ArticleDevelopment (Cambridge, England)2022
Selective requirement for polycomb repressor complex 2 in the generation of specific hypothalamic neuronal subtypes.
Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Single cell transcriptomics of the cerebral cortex of mice lacking the PRC2 gene eed.BMC research notes · 2024Article
- Concerted transcriptional regulation of the morphogenesis of hypothalamic neurons by ONECUT3.Nature communications · 2024Article
- Polycomb repressive complex 2 is critical for mouse cortical glutamatergic neuron development.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Cytocipher determines significantly different populations of cells in single-cell RNA-seq data.Bioinformatics (Oxford, England) · 2023Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hypothalamus displays staggering cellular diversity, chiefly established during embryogenesis by the interplay of several signalling pathways and a battery of transcription factors. However, the contribution of epigenetic cues to hypothalamus development remains unclear. We mutated the polycomb repressor complex 2 gene Eed in the developing mouse hypothalamus, which resulted in the loss of H3K27me3, a fundamental epigenetic repressor mark. This triggered ectopic expression of posteriorly expressed regulators (e.g. Hox homeotic genes), upregulation of cell cycle inhibitors and reduced proliferation. Surprisingly, despite these effects, single cell transcriptomic analysis revealed that most neuronal subtypes were still generated in Eed mutants. However, we observed an increase in glutamatergic/GABAergic double-positive cells, as well as loss/reduction of dopamine, hypocretin and Tac2-Pax6 neurons. These findings indicate that many aspects of the hypothalamic gene regulatory flow can proceed without the key H3K27me3 epigenetic repressor mark, but points to a unique sensitivity of particular neuronal subtypes to a disrupted epigenomic landscape.
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Registered trials
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