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RNA sequencing of wild-type liver at stage 54, stage 61, stage 66 and T3 treated liver.

ABSTRACT: RNA sequencing of wild-type liver at stage 54, stage 61, stage 66 and T3 treated liver.

PROVIDER: PRJNA828585 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18840331_1.fastq.gz	Fastqsanger.gz
	SRR18840331_2.fastq.gz	Fastqsanger.gz
	SRR18840332_1.fastq.gz	Fastqsanger.gz
	SRR18840332_2.fastq.gz	Fastqsanger.gz
	SRR18840333_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of wild-type liver at stage 54, stage 61, stage 66 and T3 treated liver.

Project description:Conclusions: Our study represents the first detailed analysis of liver transcriptomes in wild-type tadpoles, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles.

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Expression data from stage 54 Xenopus laevis larvae treated with 20 nM triiodothyronine (T3)

Project description:Induction of Xenopus laevis larvae metamorphosis is dependent on exposure to TH. Metamorphosis involves the regression, growth or remodeling of almost all the tissues in the animals body. Metamorphosis in frogs is induced by thyroid hormone. Each organ system has a unique morphological and genetic program that it follows while undergoing metamorphosis involving both the upregulation and downregulation of genes. In this array we examined the change in gene expression in the tail of larvae undergoing precocious metamorphosis following induction with thyroid hormone. Whole stage 54 xenopus larvae were exposed to either vehicle for 48 hours or 20 nM T3 for 6 or 48 hours. Total RNA was then purified from tail tissue and the samples were examined by hybridization to the Affymetrix Xenopus array. Developmental stage 51-54 Xenopus larvae were selected because these stages do not express high levels of endogenous T3 but are still capable of morphologically responding to exposure.

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Project description:Diurnal (i.e., 24-hour) physiological rhythms depend on transcriptional programs controlled by a set of circadian clock genes/proteins. Systemic factors like humoral and neuronal signals, oscillations in body temperature, and food intake align physiological circadian rhythms with external time. Thyroid hormones (THs) are major regulators of circadian clock target processes such as energy metabolism, but little is known about how fluctuations in TH levels affect the circadian coordination of tissue physiology. In this study, a high triiodothyronine (T3) state was induced in mice by supplementing T3 in the drinking water, which affected body temperature, and oxygen consumption in a time-of-day dependent manner. 24-hour transcriptome profiling of liver tissue identified 37 robustly and time independently T3 associated transcripts as potential TH state markers in the liver. Such genes participated in xenobiotic transport, lipid and xenobiotic metabolism. We also identified 10 – 15 % of the liver transcriptome as rhythmic in control and T3 groups, but only 4 % of the liver transcriptome (1,033 genes) were rhythmic across both conditions – amongst these several core clock genes. In-depth rhythm analyses showed that most changes in transcript rhythms were related to mesor (50%), followed by amplitude (10%), and phase (10%). Gene set enrichment analysis revealed TH state dependent reorganization of metabolic processes such as lipid and glucose metabolism. At high T3 levels, we observed weakening or loss of rhythmicity for transcripts associated with glucose and fatty acid metabolism, suggesting increased hepatic energy turnover. In sum, we provide evidence that tonic changes in T3 levels restructure the diurnal liver metabolic transcriptome independent of local molecular circadian clocks.

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Project description:Thyroid hormone (TH) influences metabolic pathways by binding to specific receptors (TRs), which are conditional transcription factors. T3 works through TRs to induce fibroblast growth factor (FGF) 21, a peptide hormone that is usually induced in fasting and influences lipid and carbohydrate metabolism via local hepatic and systemic endocrine effects. While administered TH and FGF21 display overlapping actions, including reductions in serum lipids, current models suggest that these hormones act independently in vivo. Here, we examined mechanisms of TH regulation of FGF21 expression and tested the possibility that FGF21 is required for induction of hepatic TH-responsive genes. We confirm that active TH (T3) and the TRβ selective thyromimetic GC-1 increase FGF21 transcript and peptide levels in mouse liver and that this effect requires TRβ. T3 also induces FGF21 in cultured hepatocytes and this effect involves direct actions of TRβ1, which binds a TRE within intron 2 of FGF21. Gene expression profiles in wild type and FGF21 knockout mice are highly similar indicating that FGF21 is dispensable for the majority of hepatic T3 gene responses. A small subset of genes displays diminished T3 response in the absence of FGF21. However, most of these are not obviously involved in T3-dependent hepatic lipid and carbohydrate metabolic processes. Accordingly, T3-dependent effects upon serum lipids are maintained in the FGF21-/- background. Our findings suggest that T3 regulates genes involved in classical hepatic metabolic responses independently of FGF21.

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