Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8559987.fastq.gz | Fastqsanger.gz | |||
| SRR8559988.fastq.gz | Fastqsanger.gz |
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Project description:We performed an original protocol called synthetic STARR-seq (PMID: 30427832) in which a library of putative response elements are tested for their capacity to bind thyroid hormone (T3) nuclear receptors and convey T3 transactivation More than 10 000 putative T3 response elements (T3RE) were cloned in the hSTARR-seq-ORI vector with a minimal promoter, in the 3' end of the transcribed sequence. These are variant of the consensus T3RE (5'NGGTCANNNNRGGNNA3') Therefore the most active T3RE are over-represented in the RNA of cells transfected with the plasmid library and treated with T3.
2022-07-06 | GSE196145 | GEO
Project description:The first GSSM of V. vinifera was reconstructed (MODEL2408120001). Tissue-specific models for stem, leaf, and berry of the Cabernet Sauvignon cultivar were generated from the original model, through the integration of RNA-Seq data. These models have been merged into diel multi-tissue models to study the interactions between tissues at light and dark phases.
2024-09-02 | MODEL2408160001 | BioModels
Project description:Thyroid hormones, thyroxine and triiodothyronine (T3) are crucial for cerebral cortex development acting through regulation of gene expression. To define the transcriptional program under T3 regulation we have performed RNA-Seq of T3-treated and untreated primary mouse cerebrocortical cells. The expression of 1,145 genes or 7.7% of expressed genes was changed upon T3 addition, of which 371 responded to T3 in the presence of cycloheximide indicating direct transcriptional regulation. The results were compared with available transcriptomic datasets of defined cellular types. In this way we could identify genomic targets of T3 in astrocytes and neurons, and in neuron subtypes, such as layer-specific neurons, and neurons expressing specific markers such as prepronociceptin, cholecystokinin, or cortistatin. T3 up-regulates mostly genes related to cell membrane events, such as G-protein signaling, neurotransmission, and ion transport, and down-regulates genes involved in nuclear events, such as cell division, M phase of cell cycle, and chromosome organization and segregation. Remarkably the transcriptomic changes induced by T3 sustain the transition from embryonic to adult patterns of gene expression. The results allowed us to define in molecular terms the elusive role of thyroid hormones on neocortical development.
2015-11-09 | GSE68949 | GEO
Project description:Background: Thyroxine (T4) is generally considered to be a pro-hormone that requires conversion to 3,5,3’-triiodothyronine (T3) to exert biological activity. Although evidence suggests that T4 has intrinsic activity, it is questionable if this activity has any physiological relevance. Methods: To answer this question, triple KO mice (Triples) that cannot express the types 1 (D1) and 2 (D2) deiodinase and the Pax8 genes were generated. Thus they lack a thyroid and cannot convert T4 to T3. Triples were injected on alternate days with either vehicle or physiological doses of T4, T3 or T3+T4 from postnatal days 2 to 14. They were euthanized at P15 and RNA-seq was employed to profile gene expression in liver. In another experiment, Pax8KO mice were injected with T3, T4 or T4 +T3, and growth rate and survival to P84 were determined. Results: The growth retardation of Triples was not improved by either T3 or T4 alone but was significantly improved by T4+T3. In liver, T4 significantly regulated the expression of genes that were also regulated by T3, but the proportion of genes that were negatively regulated was higher in mice treated with T4 than with T3. Treatment with T4+T3 identified genes that were regulated synergistically by T3 and T4, and genes that were regulated only by T4+T3. Analysis of these genes revealed enrichment in mechanisms related to cell proliferation and cholesterol physiology, suggesting a unique contribution of T4 to these biological functions. Pax8KO mice all survived to P84 when injected with T4 or T4+T3 but survival rate with T3 was 50% and 10% at 3.5 and 12 weeks of life, respectively. Conclusion: T4 has intrinsic activity in vivo and is critical for survival and growth. At a physiological level, T4 per se can up- or down-regulate many T3 target genes in the neonatal liver. While most of these genes are also regulated by T3, subsets respond exclusively to T4 or demonstrate enhanced or normalized expression only in the presence of both hormones. These studies demonstrate for the first time a complex dependency on both T4 and T3 for normal mammalian growth and development.
