ArticleNucleus (Austin, Tex.)2017
L1 retrotransposition is activated by Ten-eleven-translocation protein 1 and repressed by methyl-CpG binding proteins.
Article in Nucleus (Austin, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- Heterochromatome wide analyses reveal MBD2 as a phase separation scaffold for heterochromatin compartmentalization and composition.Nucleic acids research · 2025Article
- Article
- Binding of zebrafish lipovitellin and L1‑ORF2 increases the accessibility of L1‑ORF2 via interference with histone wrapping.International journal of molecular medicine · 2025Article
- Histone variant macroH2A1 regulates synchronous firing of replication origins in the inactive X chromosome.Nucleic acids research · 2024Article
- A pilot study of LINE-1 copy number and telomere length with aging in human sperm.Journal of assisted reproduction and genetics · 2023Article
- Isoform-specific and ubiquitination dependent recruitment of Tet1 to replicating heterochromatin modulates methylcytosine oxidation.Nature communications · 2022Article
- Optochemical Control of TET Dioxygenases Enables Kinetic Insights into the Domain-Dependent Interplay of TET1 and MBD1 while Oxidizing and Reading 5-Methylcytosine.ACS chemical biology · 2022Article
- Cytosine base modifications regulate DNA duplex stability and metabolism.Nucleic acids research · 2021Article
- DysregulatedCancers · 2021Review
- The Molecular Functions of MeCP2 in Rett Syndrome Pathology.Frontiers in genetics · 2021Review
- SIRT6 Through the Brain Evolution, Development, and Aging.Frontiers in aging neuroscience · 2021Article
- MeCP2 and Chromatin Compartmentalization.Cells · 2020Review
- Structural analysis of healthy and cancerous epithelial-type breast cells by nanomechanical spectroscopy allows us to obtain peculiarities of the skeleton and junctions.Nanoscale advances · 2019Article
- Regulation of transposable elements by DNA modifications.Nature reviews. Genetics · 2019Review
- The impact of transposable element activity on therapeutically relevant human stem cells.Mobile DNA · 2019Review
- Post-transcriptional regulation of LINE-1 retrotransposition by AID/APOBEC and ADAR deaminases.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2018Review
- L1 retrotransposition in the soma: a field jumping ahead.Mobile DNA · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the major functions of DNA methylation is the repression of transposable elements, such as the long-interspersed nuclear element 1 (L1). The underlying mechanism(s), however, are unclear. Here, we addressed how retrotransposon activation and mobilization are regulated by methyl-cytosine modifying ten-eleven-translocation (Tet) proteins and how this is modulated by methyl-CpG binding domain (MBD) proteins. We show that Tet1 activates both, endogenous and engineered L1 retrotransposons. Furthermore, we found that Mecp2 and Mbd2 repress Tet1-mediated activation of L1 by preventing 5hmC formation at the L1 promoter. Finally, we demonstrate that the methyl-CpG binding domain, as well as the adjacent non-sequence specific DNA binding domain of Mecp2 are each sufficient to mediate repression of Tet1-induced L1 mobilization. Our study reveals a mechanism how L1 elements get activated in the absence of Mecp2 and suggests that Tet1 may contribute to Mecp2/Mbd2-deficiency phenotypes, such as the Rett syndrome. We propose that the balance between methylation "reader" and "eraser/writer" controls L1 retrotransposition.
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.