Evidence map›Paper›PMID 41727113›Full record

ArticlebioRxiv : the preprint server for biology2026

Multiple redundant mechanisms account for the majority of gene silencing downstream of DNA methylation.

Shuya Wang, Zhongshou Wu, Zheng Li, Andrea Movilli, Li He, Yuxing Zhou, Evan K Lin, Russell Chuang, Wai Wai Thiri, Sean Convery and 3 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Shuya WangMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0001-9850-4634
Zhongshou WuMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Zheng LiMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Andrea MovilliDepartment of Molecular Biology, Max Planck Institute for Biology Tübingen, Tübingen, Germany.
Li HeDepartment of Molecular Biology, Max Planck Institute for Biology Tübingen, Tübingen, Germany.
Yuxing ZhouMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Evan K LinDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Russell ChuangDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Wai Wai ThiriDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Sean ConveryDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Suhua FengMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Detlef WeigelDepartment of Molecular Biology, Max Planck Institute for Biology Tübingen, Tübingen, Germany.
Steven E JacobsenMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.

Funding

Epigenetic gene regulation in ArabidopsisR35GM130272 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JACOBSEN, STEVEN E · 2019 to 2023
$1.6M
NIGMS NIH HHS R35 GM130272
6 · The paper itself

Abstract

DNA methylation is a conserved epigenetic modification crucial for silencing genes and transposable elements (TEs). However, the mechanisms that cause silencing remain unclear, partly because methyl reader protein mutants in both plants and animals show minimal transcriptional changes. To explore the possibility of redundancy among these silencing mechanisms, we generated combinatorial mutants of H1.1, H1.2, ADCP1, MOM1, MBD2, MBD5, and MBD6 lacking key methyl readers and related silencing pathways. We observed massive derepression of genes and TEs at DNA-methylated loci, showing that these pathways account for 73% of silencing compared to DNA methylation-free mutants. We also observed that immune response genes were upregulated, causing an imbalance between growth and defense. Loss of downstream silencing pathways further disrupted 3D genome organization, leading to increased euchromatin-heterochromatin interactions. These findings highlight the cooperative action of multiple downstream mechanisms in DNA methylation-mediated silencing and genome organization.

Identifiers

PMID41727113
PMCPMC12918867

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Registered trials

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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.