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Taurocholate acid signals a specific gene expression reprogramming affecting amino-acids and nucleotides metabolisms

ABSTRACT: Taurocholate acid signals a specific gene expression reprogramming affecting amino-acids and nucleotides metabolisms

PROVIDER: PRJNA798735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17665448.fastq.gz	Fastqsanger.gz
	SRR17665449.fastq.gz	Fastqsanger.gz
	SRR17665450.fastq.gz	Fastqsanger.gz
	SRR17665451.fastq.gz	Fastqsanger.gz
	SRR17665452.fastq.gz	Fastqsanger.gz

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Taurocholate acid signals a specific gene expression reprogramming affecting amino-acids and nucleotides metabolisms

Project description:Enterococcus faecalis is a natural inhabitant of the human gastrointestinal tract. In a healthy physiological state of the gut (eubiosis), E. faecalis is a subdominant species in the intestinal microbiota. When the intestinal homeostasis is disrupted (dysbiosis), it becomes dominant species and can cause infections. The taurocholate bile acid (TCA) becomes prominent during dysbiosis. This experiment aimed to better understand how E. faecalis adapts to TCA. We showed that TCA reprograms genes involved in the pool management of amino acids and nucleotides.

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Response of Candida albicans to taurocholate

Project description:Presence of taurocholate (TC), a constituent of bile, confers resistance of Candida albicans to antifungals like Caspofungin and Amphotericin B. Transcriptional profiles in presence and absence of TC were compared to determine whether an upregulation of known resistance genes is responsible for this effect. No upregulation was found, and the resistance seemed to be rather based on a direct interaction of TC with the antifungals.

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Increased sulfation of bile acids in mice and human subjects with sodium taurocholate cotransporting polypeptide deficiency

Project description:Purpose: To decipher the biochemical basis for the declining of total bile acids (TBA) levels in the late age of Slc10a1-/- mice, we performed a serial liver RNA-Seq analysis of mRNA expression with male mice at different ages. Methods: Liver mRNA profiles of 4-week, 8-week, 20-month-old wild-type (WT) and sodium taurocholate cotransporting polypeptide knockout (Slc10a1-/-) mice were generated by deep sequencing, in triplicate, quadruplicate or sextuplicate, using Illumina Hiseq-2500 platform. Clean mRNA-seq reads were aligned to the mouse reference genome (GRCm38) with TopHat (v2.0.13), guided by Ensembl gene annotation v83. Only uniquely aligned and properly paired reads were retained for further analysis. Gene-level read counts were calculated with HTseq (v0.6.1p1) with the union mode. Genes with less than a total of 11 non-normalized reads across all samples were excluded. Data normalization and statistical analysis of differential expression were performed with the DEseq2 (v1.10.0) R package. Pair-wise Spearman correlation between samples across all quantified genes used for hierarchical clustering. Results: At 4 weeks and 8 weeks, WT and Slc10a1-/- mice exhibited clear different pattern in terms of transcriptome similarity and were well separated, however, the difference was indistinguishable at 20 months.And changes of pathways involved in the metabolism of xenobiotics in Slc10a1-/- mice. Conclusions: Our study reveal that enhanced BA sulfation is a major mechanism for BA detoxification and elimination in Slc10a1-/- mice with hypercholanemia.

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Nucleotides affect zebrafish microbiota

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Project description:Contrasted effects of deoxycholate and taurocholate bile acids on the gut pathobiont Enterococcus faecalis

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Project description:Acute pancreatitis (AP) is a common digestive disorder with high morbidity and mortality. At present, the pathogenic mechanisms of AP remain unclear. Pancreatic acinar intracellular trypsinogen activation is considered to be an important cause of AP and is an important event in the early stages of AP. The activation of trypsinogen is a key factor for the pancreas to maintain normal function and that the abnormal activation of trypsinogen in pancreatic acinar cells is an initiating factor for the occurrence of AP. In the past decade, microRNA-related research results suggest that small non-coding RNAs play an important role in AP. Recently, endogenous transfer RNA-derived small RNA (tsRNA), a newly identified non-coding small RNA, is reported to be associated with multiple diseases. tsRNAs can be broadly classified into two main groups: tiRNAs (tRNA halves) and tRFs (tRNA-derived fragments). tiRNAs are produced by specific cleavage in the anticodon loop under various stress conditions (29-50 nucleotides). tRFs are separated to 4 subtypes by their sites of origin in pre-tRNA or mature tRNA, and generally shorter than tiRNAs (16-28 nucleotides). Similar to the function of microRNA, tsRNA can inhibit their functions by binding to target genes. However, the role of tsRNA in regulating AP pathogenesis has not been investigated. In this experiment, sodium taurocholate was used to treat the rat pancreatic acinar cell (AR42J) to establish the AP-related intracellular activation of trypsinogen model. Then we used RNA sequencing to identify the differentially expressed non-coding small RNAs including microRNA and tsRNA in the cell model.

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Sodium taurocholate co-transporting polypeptide deficiency attenuates hepatocarcinogenesis in mice

Project description:Sodium taurocholate co-transporting polypeptide (NTCP) is a liver specific bile acid (BA) transporter; this transporter also serves as a functional receptor for hepatitis B virus (HBV) and hepatitis D virus (HDV). Here, we generated mouse models to investigate the role of NTCP in hepatocarcinogenesis. We report that NTCP-deficient (Slc10a1-/-) mice with long-term hypercholanemia do not develop spontaneous hepatocellular carcinoma (HCC). Using a diethylnitrosamine (DEN)-induced mouse model of HCC, we found that Slc10a1-/- mice exhibited fewer liver tumors, while transgenic mice constitutively overexpressing mouse NTCP in hepatocytes Tg(mNTCP-C9) experienced increased tumor burdens. Intriguingly, the subset of male Slc10a1-/- mice with hypercholanemia exhibited a hepatic female-biased gene expression. Importantly, a majority of the human homologs of genes with significantly hepatic female-biased expression were found to be correlated with improved prognosis in human patients with liver cancer. Our ﬁndings indicate that pharmacological manipulation of NTCP function can have a clinical impact on decreasing risk of development or decreasing risk of death liver cancer.

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