ArticleHuman molecular genetics2023
Genes positively regulated by Mef2c in cortical neurons are enriched for common genetic variation associated with IQ and educational attainment.
Article in Human molecular genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Modeling Late-Onset Sporadic Alzheimer's Disease Using Patient-Derived Cells: A Review.Neurology international · 2026Review
- Loss of MEF2C function by enhancer mutation leads to neuronal mitochondria dysfunction and motor deficits in mice.Molecular neurodegeneration · 2025Article
- Developmental Disruption of Mef2c in Medial Ganglionic Eminence-Derived Cortical Inhibitory Interneurons Impairs Cellular and Circuit Function.Biological psychiatry · 2024Article
- Pre- and Postsynaptic MEF2C Promotes Experience-Dependent, Input-Specific Development of Cortical Layer 4 to Layer 2/3 Excitatory Synapses and Regulates Activity-Dependent Expression of Synaptic Cell Adhesion Molecules.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- The function ofFrontiers in cellular neuroscience · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The myocyte enhancer factor 2 C (MEF2C) gene encodes a transcription factor important for neurogenesis and synapse development and contains common variants associated with intelligence (IQ) and educational attainment (EA). Here, we took gene expression data from the mouse cortex of a Mef2c mouse model with a heterozygous DNA binding-deficient mutation of Mef2c (Mef2c-het) and combined these data with MEF2C ChIP-seq data from cortical neurons and single-cell data from the mouse brain. This enabled us to create a set of genes that were differentially regulated in Mef2c-het mice, represented direct target genes of MEF2C and had elevated in expression in cortical neurons. We found this gene-set to be enriched for genes containing common genetic variation associated with IQ and EA. Genes within this gene-set that were down-regulated, i.e. have reduced expression in Mef2c-het mice versus controls, were specifically significantly enriched for both EA and IQ associated genes. These down-regulated genes were enriched for functionality in the adenylyl cyclase signalling system, which is known to positively regulate synaptic transmission and has been linked to learning and memory. Within the adenylyl cyclase signalling system, three genes regulated by MEF2C, CRHR1, RGS6, and GABRG3, are associated at genome-wide significant levels with IQ and/or EA. Our results indicate that genetic variation in MEF2C and its direct target genes within cortical neurons contribute to variance in cognition within the general population, and the molecular mechanisms involved include the adenylyl cyclase signalling system's role in synaptic function.
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