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TBX3 defines the functional identity of hypothalamic melanocortin neurons

ABSTRACT: TBX3 defines the functional identity of hypothalamic melanocortin neurons

PROVIDER: PRJNA490554 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7824090_1.fastq.gz	Fastqsanger.gz
	SRR7824090_2.fastq.gz	Fastqsanger.gz
	SRR7824100_1.fastq.gz	Fastqsanger.gz
	SRR7824100_2.fastq.gz	Fastqsanger.gz
	SRR7824110_1.fastq.gz	Fastqsanger.gz

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TBX3 defines the functional identity of hypothalamic melanocortin neurons

Project description:Purpose: Identify cellular pathways controlled by Tbx3 Methods: RNA sequencing of hypothalamic primary neurons from Tbx3 loxP/loxP mice infected with Ad-Cre or Ad-GFP viruses. Results: Unbiased pathway analysis revealed that Tbx3 deletion in primary neurons significantly affected the expression of genes involved in several pathways responsible for controlling cellular proliferation, differentiation and determination of cellular fate. Conclusions: Tbx3 in primary neurons might be implicated in the development and maintenance of neuronal identity.

2019-01-22 | GSE119883 | GEO

Functional identity of hypothalamic melanocortin neurons depends on Tbx3.

Project description:Heterogeneous populations of hypothalamic neurons orchestrate energy balance via the release of specific signatures of neuropeptides. However, how specific intracellular machinery controls peptidergic identities and function of individual hypothalamic neurons remains largely unknown. The transcription factor T-box 3 (Tbx3) is expressed in hypothalamic neurons sensing and governing energy status, whereas human TBX3 haploinsufficiency has been linked with obesity. Here, we demonstrate that loss of Tbx3 function in hypothalamic neurons causes weight gain and other metabolic disturbances by disrupting both the peptidergic identity and plasticity of Pomc/Cart and Agrp/Npy neurons. These alterations are observed after loss of Tbx3 in both immature hypothalamic neurons and terminally differentiated mouse neurons. We further establish the importance of Tbx3 for body weight regulation in Drosophila melanogaster and show that TBX3 is implicated in the differentiation of human embryonic stem cells into hypothalamic Pomc neurons. Our data indicate that Tbx3 directs the terminal specification of neurons as functional components of the melanocortin system and is required for maintaining their peptidergic identity. In summary, we report the discovery of a key mechanistic process underlying the functional heterogeneity of hypothalamic neurons governing body weight and systemic metabolism.

| S-EPMC8291379 | biostudies-literature

Hierarchical deployment of Tbx3 dictating the identity of hypothalamic Tac2/Kiss1 neurons

Project description:Hierarchical deployment of Tbx3 dictating the identity of hypothalamic Tac2/Kiss1 neurons

| PRJNA800757 | ENA

Hierarchical deployment of Tbx3 dictating the identity of hypothalamic Tac2/Kiss1 neurons

Project description:To investigate how Tbx3 regulates the fate determination of arcuate piptidergic neruons, we performed scRNA-seq, snRNA-seq and CUT&Tag to reveal the function of Tbx3 in fate specification and maintenance of neurons

2022-01-30 | GSE195472 | GEO

Estrogen Drives Melanocortin Neurons To Reduce Sedentary Behavior

Project description:Estrogen depletion in both rodents and humans leads to inactivity, unhealthy fat accumulation, and metabolic syndrome, underscoring the conserved metabolic benefits of estrogen signaling that inevitably decline with aging. Here, we uncover a hypothalamic node that integrates estrogen and melanocortin-4 receptor (MC4R) signaling to drive episodic bursts in activity prior to ovulation. Skirting the estrogen-dependent gating of this node by CRISPR activation of Mc4r reduces sedentary behavior long-term in both males and females. Our findings expand the impact of MC4R signaling beyond food intake regulation and rationalize reported sex-differences in melanocortin signaling including increased disease severity for women with MC4R-insuffciency. This newly identified hormone-dependent activity node illustrates the potency of estrogen in maintaining an active lifestyle.

2021-03-01 | GSE141434 | GEO

Neuronal identity defines a-synuclein and tau toxicity

Project description:Neuronal identity defines a-synuclein and tau toxicity

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Forebrain neuronal Smc3 regulates weight and metabolic parameters partly through regulation of hypothalamic Melanocortin 4 receptor

Project description:Forebrain neuronal Smc3 regulates weight and metabolic parameters partly through regulation of hypothalamic Melanocortin 4 receptor

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Forebrain neuronal Smc3 regulates weight and metabolic parameters associated with regulation of hypothalamic Melanocortin 4 receptor

Project description:Forebrain neuronal Smc3 regulates weight and metabolic parameters associated with regulation of hypothalamic Melanocortin 4 receptor

| PRJNA1060298 | ENA

Hierarchical deployment of Tbx3 dictates the identity of hypothalamic KNDy neurons to control puberty onset.

Project description:The neuroendocrine system consists of a heterogeneous collection of neuropeptidergic neurons in the brain, among which hypothalamic KNDy neurons represent an indispensable cell subtype controlling puberty onset. Although neural progenitors and neuronal precursors along the cell lineage hierarchy adopt a cascade diversification strategy to generate hypothalamic neuronal heterogeneity, the cellular logic operating within the lineage to specify a subtype of neuroendocrine neurons remains unclear. As human genetic studies have recently established a link between TBX3 mutations and delayed puberty onset, we systematically studied Tbx3-derived neuronal lineage and Tbx3-dependent neuronal specification and found that Tbx3 hierarchically established and maintained the identity of KNDy neurons for triggering puberty. Apart from the well-established lineage-dependent fate determination, we uncovered rules of interlineage interaction and intralineage retention operating through neuronal differentiation in the absence of Tbx3. Moreover, we revealed that human TBX3 mutations disturbed the phase separation of encoded proteins and impaired transcriptional regulation of key neuropeptides, providing a pathological mechanism underlying TBX3-associated puberty disorders.

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Comparative transcriptomic analyses of developing melanocortin neurons reveal new regulators for the anorexigenic neuron identity

Project description:Comparative transcriptomic analyses of developing melanocortin neurons reveal new regulators for the anorexigenic neuron identity

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