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Transgenerational effects of thyroid hormone in the hypothalamus of the F2 generation

ABSTRACT: Transgenerational effects of thyroid hormone in the hypothalamus of the F2 generation

PROVIDER: PRJNA479419 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7467030.fastq.gz	Fastqsanger.gz
	SRR7467031.fastq.gz	Fastqsanger.gz
	SRR7467032.fastq.gz	Fastqsanger.gz
	SRR7467023.fastq.gz	Fastqsanger.gz
	SRR7467033.fastq.gz	Fastqsanger.gz

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Transgenerational effects of thyroid hormone in the hypothalamus of the F2 generation

Project description:Genetic factors do not fully account for the relatively high heritability of neurodevelopmental conditions, suggesting that non-genetic heritable factors contribute to their etiology. To evaluate the potential contribution of aberrant thyroid hormone status to the epigenetic inheritance of neurological phenotypes, we examined genetically normal mice with paternal grandparents that were developmentally overexposed to thyroid hormone due to a Dio3 mutation. Hypothalamic gene expression profiling in postnatal day 15 mice with control ancestry (Control), with a Dio3KO paternal grandmother (PGM), with Dio3KO paternal grandfather (PGF), with a heterozygous DIo3KO mother (HM) and with a heterozygous DIO3KO father (HF).

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Project description:We profiled gene expression in hypothalamus tissue from F2 progeny from a cross between the outbred M16 (selectively bred for rapid weight gain) and ICR (control) mouse strains. We developed a framework for reconstructing tissue-to-tissue coexpression networks between genes in hypothalamus, liver or hypothalamus tissues that are independent of networks constructed from single tissue analyses. The subnetworks we identify as specific to tissue-to-tissue interactions associate with multiple obesity-relevant biological functions like circadian rhythm, energy balance, stress response, or immune response. Keywords: Tissue profiling in a mouse F2 cross.

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Profiling of hypothalamus tissue from the F2 M16xICR mouse cross.

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Project description:Perfluorooctanesulfonic acid (PFOS) is a persistent anthropogenic chemical that can affect the thyroid hormone system in humans. In experimental animals, PFOS exposure decreases thyroxine (T4) and triiodothyronine (T3) levels, without a compensatory upregulation of thyroid stimulating hormone (TSH). In adults, THs are regulated by the hypothalamus-pituitary-thyroid (HPT) axis, but also organs such as the liver and potentially the gut microbiota. PFOS and other xenobiotics can therefore potentially disrupt the TH system through various entry points of disruption. To start addressing this issue, we performed a PFOS exposure study to identify effects in multiple organs and pathways simultaneously.

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Project description:The obesity epidemic is a significant global health issue. Improved understanding of the mechanisms which regulate appetite and body weight will provide the rationale for the design of novel anti-obesity therapies. Thyroid hormones play a key role in metabolic homeostasis through their interaction with thyroid hormone receptors (TR) which function as ligand inducible transcription factors. The TR beta isoform (TRβ) is expressed in the ventromedial hypothalamus (VMH), a brain area important for control of energy homeostasis. Here we report that selective knock down of TRβ in the VMH of adult mice results in severe obesity due to hyperphagia and reduced energy expenditure. The observed increase in body weight is of a similar magnitude to murine models of the most extreme forms of monogenic obesity. These data identify TRβ in the VMH as a major physiological regulator of food intake and energy homeostasis.

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