Evidence map›Paper›PMID 17464364›Full record

ArticleEpigenetics

Dynamic changes in Histone H3 lysine 9 acetylation localization patterns during neuronal maturation require MeCP2.

Karen N Thatcher, Janine M LaSalle

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Rett syndrome and MeCP2.Neuromolecular medicine · 2014
    Review
  10. Article
  11. Article
  12. Review
  13. Setdb1 histone methyltransferase regulates mood-related behaviors and expression of the NMDA receptor subunit NR2B.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  14. Review
  15. Article
  16. High throughput characterization of combinatorial histone codes.Molecular & cellular proteomics : MCP · 2009
    Article
  17. Article
  18. Epigenetic regulation of mammalian stem cells.Stem cells and development · 2008
    Review
  19. MECP2 promoter methylation and X chromosome inactivation in autism.Autism research : official journal of the International Society for Autism Research · 2008
    Article
  20. MicroRNAs and epigenetic regulation in the mammalian inner ear: implications for deafness.Mammalian genome : official journal of the International Mammalian Genome Society
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Karen N ThatcherMedical Microbiology and Immunology, Rowe Program in Human Genetics, School of Medicine, One Shields Ave, University of California, Davis, CA 95616, USA.
Janine M LaSalle
Moscow State University of Technologies and Management named after K.G. Razumovskiy · RU

Funding

The Role of MeCP2 in Rett SyndromeR01HD041462 · NICHD · UNIVERSITY OF CALIFORNIA DAVIS · PI LASALLE, JANINE M · 2002 to 2011
$2.8M
NICHD NIH HHS R01 HD041462
6 · The paper itself

Abstract

Mutations within the gene encoding methyl CpG binding protein 2 (MECP2) cause the autism-spectrum neurodevelopmental disorder Rett Syndrome (RTT). MECP2 recruits histone deacetylase to methylated DNA and acts as a long-range regulator of methylated genes. Despite ubiquitous MECP2 expression, the phenotype of RTT and the Mecp2-deficient mouse is largely restricted to the postnatal brain. Since Mecp2-deficient mice have a defect in neuronal maturation, we sought to understand how MECP2/Mecp2 mutations globally affect histone modifications during postnatal brain development by an immunofluorescence approach. Using an antibody specific to acetylated histone H3 lysine 9 (H3K9ac), a bright punctate nuclear staining pattern was observed as MECP2 expression increased in early postnatal neuronal nuclei. As neurons matured in juvenile and adult brain samples, the intensity of H3K9ac staining was reduced. Mecp2-deficient mouse and RTT cerebral neurons lacked this developmental reduction in H3K9ac staining compared to age-matched controls, resulting in a significant increase in neuronal nuclei with bright H3K9ac punctate staining. In contrast, trimethylated histone H3 lysine 9 (H3K9me3) localized to heterochromatin independent of MeCP2, but showed significantly reduced levels in Mecp2 deficient mouse and RTT brain. Autism brain with reduced MECP2 expression displayed similar histone H3 alterations as RTT brain. These observations suggest that MeCP2 regulates global histone modifications during a critical postnatal stage of neuronal maturation. These results have implications for understanding the molecular pathogenesis of RTT and autism in which MECP2 mutation or deficiency corresponds with arrested neurodevelopment.

Indexed as

AcetylationAnimalsFluorescent Antibody TechniqueHistonesLysineMethyl-CpG-Binding Protein 2MiceMice, Inbred C57BLNeuronsPhenotypeRett SyndromeHistonesLysineMecp2 protein, mouseMethyl-CpG-Binding Protein 2

Identifiers

PMID17464364
PMCPMC1857283
OpenAlexW2002509683

What OpenQuestion holds

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Registered trials

None linked

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.