ArticleCell and tissue research2009
Defects in the cerebella of conditional Neurod1 null mice correlate with effective Tg(Atoh1-cre) recombination and granule cell requirements for Neurod1 for differentiation.
Article in Cell and tissue research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 82 citations in OpenAlex.
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- Conditional Deletion of Isl1 Disrupts Cochlear Sensory and Neuronal Development, Leading to Hearing Loss.Molecular neurobiology · 2026Article
- Neuronal Activity Suppresses NEUROD-Dependent Transcription and Genome Organization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Hierarchical regulation of cerebellar neurogenesis by Sin3A-mediated gene repression.bioRxiv : the preprint server for biology · 2025Article
- An EED/PRC2-H19 Loop Regulates Cerebellar Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Joubert syndrome-derived induced pluripotent stem cells show altered neuronal differentiation in vitro.Cell and tissue research · 2024Article
- SMARCA4 Loss and Mutated β-Catenin Induce Proliferative Lesions in the Murine Embryonic Cerebellum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Commissural and monosynaptic inputs to medial vestibular nucleus GABAergic neurons in mice.Frontiers in neurology · 2024Article
- NEUROD1: transcriptional and epigenetic regulator of human and mouse neuronal and endocrine cell lineage programs.Frontiers in cell and developmental biology · 2024Review
- Generation of advanced cerebellar organoids for neurogenesis and neuronal network development.Human molecular genetics · 2023Article
- Identification and characterization of transcribed enhancers during cerebellar development through enhancer RNA analysis.BMC genomics · 2023Article
- Protective Effect of Dexmedetomidine against Hyperoxia-Damaged Cerebellar Neurodevelopment in the Juvenile Rat.Antioxidants (Basel, Switzerland) · 2023Article
- Early Steps towards Hearing: Placodes and Sensory Development.International journal of molecular sciences · 2023Review
- Disease-causing mutations in genes encoding transcription factors critical for photoreceptor development.Frontiers in molecular neuroscience · 2023Review
- Molecular mechanisms governing development of the hindbrain choroid plexus and auditory projection: A validation of the seminal observations of Wilhelm His.IBRO neuroscience reports · 2022Review
- BiallelicNeurology. Genetics · 2022Article
- The Transcription Factor Pou3f1 Sheds Light on the Development and Molecular Diversity of Glutamatergic Cerebellar Nuclear Neurons in the Mouse.Frontiers in molecular neuroscience · 2022Article
- Transcription factors regulating the specification of brainstem respiratory neurons.Frontiers in molecular neuroscience · 2022Review
- Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Neurod1 is a crucial basic helix-loop-helix gene for most cerebellar granule cells and mediates the differentiation of these cells downstream of Atoh1-mediated proliferation of the precursors. In Neurod1 null mice, granule cells die throughout the posterior two thirds of the cerebellar cortex during development. However, Neurod1 is also necessary for pancreatic beta-cell development, and therefore Neurod1 null mice are diabetic, which potentially influences cerebellar defects. Here, we report a new Neurod1 conditional knock-out mouse model created by using a Tg(Atoh1-cre) line to eliminate Neurod1 in the cerebellar granule cell precursors. Our data confirm and extend previous work on systemic Neurod1 null mice and show that, in the central lobules, granule cells can be eradicated in the absence of Neurod1. Granule cells in the anterior lobules are partially viable and depend on as yet unknown genes, but the Purkinje cells show defects not previously recognized. Interestingly, delayed and incomplete Tg(Atoh1-cre) upregulation occurs in the most posterior lobules; this leads to near normal expression of Neurod1 with a concomitant normal differentiation of granule cells, Purkinje cells, and unipolar brush cells in lobules IX and X. Our analysis suggests that Neurod1 negatively regulates Atoh1 to ensure a rapid transition from proliferative precursors to differentiating neurons. Our data have implications for research on medulloblastoma, one of the most frequent brain tumors of children, as the results suggest that targeted overexpression of Neurod1 under Atoh1 promoter control may initiate the differentiation of these tumors.
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