ArticleNucleic acids research2019
DOT1L promotes progenitor proliferation and primes neuronal layer identity in the developing cerebral cortex.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- Loss of DOT1L disrupts neuronal transcription and leads to a neurodevelopmental disorder.Brain : a journal of neurology · 2026Article
- Neurod2 knockdown inmicroPublication biology · 2026Article
- "Stand by me": astrocyte-microglia crosstalk in central nervous system development, homeostasis, injury, and disease.Frontiers in network physiology · 2026Review
- 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
- Combined small-molecule treatment accelerates maturation of human pluripotent stem cell-derived neurons.Nature biotechnology · 2024Article
- Endogenous mutant Huntingtin alters the corticogenesis via lowering Golgi recruiting ARF1 in cortical organoid.Molecular psychiatry · 2024Article
- Folate deficiency reduced aberrant level of DOT1L-mediated histone H3K79 methylation causes disruptive SHH gene expression involved in neural tube defects.Epigenetics & chromatin · 2023Article
- DOT1L is a barrier to histone acetylation during reprogramming to pluripotency.Science advances · 2023Article
- Rare de novo gain-of-function missense variants in DOT1L are associated with developmental delay and congenital anomalies.American journal of human genetics · 2023Article
- 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 deletion impairs the development of cortical parvalbumin-expressing interneurons.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- DOT1L activity affects neural stem cell division mode and reduces differentiation and ASNS expression.EMBO reports · 2023Article
- KDM6B Negatively Regulates the Neurogenesis Potential of Apical Papilla Stem Cells via HES1.International journal of molecular sciences · 2023Article
- The TUDOR domain of SMN is an H3K79Life science alliance · 2023Article
- Prediction of Neurodevelopmental Disorders Based on De Novo Coding Variation.Journal of autism and developmental disorders · 2023Article
- Neuronal Dot1l Activity Acts as a Mitochondrial Gene-Repressor Associated with Human Brain Aging via H3K79 Hypermethylation.International journal of molecular sciences · 2023Article
- Molecular mechanisms of corpus callosum development: a four-step journey.Frontiers in neuroanatomy · 2023Review
- DOT-1.1 (DOT1L) deficiency inBBA advances · 2023Article
- The role of histone modifications: from neurodevelopment to neurodiseases.Signal transduction and targeted therapy · 2022Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cortical development is controlled by transcriptional programs, which are orchestrated by transcription factors. Yet, stable inheritance of spatio-temporal activity of factors influencing cell fate and localization in different layers is only partly understood. Here we find that deletion of Dot1l in the murine telencephalon leads to cortical layering defects, indicating DOT1L activity and chromatin methylation at H3K79 impact on the cell cycle, and influence transcriptional programs conferring upper layer identity in early progenitors. Specifically, DOT1L prevents premature differentiation by increasing expression of genes that regulate asymmetric cell division (Vangl2, Cenpj). Loss of DOT1L results in reduced numbers of progenitors expressing genes including SoxB1 gene family members. Loss of DOT1L also leads to altered cortical distribution of deep layer neurons that express either TBR1, CTIP2 or SOX5, and less activation of transcriptional programs that are characteristic for upper layer neurons (Satb2, Pou3f3, Cux2, SoxC family members). Data from three different mouse models suggest that DOT1L balances transcriptional programs necessary for proper neuronal composition and distribution in the six cortical layers. Furthermore, because loss of DOT1L in the pre-neurogenic phase of development impairs specifically generation of SATB2-expressing upper layer neurons, our data suggest that DOT1L primes upper layer identity in cortical progenitors.
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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.