ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2017
Associations of the Intellectual Disability Gene MYT1L with Helix-Loop-Helix Gene Expression, Hippocampus Volume and Hippocampus Activation During Memory Retrieval.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Stimulus-Dependent Expression ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Autism- and intellectual disability-associated MYT1L mutation alters human cortical interneuron differentiation, maturation, and physiology.Stem cell reports · 2025Article
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- MYT1L deficiency impairs excitatory neuron trajectory during cortical development.Nature communications · 2024Article
- Shared genetic architecture of psychiatric disorders and hemorrhoidal disease: a large-scale genome-wide cross-trait analysis.Frontiers in psychiatry · 2024Article
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- St18 specifies globus pallidus projection neuron identity in MGE lineage.Nature communications · 2022Article
- A causal association of ANKRD37 with human hippocampal volume.Molecular psychiatry · 2022Article
- MYT1L in the making: emerging insights on functions of a neurodevelopmental disorder gene.Translational psychiatry · 2022Review
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- Neuroprotective Effect of α-Mangostin in the Ameliorating Propionic Acid-Induced Experimental Model of Autism in Wistar Rats.Brain sciences · 2021Article
- Daughterless, theDisease models & mechanisms · 2020Article
- Downregulation of transcription factor TCTP elevates microRNA-200a expression to restrain Myt1L expression, thereby improving neurobehavior and oxidative stress injury in cerebral palsy rats.Cell cycle (Georgetown, Tex.) · 2020Article
- KMT2B and Neuronal Transdifferentiation: Bridging Basic Chromatin Mechanisms to Disease Actionability.Neuroscience insights · 2020Article
- Intellectual disability and autism spectrum disorders 'on the fly': insights fromDisease models & mechanisms · 2019Review
- Contribution of Inhibitor of Differentiation and Estrogenic Endocrine Disruptors to Neurocognitive Disorders.Medical sciences (Basel, Switzerland) · 2018Review
- Article
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Authors and funding
20 authors at 9 institutions in 4 countries.
Funding
Abstract
The fundamental role of the brain-specific myelin transcription factor 1-like (MYT1L) gene in cases of intellectual disability and in the etiology of neurodevelopmental disorders is increasingly recognized. Yet, its function remains under-investigated. Here, we identify a network of helix-loop-helix (HLH) transcriptional regulators controlled by MYT1L, as indicated by our analyses in human neural stem cells and in the human brain. Using cell-based knockdown approaches and microarray analyses we found that (1) MYT1L is required for neuronal differentiation and identified ID1, a HLH inhibitor of premature neurogenesis, as a target. (2) Although MYT1L prevented expression of ID1, it induced expression of a large number of terminal differentiation genes. (3) Consistently, expression of MYT1L in the human brain coincided with neuronal maturation and inversely correlated with that of ID1 and ID3 throughout the lifespan. (4) Genetic polymorphisms that reduced expression of MYT1L in the hippocampus resulted in increased expression of ID1 and ID3, decreased levels of the proneural basic HLH (bHLH) transcriptional regulators TCF4 and NEUROD6 and decreased expression of genes involved in long-term potentiation and synaptic transmission, cancer and neurodegeneration. Furthermore, our neuroimaging analyses indicated that MYT1L expression associated with hippocampal volume and activation during episodic memory recall, as measured by blood-oxygen-level-dependent (BOLD) signals. Overall, our findings suggest that MYT1L influences memory-related processes by controlling a neuronal proliferation/differentiation switch of ID-bHLH factors.
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