperfusion through CCR2-Mediated Macrophage Infiltration

Project description:Inflammation plays a crucial role in the development of acute kidney injury (AKI) and subsequent chronic kidney disease (CKD) following renal ischemia-reperfusion (IR). It has been demonstrated that metabolites from the gut microbiota can trigger inflammatory responses and modulate renal damage induced by IR. However, the exact driving factors and underlying mechanisms of this process remain unclear. Trimethylamine N-oxide (TMAO), a choline metabolite derived from the gut, has been observed to increase in AKI and CKD patients. Our study reveals that glycyrrhizic acid (GA) exacerbates IR-induced AKI and subsequent CKD through TMAO. To delve into the underlying mechanisms, we employed single-cell sequencing to construct a molecular map of kidney cells.

2024-09-09 | GSE244890 | GEO

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