ArticleHuman molecular genetics2010
The distribution of repressive histone modifications on silenced FMR1 alleles provides clues to the mechanism of gene silencing in fragile X syndrome.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 88 citations in OpenAlex.
- SMCHD1 Is Dispensable for Repeat-Induced FMR1 Hypermethylation in Fragile X Pluripotent Stem Cells.International journal of molecular sciences · 2026Article
- Article
- Targeting Histone H3K9 Methyltransferase G9a as a Potential Therapeutic Strategy for Neuropsychiatric Disorders.Medicinal research reviews · 2025Review
- Long-read sequencing reveals extensivebioRxiv : the preprint server for biology · 2025Article
- MSH2 is not required for either maintenance of DNA methylation or repeat contraction at the FMR1 locus in fragile X syndrome or the FXN locus in Friedreich's ataxia.Epigenetics & chromatin · 2025Article
- Chromatin modifiers in neurodevelopment.Frontiers in molecular neuroscience · 2025Review
- Review
- Cage effects on synaptic plasticity and its modulation in a mouse model of fragile X syndrome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
- Article
- Epigenetic insights into Fragile X Syndrome.Frontiers in cell and developmental biology · 2024Review
- EZH2 inhibition reactivates epigenetically silencedFrontiers in neuroscience · 2024Article
- Spatially coordinated heterochromatinization of long synaptic genes in fragile X syndrome.Cell · 2023Article
- Histone 4 lysine 20 tri-methylation: a key epigenetic regulator in chromatin structure and disease.Frontiers in genetics · 2023Review
- 3D genome, on repeat: Higher-order folding principles of the heterochromatinized repetitive genome.Cell · 2022Review
- Epigenome editing and epigenetic gene regulation in disease phenotypes.The Korean journal of chemical engineering · 2022Article
- Genome-wide screening for genes involved in the epigenetic basis of fragile X syndrome.Stem cell reports · 2022Article
- Genetic and Epigenetic Interplay Define Disease Onset and Severity in Repeat Diseases.Frontiers in aging neuroscience · 2022Review
- DNMT1 reads heterochromatic H4K20me3 to reinforce LINE-1 DNA methylation.Nature communications · 2021Article
- DNA Methylation, Mechanisms ofBiomolecules · 2021Review
- Three-dimensional chromatin interactions remain stable upon CAG/CTG repeat expansion.Science advances · 2020Article
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 1 institution in 1 country.
Funding
Abstract
Fragile X syndrome (FXS) is the most common heritable cause of intellectual disability and the most common known cause of autism. Most cases of FXS result from the expansion of a CGG·CCG repeat in the 5' UTR of the FMR1 gene that leads to gene silencing. It has previously been shown that silenced alleles are associated with histone H3 dimethylated at lysine 9 (H3K9Me2) and H3 trimethylated at lysine 27 (H3K27Me3), modified histones typical of developmentally repressed genes. We show here that these alleles are also associated with elevated levels of histone H3 trimethylated at lysine 9 (H3K9Me3) and histone H4 trimethylated at lysine 20 (H4K20Me3). All four of these modified histones are present on exon 1 of silenced alleles at levels comparable to that seen on pericentric heterochromatin. The two groups of histone modifications show a different distribution on fragile X alleles: H3K9Me2 and H3K27Me3 have a broad distribution, whereas H3K9Me3 and H4K20Me3 have a more focal distribution with the highest level of these marks being present in the vicinity of the repeat. This suggests that the trigger for gene silencing may be local to the repeat itself and perhaps involves a mechanism similar to that involved in the formation of pericentric heterochromatin.
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.