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Thyroid hormone receptor is essential for larval eptiehlial apoptosis and adult epithelial stem cell development

ABSTRACT: Thyroid hormone receptor is essential for larval eptiehlial apoptosis and adult epithelial stem cell development

PROVIDER: PRJNA679241 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13080669_1.fastq.gz	Fastqsanger.gz
	SRR13080669_2.fastq.gz	Fastqsanger.gz
	SRR13080670_1.fastq.gz	Fastqsanger.gz
	SRR13080670_2.fastq.gz	Fastqsanger.gz
	SRR13080671_1.fastq.gz	Fastqsanger.gz

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Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

Project description:Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

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Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

Project description:Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered an important site for thyroid action, the contribution of thyroid hormone receptor signaling, in muscle, to whole-body energy metabolism and body temperature has not been resolved. Here, we show that thyroid hormone-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRa1) in skeletal muscle, but that thyroid hormone induced elevation in body temperature is independent of muscle-TRa1. In slow-twitch soleus muscle, ablation of TRa1 leads to an altered fiber type composition toward a more oxidative phenotype, which, however, does not influence running capacity or motivation to voluntary running. RNA-sequencing of soleus muscle from WT mice and TRaHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, thus providing molecular clues pertaining to the mechanistic underpinnings of TRa1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in thyroid hormone-stimulated increase in whole-body energy expenditure.

2020-09-21 | GSE146336 | GEO

Thyroid hormone receptor is essential for larval eptiehlial apoptosis and adult epithelial stem cell development

Project description:Our experiment revealed that TR double knockout completely blocks intestinal length shortening, larval cell death, and adult stem cell development, demonstrating a requirement for TR in adult intestinal development.

2021-03-31 | GSE161714 | GEO

Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

Project description:Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

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Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis

Project description:Using tadpoles mutant for thyroid hormone receptor alpha (thra), we show that TRa is required for thyroid hormone (T3) induction of cell proliferation in the brain. RNA-sequencing showed that the TRa is required for 95% of the gene regulation responses to T3.

2019-05-13 | GSE130816 | GEO

Thyroid Hormone Promotes Fetal Neurogenesis [CosMx]

Project description:Maternal low thyroxine (T4) serum levels during the first trimester of pregnancy correlate with cerebral cortex volume and mental development of the progeny, but why neural cells during early fetal brain development are vulnerable to maternal T4 levels remains unknown. In this study, using iPSCs obtained from a boy with a loss-of-function mutation in MCT8—a transporter previously identified as critical for thyroid hormone uptake and action in neural cells—we demonstrate that thyroid hormones induce transcriptional changes that promote the progression of human neural precursor cells along the dorsal projection trajectory. Consistent with these findings, single-cell, spatial, and bulk transcriptomics from MCT8-deficient cerebral organoids and cultures of human neural precursor cells underscore the necessity for optimal thyroid hormone levels for these cells to differentiate into neurons. The controlled intracellular activation of T4 signaling occurs through the transient expression of the enzyme type 2 deiodinase, which converts T4 into its active form, T3, alongside the coordinated expression of thyroid hormone nuclear receptors. The intracellular activation of T4 in NPCs results in transcriptional changes important for their division mode and cell cycle progression. Thus, T4 is essential for fetal neurogenesis, highlighting the importance of adequate treatment for mothers with hypothyroidism.

2025-08-22 | GSE305978 | GEO

Target genes of thyroid hormone in cerebellum neurons

Project description:Cerebellar post-natal development is particularly sensitive to thyroid hormone and low levels of thyroid hormone (hypothyroidism) result in permanent defects in cerebellar architecture and function. All cell types of the cerebellum are affected, but the main sign of hypothyroidism in mice is the persistence of the external granular layer, composed of mitotic neuronal precursors at P21. To make the genetic link between thyroid hormone and cerebellar development, we sought to identify new thyroid hormone target genes, in particular in granule cells which represent the vast majority of cerebellar cells.

2012-03-30 | GSE24793 | GEO

Functional Role of THRAP3 in Modulating Thyroid Hormone–Mediated Gene Networks in C2C12 Myotubes

Project description:Thyroid hormone (TH) secreted by the thyroid gland plays essential roles in regulating metabolism, development, and nervous system function. Thyroid hormone receptor-associated protein 3 (THRAP3) is a nuclear coactivator that interacts with the thyroid hormone receptor (TR) and facilitates target gene regulation through the mediator complex. Although this mechanism has been well studied in other tissues, the specific role of THRAP3 in skeletal muscle remains unclear. Here we investigated the function of THRAP3 in skeletal muscle using Thrap3 knockout (KO) C2C12 cells. Loss of THRAP3 significantly suppressed the expression of key myogenic regulatory factors, including Myod1, Mef2c, and myosin heavy chain genes, resulting in impaired myogenic differentiation and muscle diameter. Furthermore, we found that THRAP3 influences triiodothyronine (T3)-induced gene expression, suggesting that it cooperatively modulates thyroid hormone signaling in muscle cells. Taken together, our findings identify THRAP3 as a novel regulator of myogenesis and indicate that it supports T3 activity by coordinating thyroid hormone–responsive gene expression in skeletal muscle.

2025-12-11 | GSE306461 | GEO

Thyroid Hormone Promotes Fetal Neurogenesis [scRNA-Seq]

2025-08-11 | GSE304918 | GEO

Thyroid hormone receptor α controls larval intestinal epithelial cell death by regulating the CDK1 pathway

Project description:Thyroid hormone receptor α controls larval intestinal epithelial cell death by regulating the CDK1 pathway

| PRJNA679246 | ENA