ArticleDevelopment (Cambridge, England)2024
Engrailed transcription factors direct excitatory cerebellar neuron diversity and survival.
Article in Development (Cambridge, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- FromProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Developmental determinants of male bias in medulloblastoma.bioRxiv : the preprint server for biology · 2026Article
- Autism Spectrum Disorder: The Cerebellum, Genes, and Pathways.Neurology international · 2025Review
- Conference Report: Cerebellar Development and Disease at Single-Cell Resolution.Cerebellum (London, England) · 2025Article
- Parp1 deletion rescues cerebellar hypotrophy in xrcc1 mutant zebrafish.Scientific reports · 2025Article
- Cerebellar output neurons can impair non-motor behaviors by altering development of extracerebellar connectivity.Nature communications · 2025Article
- Article
- Conserved roles of engrailed: patterning tissues and specifying cell types.Development (Cambridge, England) · 2024Review
- Cerebellar output neurons impair non-motor behaviors by altering development of extracerebellar connectivity.bioRxiv : the preprint server for biology · 2024Article
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Abstract
The neurons of the three cerebellar nuclei (CN) are the primary output neurons of the cerebellum. The excitatory neurons (e) of the medial (m) CN (eCNm) were recently divided into molecularly defined subdomains in the adult; however, how they are established during development is not known. We define molecular subdomains of the mouse embryonic eCNm using single-cell RNA-sequencing and spatial expression analysis, showing that they evolve during embryogenesis to prefigure the adult. Furthermore, eCNm are transcriptionally divergent from cells in the other nuclei by embryonic day 14.5. We previously showed that loss of the homeobox genes En1 and En2 leads to loss of approximately half of the embryonic eCNm. We demonstrate that mutation of En1/2 in the embryonic eCNm results in death of specific posterior eCNm molecular subdomains and downregulation of TBR2 (EOMES) in an anterior embryonic subdomain, as well as reduced synaptic gene expression. We further reveal a similar function for EN1/2 in mediating TBR2 expression, neuron differentiation and survival in the other excitatory neurons (granule and unipolar brush cells). Thus, our work defines embryonic eCNm molecular diversity and reveals conserved roles for EN1/2 in the cerebellar excitatory neuron lineage.
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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.