ArticleDevelopment (Cambridge, England)2014
A single allele of Hdac2 but not Hdac1 is sufficient for normal mouse brain development in the absence of its paralog.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 88 citations in OpenAlex.
- Selective histone deacetylase inhibition as a therapeutically relevant strategy in H3K27M-glioma.Neuro-oncology · 2026Article
- BRD1 haploinsufficiency alters early neuronal programming and disrupts maturation in human induced glutamatergic neurons.Research square · 2026Article
- Epigenetic Dysregulation in Neurodegeneration: The Role of Histone Deacetylases and Emerging Inhibitor Strategies.Biomolecules · 2026Review
- Review
- Epigenetic Regulation in Ischemic Neuroprotection: The Dual Role of HDACs and HATs in Neuroinflammation and Recovery.Antioxidants (Basel, Switzerland) · 2025Review
- HDAC1/2 and HDAC3 play distinct roles in controlling adult Meibomian gland homeostasis.The ocular surface · 2024Article
- Epigenetic and molecular coordination between HDAC2 and SMAD3-SKI regulates essential brain tumour stem cell characteristics.Nature communications · 2023Article
- Lactate-dependent transcriptional regulation controls mammalian eye morphogenesis.Nature communications · 2023Article
- Genetic polymorphisms of bone marrow stromal cell antigen-1 (BST-1/CD157): implications for immune/inflammatory dysfunction in neuropsychiatric disorders.Frontiers in immunology · 2023Review
- Development of a Cellular Model Mimicking Specific HDAC Inhibitors.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Paralogous Genes Involved in Embryonic Development: Lessons from the Eye and Other Tissues.Genes · 2022Review
- A toolbox for class I HDACs reveals isoform specific roles in gene regulation and protein acetylation.PLoS genetics · 2022Article
- The role of histone modifications: from neurodevelopment to neurodiseases.Signal transduction and targeted therapy · 2022Review
- Rescue of histone hypoacetylation and social deficits by ketogenic diet in a Shank3 mouse model of autism.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
- Emerging Role of HDACs in Regeneration and Ageing in the Peripheral Nervous System: Repair Schwann Cells as Pivotal Targets.International journal of molecular sciences · 2022Review
- Nonredundant, isoform-specific roles of HDAC1 in glioma stem cells.JCI insight · 2021Article
- Chromatin remodelling complexes in cerebral cortex development and neurodevelopmental disorders.Neurochemistry international · 2021Article
- Hdac1 and Hdac2 are essential for physiological maturation of a Cx3cr1 expressing subset of T-lymphocytes.BMC research notes · 2021Article
- The emerging role of chromatin remodelers in neurodevelopmental disorders: a developmental perspective.Cellular and molecular life sciences : CMLS · 2021Review
- [Role and mechanism of histone deacetylases in mouse neuronal development].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 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
17 authors at 5 institutions in 2 countries.
Funding
Abstract
The histone deacetylases HDAC1 and HDAC2 are crucial regulators of chromatin structure and gene expression, thereby controlling important developmental processes. In the mouse brain, HDAC1 and HDAC2 exhibit different developmental stage- and lineage-specific expression patterns. To examine the individual contribution of these deacetylases during brain development, we deleted different combinations of Hdac1 and Hdac2 alleles in neural cells. Ablation of Hdac1 or Hdac2 by Nestin-Cre had no obvious consequences on brain development and architecture owing to compensation by the paralog. By contrast, combined deletion of Hdac1 and Hdac2 resulted in impaired chromatin structure, DNA damage, apoptosis and embryonic lethality. To dissect the individual roles of HDAC1 and HDAC2, we expressed single alleles of either Hdac1 or Hdac2 in the absence of the respective paralog in neural cells. The DNA-damage phenotype observed in double knockout brains was prevented by expression of a single allele of either Hdac1 or Hdac2. Strikingly, Hdac1(-/-)Hdac2(+/-) brains showed normal development and no obvious phenotype, whereas Hdac1(+/-)Hdac2(-/-) mice displayed impaired brain development and perinatal lethality. Hdac1(+/-)Hdac2(-/-) neural precursor cells showed reduced proliferation and premature differentiation mediated by overexpression of protein kinase C, delta, which is a direct target of HDAC2. Importantly, chemical inhibition or knockdown of protein kinase C delta was sufficient to rescue the phenotype of neural progenitor cells in vitro. Our data indicate that HDAC1 and HDAC2 have a common function in maintaining proper chromatin structures and show that HDAC2 has a unique role by controlling the fate of neural progenitors during normal brain development.
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.