ArticleEMBO reports2023
DOT1L activity affects neural stem cell division mode and reduces differentiation and ASNS expression.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Inhibition of Dot1L Histone Methyltransferase Expands Bone Injury-Responsive CXCL12bioRxiv : the preprint server for biology · 2026Article
- Loss of DOT1L disrupts neuronal transcription and leads to a neurodevelopmental disorder.Brain : a journal of neurology · 2026Article
- A low-level Cdkn1c/p57EMBO reports · 2026Article
- Temporal control of progenitor competence shapes maturation in GABAergic neuron development in mice.Nature neuroscience · 2025Article
- BAHCC1 promotes gene expression in neuronal cells by antagonizing SIN3A-HDAC1.Nucleic acids research · 2025Article
- Loss of DOT1L disrupts neuronal transcription, behavior, and leads to a neurodevelopmental disorder.medRxiv : the preprint server for health sciences · 2025Article
- Chromatin environment-dependent effects of DOT1L on gene expression in male germ cells.Communications biology · 2025Article
- Rational design of small-sized peptidomimetic inhibitors disrupting protein-protein interaction.RSC medicinal chemistry · 2024Review
- Male-specific behavioral and transcriptomic changes in agingiScience · 2024Article
- Epigenetic control and manipulation of neuronal maturation timing.Current opinion in genetics & development · 2024Review
- Nucleophosmin 1 cooperates with the methyltransferase DOT1L to preserve peri-nucleolar heterochromatin organization by regulating H3K27me3 levels and DNA repeats expression.Epigenetics & chromatin · 2023Article
- DOT1L activity affects neural stem cell division mode and reduces differentiation and ASNS expression.EMBO reports · 2023Article
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cortical neurogenesis depends on the balance between self-renewal and differentiation of apical progenitors (APs). Here, we study the epigenetic control of AP's division mode by focusing on the enzymatic activity of the histone methyltransferase DOT1L. Combining lineage tracing with single-cell RNA sequencing of clonally related cells, we show at the cellular level that DOT1L inhibition increases neurogenesis driven by a shift of APs from asymmetric self-renewing to symmetric neurogenic consumptive divisions. At the molecular level, DOT1L activity prevents AP differentiation by promoting transcription of metabolic genes. Mechanistically, DOT1L inhibition reduces activity of an EZH2/PRC2 pathway, converging on increased expression of asparagine synthetase (ASNS), a microcephaly associated gene. Overexpression of ASNS in APs phenocopies DOT1L inhibition, and also increases neuronal differentiation of APs. Our data suggest that DOT1L activity/PRC2 crosstalk controls AP lineage progression by regulating asparagine metabolism.
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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.