Evidence map›Paper›PMID 42137983›Full record

ArticleNucleic acids research2026

Histone variant H2A.X represses deposition of active H3K4me3 marks and restricts H2A.W incorporation.

Aravind Madhu, Vivek Hari-Sundar Gandhivel, Steffi Raju, Riju Dey, Padubidri V Shivaprasad

Abstract read
In one paragraph

Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

5 authors.

Aravind MadhuNational Centre for Biological Sciences, Tata Institute of Fundamental Research, GKVK Campus, Bangalore 560 065, India.
Vivek Hari-Sundar GandhivelNational Centre for Biological Sciences, Tata Institute of Fundamental Research, GKVK Campus, Bangalore 560 065, India.
Steffi RajuNational Centre for Biological Sciences, Tata Institute of Fundamental Research, GKVK Campus, Bangalore 560 065, India.
Riju DeyNational Centre for Biological Sciences, Tata Institute of Fundamental Research, GKVK Campus, Bangalore 560 065, India.
Padubidri V ShivaprasadNational Centre for Biological Sciences, Tata Institute of Fundamental Research, GKVK Campus, Bangalore 560 065, India.ORCID 0000-0002-9296-4848

Funding

Council of Scientific and Industrial ResearchDepartment of Atomic Energy, Government of India 1303/3/2019/R&D-II/DAE/4749Department of Atomic Energy, Government of India BT/PR53711/BSA/33/312/2024Department of Biotechnology CRG/2023/003849NCBS, BangaloreNCBS-TIFRSERB
6 · The paper itself

Abstract

Histone variant H2A.X is a well-conserved histone that plays crucial roles in mediating DNA damage response across eukaryotes. Although H2A.X expresses and decorates gene bodies of actively expressed genes even without stress, it is not known if H2A.X has functions beyond DNA damage repair. Using genetic, high-throughput genomics, and molecular approaches, we identified a previously unappreciated role of H2A.X in regulating development-associated genes. Using custom-made antibodies specific to the rice H2A.X variant, we show that it repressed the deposition of active H3K4me3 marks over gene bodies and transposable elements (TEs), specifically regulating root development, photosynthesis, and pigmentation-related genes, as seen by the impairment of these processes in rice h2a.x knockout (ko) plants. H2A.X also repressed global deposition of repressive mark H3K9me2 by restricting the activity of H2A variant H2A.W. In agreement with this, there was a genome-wide relocalization of H2A.W to TEs and a few genes in ko plants. H2A.X-overexpressing plants exhibited stress phenotypes, including increased anthocyanin levels, mimicking the transcriptome of DNA-damaged wild-type (WT) plants. The transcriptome of knockdown (kd) lines of facilitates chromatin transcription (FACT) complex, a known chaperone of H2A.X, was largely similar to that of h2a.x ko plants, suggesting that the development-associated functions of FACT are at least partially due to H2A.X. These results suggest a specific role of H2A.X in regulating competing histone marks, a function that might also be conserved across plants.

Indexed as

HistonesPlant ProteinsDNA Transposable ElementsGene Expression Regulation, PlantOryzaPhotosynthesisPlant RootsDNA Transposable Elementshistone H3 trimethyl Lys4HistonesPlant Proteins

Identifiers

PMID42137983
PMCPMC13176775

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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.