ArticleThe EMBO journal2022
Postnatal expression of the lysine methyltransferase SETD1B is essential for learning and the regulation of neuron-enriched genes.
Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- Ythdf2/Setd1b regulatory axis is essential for cerebellar development through regulating epigenetic reprogramming.Molecular psychiatry · 2026Article
- Ketogenic Diet as an Epigenetic Therapy in SETD1B-Related Epilepsy.Annals of clinical and translational neurology · 2026Article
- From epigenetic scripts to kinase signals: linking DOT1L and RIPK1 in the neurobiology of degeneration.Molecular biology reports · 2026Review
- Neuid: A Novel Neuron-Enriched LncRNA that Connects Epigenetic Gene Silencing to Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Reducing methylation of histone 3.3 lysine 4 in the medial ganglionic eminence and hypothalamus recapitulates neurodevelopmental disorder phenotypes.Nature communications · 2026Article
- Canonical and Non-Canonical Functions of Histone H3K4 Methylation Modifiers in Cancer.Cancer science · 2025Review
- lncRNAbioRxiv : the preprint server for biology · 2025Article
- The Extremely Low Mechanical Force Generated by Nano-Pulling Induces Global Changes in the Microtubule Network, Nuclear Morphology, and Chromatin Transcription in Neurons.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Regulation of H3K4me3 breadth and MYC expression by the SETD1B catalytic domain in MLL-rearranged leukemia.Leukemia · 2025Article
- [Clinical characteristics of epilepsy with intellectual disability associated withZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Review
- Genomic landscape of diffuse glioma revealed by whole genome sequencing.Nature communications · 2025Article
- SETD1B-mediated broad H3K4me3 controls proper temporal patterns of gene expression critical for spermatid development.Cell research · 2025Article
- LncRNANon-coding RNA · 2025Article
- PRDM16-DT is a novel lncRNA that regulates astrocyte function in Alzheimer's disease.Acta neuropathologica · 2024Article
- Unveiling the hidden dangers: a review of non-apoptotic programmed cell death in anesthetic-induced developmental neurotoxicity.Cell biology and toxicology · 2024Review
- PRDM16-DT: A Brain and Astrocyte-Specific lncRNA Implicated in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
- KMT2 Family of H3K4 Methyltransferases: Enzymatic Activity-dependent and -independent Functions.Journal of molecular biology · 2024Review
- Role of the histone methyltransferases Ezh2 and Suv4-20h1/Suv4-20h2 in neurogenesis.Neural regeneration research · 2023Review
- Conserved reduction of mProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The role of histone methyltransferases in neurocognitive disorders associated with brain size abnormalities.Frontiers in neuroscience · 2023Review
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, histone 3 lysine 4 methylation (H3K4me) is mediated by six different lysine methyltransferases. Among these enzymes, SETD1B (SET domain containing 1b) has been linked to syndromic intellectual disability in human subjects, but its role in the mammalian postnatal brain has not been studied yet. Here, we employ mice deficient for Setd1b in excitatory neurons of the postnatal forebrain, and combine neuron-specific ChIP-seq and RNA-seq approaches to elucidate its role in neuronal gene expression. We observe that Setd1b controls the expression of a set of genes with a broad H3K4me3 peak at their promoters, enriched for neuron-specific genes linked to learning and memory function. Comparative analyses in mice with conditional deletion of Kmt2a and Kmt2b histone methyltransferases show that SETD1B plays a more pronounced and potent role in regulating such genes. Moreover, postnatal loss of Setd1b leads to severe learning impairment, suggesting that SETD1B-dependent regulation of H3K4me levels in postnatal neurons is critical for cognitive function.
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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.