ArticleCell death and differentiation2017
Histone variant H3.3 orchestrates neural stem cell differentiation in the developing brain.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 64 citations in OpenAlex.
- CRL4EMBO reports · 2026Article
- Reducing methylation of histone 3.3 lysine 4 in the medial ganglionic eminence and hypothalamus recapitulates neurodevelopmental disorder phenotypes.Nature communications · 2026Article
- Histone H3 availability is more important for development than H3.2 versus H3.3 subtype identity.bioRxiv : the preprint server for biology · 2026Article
- Histone variants: expanding the epigenetic potential of neurons one amino acid at a time.Trends in biochemical sciences · 2025Review
- Unraveling Neurodevelopment: Synergistic Effects of Intrinsic Genetic Programs and Extrinsic Environmental Cues.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Multifunctional histone variants in genome function.Nature reviews. Genetics · 2025Review
- Roles of Histone H2B, H3 and H4 Variants in Cancer Development and Prognosis.International journal of molecular sciences · 2024Review
- Fucosyltransferase 8 regulates adult neurogenesis and cognition of mice by modulating the Itga6-PI3K/Akt signaling pathway.Science China. Life sciences · 2024Article
- Beyond the Usual Suspects: Examining the Role of Understudied Histone Variants in Breast Cancer.International journal of molecular sciences · 2024Review
- Involvement of the H3.3 Histone Variant in the Epigenetic Regulation of Gene Expression in the Nervous System, in Both Physiological and Pathological Conditions.International journal of molecular sciences · 2023Review
- Human SERPINA3 induces neocortical folding and improves cognitive ability in mice.Cell discovery · 2022Article
- Loss of Nexmif results in the expression of phenotypic variability and loss of genomic integrity.Scientific reports · 2022Article
- Postmitotic accumulation of histone variant H3.3 in new cortical neurons establishes neuronal chromatin, transcriptome, and identity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The role of histone modifications: from neurodevelopment to neurodiseases.Signal transduction and targeted therapy · 2022Review
- Multi-omic profiling of histone variant H3.3 lysine 27 methylation reveals a distinct role from canonical H3 in stem cell differentiation.Molecular omics · 2022Article
- Review
- RYBP modulates embryonic neurogenesis involving the Notch signaling pathway in a PRC1-independent pattern.Stem cell reports · 2021Article
- Epigenetic regulation of neural stem cells: The emerging role of nucleoporins.Stem cells (Dayton, Ohio) · 2021Review
- Nuclear deformation guides chromatin reorganization in cardiac development and disease.Nature biomedical engineering · 2021Article
- The H3.3K27M oncohistone affects replication stress outcome and provokes genomic instability in pediatric glioma.PLoS genetics · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the brain development, the process of neural stem cells (NSCs) proliferation and differentiation is precisely regulated. The deficiency in the embryonic brain development will cause serious developmental disorders. Epigenetic modifications play critical roles in controlling proliferation and differentiation in different types of stem cells. Histone variants, as one of epigenetic regulators, have been reported to be associated with many bioprocesses. Among different variants, H3.3 is one of the important epigenetic regulators, but its role in embryonic NSCs remains unclear. Here we demonstrate that H3.3 is intrinsically required for NSCs proliferation and differentiation. Suppression of the H3.3 mediated by shRNAs causes the reduction of the PAX6-positive NSCs proliferation, and promotes the premature terminal mitosis and neuronal differentiation. Particularly, the level of the H4K16ac is selectively reduced in the H3.3 knockdown NSCs. We further confirm that H3.3 is directly interacted with the MOF, a specific H4K16 acetyltransferase. Interestingly, H3.3/MOF increases the level of H4K16ac by a mutual cooperation manner. However, the H3.3K36R mutant could not increase the level of H4K16ac. RNA-seq data show the GLI1, a transcriptional regulator, is downregulated in H3.3 knockdown NSCs. Furthermore, the neurogenesis phenotype of the GLI1 knockdown is consistent with the H3.3 knockdown. Overexpression of the H3.3, MOF, and GLI1 could rescue the abnormal phenotype caused by H3.3 knockdown in the embryonic brain, but H3.1 or H3.3K36R overexpression can not rescue it. Taken together, these results suggest that H3.3 cooperates with MOF to increase the level of the H4K16ac and the GLI1, and then regulates the NSCs proliferation and differentiation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.