ArticleDevelopmental biology2015
Gbx2 is essential for maintaining thalamic neuron identity and repressing habenular characters in the developing thalamus.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 50 citations in OpenAlex.
- Spatial chromatin architecture and accessibility co-profiling of mammalian tissues.Nature methods · 2026Article
- Sensory modality-specific wiring of thalamocortical circuits.Nature reviews. Neuroscience · 2025Review
- A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer.Oncogene · 2025Article
- CHOIR improves significance-based detection of cell types and states from single-cell data.Nature genetics · 2025Article
- Astrocyte involvement in metabolic regulation and disease.Trends in endocrinology and metabolism: TEM · 2025Review
- Development of the early fetal human thalamus: from a protomap to emergent thalamic nuclei.Frontiers in neuroanatomy · 2025Article
- CpG island turnover events predict evolutionary changes in enhancer activity.Genome biology · 2024Article
- A high-resolution transcriptomic and spatial atlas of cell types in the whole mouse brain.Nature · 2023Article
- Spatiotemporal molecular dynamics of the developing human thalamus.Science (New York, N.Y.) · 2023Article
- Building thalamic neuronal networks during mouse development.Frontiers in neural circuits · 2023Review
- Astrocytes and neurons share region-specific transcriptional signatures that confer regional identity to neuronal reprogramming.Science advances · 2021Article
- Gbx2 Identifies Two Amacrine Cell Subtypes with Distinct Molecular, Morphological, and Physiological Properties.Cell reports · 2020Article
- A human cell atlas of fetal gene expression.Science (New York, N.Y.) · 2020Article
- TCF7L2 regulates postmitotic differentiation programmes and excitability patterns in the thalamus.Development (Cambridge, England) · 2020Article
- Self-organizing neuruloids model developmental aspects of Huntington's disease in the ectodermal compartment.Nature biotechnology · 2019Article
- Defining developmental diversification of diencephalon neurons through single cell gene expression profiling.Development (Cambridge, England) · 2019Article
- Thalamocortical Afferents Innervate the Cortical Subplate much Earlier in Development in Primate than in Rodent.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Developmental Requirement of Homeoprotein Otx2 for Specific Habenulo-Interpeduncular Subcircuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Molecular guidance cues in the development of visual pathway.Protein & cell · 2018Review
- Development and connectivity of the habenular nuclei.Seminars in cell & developmental biology · 2018Review
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
The thalamus and habenula, two important nodes of the forebrain circuitry, are derived from a single developmental compartment, called prosomere 2, in the diencephalon. Habenular and thalamic neurons display distinct molecular identity, neurochemistry, and connectivity. Furthermore, their progenitors exhibit distinctive neurogenic patterns with a marked delay in the onset of neurogenesis in the thalamus. However, the progenitors in prosomere 2 express many common developmental regulators and the mechanism underlying the specification and differentiation of these two populations of neurons remains unknown. Gbx2, coding for a homeodomain transcription factor, is initially expressed in thalamic neuronal precursors that have just exited the cell cycle, and its expression is maintained in many mature thalamic neurons in adults. Deletion of Gbx2 severely disrupts histogenesis of the thalamus and abolishes thalamocortical projections in mice. Here, by using genome-wide transcriptional profiling, we show that Gbx2 promotes thalamic but inhibits habenular molecular characters. Remarkably, although Gbx2 is expressed in postmitotic neuronal precursors, deletion of Gbx2 changes gene expression and cell proliferation in dividing progenitors in the developing thalamus. These defects are partially rescued by the mosaic presence of wild-type cells, demonstrating a cell non-autonomous role of Gbx2 in regulating the development of thalamic progenitors. Our results suggest that Gbx2 is essential for the acquisition of the thalamic neuronal identity by repressing habenular identity through a feedback signaling from postmitotic neurons to progenitors.
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