ArticleNature communications2024
MYT1L deficiency impairs excitatory neuron trajectory during cortical development.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Multi-omics profiling reveals MAGEL2-driven defects in human corticogenesis shared across Prader-Willi and Schaaf-Yang syndromes.bioRxiv : the preprint server for biology · 2026Article
- Genome-scale functional mapping of the mammalian whole brain with in vivo Perturb-seq.bioRxiv : the preprint server for biology · 2026Article
- Article
- Cortical versus hippocampal network dysfunction in a human brain assembloid model of epilepsy and intellectual disability.Cell reports · 2025Article
- A survey of hypothalamic phenotypes identifies molecular and behavioral consequences of MYT1L haploinsufficiency in male and female mice.Hormones and behavior · 2025Article
- Single-cell technology grows up: Leveraging high-resolution omics approaches to understand neurodevelopmental disorders.Current opinion in neurobiology · 2025Review
- Chromosomal and gonadal sex have differing effects on social motivation in mice.Biology of sex differences · 2025Article
- Lifespan in rodents with MYT1L heterozygous mutation.Scientific reports · 2025Article
- Article
- Chromosomal and gonadal sex have differing effects on social motivation in mice.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
13 authors.
Funding
Abstract
Mutations reducing the function of MYT1L, a neuron-specific transcription factor, are associated with a syndromic neurodevelopmental disorder. MYT1L is used as a pro-neural factor in fibroblast-to-neuron transdifferentiation and is hypothesized to influence neuronal specification and maturation, but it is not clear which neuron types are most impacted by MYT1L loss. In this study, we profile 412,132 nuclei from the forebrains of wild-type and MYT1L-deficient mice at three developmental stages: E14 at the peak of neurogenesis, P1 when cortical neurons have been born, and P21 when neurons are maturing, to examine the role of MYT1L levels on neuronal development. MYT1L deficiency disrupts cortical neuron proportions and gene expression, primarily affecting neuronal maturation programs. Effects are mostly cell autonomous and persistent through development. While MYT1L can both activate and repress gene expression, the repressive effects are most sensitive to haploinsufficiency, likely mediating MYT1L syndrome. These findings illuminate MYT1L's role in orchestrating gene expression during neuronal development, providing insights into the molecular underpinnings of MYT1L syndrome.
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Registered trials
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 Socratic graph.