ArticleDevelopment (Cambridge, England)2013
Notch/Rbpjκ signaling regulates progenitor maintenance and differentiation of hypothalamic arcuate neurons.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- In vitro differentiation of the hypothalamic KNDy neuron, a master regulator for reproduction, from mouse embryonic stem cells.Reproductive biology and endocrinology : RB&E · 2026Article
- The long-term impact of obesity in pregnancy on offspring hypothalamic feeding pathways.Royal Society open science · 2025Review
- Proneural gene Mash1 (Ascl1) is expressed in multiple lineages and regulates their differentiation and specification.Histochemistry and cell biology · 2025Review
- Klf10 Regulates the Emergence of Glial Phenotypes During Hypothalamic Development.Journal of neuroscience research · 2025Article
- Control of tuberal hypothalamic development and its implications in metabolic disorders.Nature reviews. Endocrinology · 2025Review
- Differentiation of mesenchymal stem cells towards lens epithelial stem cells based on three-dimensional bio-printed matrix.Frontiers in cell and developmental biology · 2024Article
- Casein kinase 1α is required to maintain murine hypothalamic pro-opiomelanocortin expression.iScience · 2023Article
- A neuroepithelial wave of BMP signalling drives anteroposterior specification of the tuberal hypothalamus.eLife · 2023Article
- Zebrafish: A New Promise to Study the Impact of Metabolic Disorders on the Brain.International journal of molecular sciences · 2022Review
- Developmental programming of hypothalamic melanocortin circuits.Experimental & molecular medicine · 2022Review
- Aberrant Notch Signaling Pathway as a Potential Mechanism of Central Precocious Puberty.International journal of molecular sciences · 2022Review
- Mechanisms mediating the impact of maternal obesity on offspring hypothalamic development and later function.Frontiers in endocrinology · 2022Review
- Epigenetic modifier Kdm6a/Utx controls the specification of hypothalamic neuronal subtypes in a sex-dependent manner.Frontiers in cell and developmental biology · 2022Article
- SHH and Notch regulate SOX9+ progenitors to govern arcuate POMC neurogenesis.Frontiers in neuroscience · 2022Article
- Methylation status of hypothalamicFrontiers in endocrinology · 2022Article
- GAS1 is required for NOTCH-dependent facilitation of SHH signaling in the ventral forebrain neuroepithelium.Development (Cambridge, England) · 2021Article
- Lens regeneration: scientific discoveries and clinical possibilities.Molecular biology reports · 2021Review
- Maternal obesity causes fetal hypothalamic insulin resistance and disrupts development of hypothalamic feeding pathways.Molecular metabolism · 2020Article
- Molecular design of hypothalamus development.Nature · 2020Article
- Pro-opiomelanocortin (POMC) neuron translatome signatures underlying obesogenic gestational malprogramming in mice.Molecular metabolism · 2020Article
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4 authors at 1 institution in 1 country.
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Abstract
The hypothalamic arcuate nucleus (Arc), containing pro-opoiomelanocortin (POMC), neuropeptide Y (NPY) and growth hormone releasing hormone (GHRH) neurons, regulates feeding, energy balance and body size. Dysregulation of this homeostatic mediator underlies diseases ranging from growth failure to obesity. Despite considerable investigation regarding the function of Arc neurons, mechanisms governing their development remain unclear. Notch signaling factors such as Hes1 and Mash1 are present in hypothalamic progenitors that give rise to Arc neurons. However, how Notch signaling controls these progenitor populations is unknown. To elucidate the role of Notch signaling in Arc development, we analyzed conditional loss-of-function mice lacking a necessary Notch co-factor, Rbpjκ, in Nkx2.1-cre-expressing cells (Rbpjκ cKO), as well as mice with expression of the constitutively active Notch1 intracellular domain (NICD) in Nkx2.1-cre-expressing cells (NICD Tg). We found that loss of Rbpjκ results in absence of Hes1 but not of Hes5 within the primordial Arc at E13.5. Additionally, Mash1 expression is increased, coincident with increased proliferation and accumulation of Arc neurons at E13.5. At E18.5, Rbpjκ cKO mice have few progenitors and show increased numbers of differentiated Pomc, NPY and Ghrh neurons. By contrast, NICD Tg mice have increased hypothalamic progenitors, show an absence of differentiated Arc neurons and aberrant glial differentiation at E18.5. Subsequently, both Rbpjκ cKO and NICD Tg mice have changes in growth and body size during postnatal development. Taken together, our results demonstrate that Notch/Rbpjκ signaling regulates the generation and differentiation of Arc neurons, which contribute to homeostatic regulation of body size.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.