2021-03-31 | GSE154156 | GEO
Project description:Traumatic Brain Injury (TBI) is associated with disruption of cerebral blood flow leading to localized brain hypoxia. Thyroid hormone (TH) treatment, when administered shortly after injury, has been shown to promote neural protection in rodent TBI models. The mechanism of TH protection, however, is not established. We used mouse primary cortical neurons to investigate the effectiveness and mechanism of T3-promoted cell survival after exposure to hypoxic injury. Cultured primary cortical neurons were exposed to hypoxia (0.2% oxygen) for 7 hours, in either the presence or absence of T3 (5 nM). T3 treatment enhanced DNA 5-hydroxymethylcytosin (5-hmc) levels and attenuated the hypoxia-induced increase in DNA 5-methylcytosin (5-mc). In the presence of T3, mRNA expression of Tet family genes was increased and DNA methyltransferases, (Dnmt) 3a and Dnmt3b, were downregulated, compared to conditions in the absence of T3. These T3-induced changes decreased hypoxia-induced DNA de novo methylation, which reduced hypoxia-induced neuronal damage and apoptosis. We utilized RNA-seq to characterize T3-regulated genes in cortical neurons under hypoxic conditions and identified 22 genes that were upregulated and 15 genes that were downregulated. Krupple-like factor 9 (KLF9), a multifunctional transcription factor that plays a key role in CNS development, was highly upregulated by T3 treatment in hypoxic conditions. Knockdown of the KLF9 gene resulted in early apoptosis and abolished the beneficial role of T3 in neuronal survival. KLF9 mediates, in part, the neuronal protective role of T3. T3 treatment reduces hypoxic damage and acts through pathways that reduce DNA methylation and apoptosis.
2020-01-21 | GSE130197 | GEO
Project description:ChIP-seq data from mouse liver over-expressing GFP and fed a PTU diet and treated with saline, or overexpressing biotinylated TRb1 and GFP and fed a PTU diet, treated with either saline or T3 Mouse liver was infected with adenovirus that either expressed only GFP or GFP and biotinylated TRb1 and were fed a PTU diet, followed by injections with only saline (GFP-only livers) or with saline or T3 (Biotinylated-TRb1 and GFP livers). ChIP assays were performed using streptavidin agarose to capture biotinylated TRb1 followed by library construction and sequencing.
2013-12-18 | E-GEOD-52613 | biostudies-arrayexpress
Project description:Epigenetic and genetic regulation mediates the response to stress at the cellular level and allows cells for adaptation and survival. Thyroid hormone has been shown to have a protective role in neuronal injury, although the mechanisms are not established. We hypothesized that the neuroprotective role of thyroid hormone was associated with epigenetic modifications of histone proteins. We used hypoxic neurons as a model system for hypoxia-induced brain injury. Mouse primary cortical neurons were exposed to 0.2% oxygen for 7 hours with or without treatment with 10 nM Triiodotyroxine (T3). We analyzed the mRNA expression of histone modifying enzymes by RNA-seq and the posttranslationally modified histone 3 proteins by ELISA assay and Western blot. We found that methylation of H3K27, associated with inactive promoters, was highly induced in hypoxic neurons, and this methylation was reduced by T3 treatment. H3K4 methylation is the hallmark of active promoters. Three (Set1db, Kmta2c and Kmt2e) out of six H3K4 methyltransferases were downregulated by hypoxia and restored by T3 treatment. H3K4me3 protein, by ELISA assay, was increased 76% in T3-treated hypoxic neurons, compared to without T3 treatment. H3K56ac, plays a critical role in transcription initiation, was markedly increased in T3-treaed hypoxic neurons, compared to those without T3 treatment, indicating that T3 treatment stimulated gene transcription. Additionally, T3 treatment restored hypoxia-induced downregulation of histone acetyltransferase, Kat6a, Kat6b and Crebbp, which function as transcription factors. These findings indicate that T3 treatment mitigates hypoxia-induced alteration of the histone modifications and protects neurons from hypoxia-induced injury.
2022-07-27 | GSE205801 | GEO
Project description:We over-expressed biotinylated-thyroid hormone receptor beta 1 (TRb1) in mouse liver using an adenovirus in order to perform ChIP-seq experiments. These microarrays were performed to determine gene expression changes in response to tri-iodothyronine (thyroid hormone; T3) stimulation. A control GFP adenovirus was used and gene expression from these livers was also done as a comparison. We performed microarrays from Ad-GFP-infected propylthiouracil (PTU)-fed livers injected with either saline or T3 and Ad-TRb1-GFP infected livers injected with either saline or T3. RNA was extracted from livers of biotin ligase (BirA)-expressing mice that had been infected with either Ad-GFP or Ad-TRb1, fed with PTU for 3 weeks followed by saline or T3 injections for 4 consecutive days.
2013-12-18 | E-GEOD-52433 | biostudies-arrayexpress