Evidence map›Paper›PMID 42409830›Full record

ArticleNature communications2026

The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers.

Jianxiang Zhang, Ye Xin, Li Cheng, Yuan Xing, Yuxin Ouyang, Mengli Zhang, Yubin Chen, Ruopeng Feng, Xiaohui Qiu, Beisi Xu and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

15 authors.

Jianxiang Zhang *Department of Blood Transfusion, The First Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, National Clinical Research Center for Hematologic Diseases, State Key Laboratory of Radiation Medicine and Protection, Collaborative Innovation Center of Hematology, Suzhou Medical College, Soochow University, Suzhou, China.ORCID http://orcid.org/0009-0000-7972-6557
Ye Xin *Department of Blood Transfusion, The First Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, National Clinical Research Center for Hematologic Diseases, State Key Laboratory of Radiation Medicine and Protection, Collaborative Innovation Center of Hematology, Suzhou Medical College, Soochow University, Suzhou, China.
Li Cheng *Department of Hematology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Yuan XingDepartment of Blood Transfusion, The First Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, National Clinical Research Center for Hematologic Diseases, State Key Laboratory of Radiation Medicine and Protection, Collaborative Innovation Center of Hematology, Suzhou Medical College, Soochow University, Suzhou, China.
Yuxin OuyangDepartment of Blood Transfusion, The First Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, National Clinical Research Center for Hematologic Diseases, State Key Laboratory of Radiation Medicine and Protection, Collaborative Innovation Center of Hematology, Suzhou Medical College, Soochow University, Suzhou, China.
Mengli ZhangDepartment of Blood Transfusion, The First Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, National Clinical Research Center for Hematologic Diseases, State Key Laboratory of Radiation Medicine and Protection, Collaborative Innovation Center of Hematology, Suzhou Medical College, Soochow University, Suzhou, China.
Yubin ChenDepartment of Blood Transfusion, The First Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, National Clinical Research Center for Hematologic Diseases, State Key Laboratory of Radiation Medicine and Protection, Collaborative Innovation Center of Hematology, Suzhou Medical College, Soochow University, Suzhou, China.
Ruopeng FengDepartment of Hematology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Xiaohui QiuDepartment of Hematology, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID http://orcid.org/0000-0002-5767-0422
Beisi XuCenter for Applied Bioinformatics, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID http://orcid.org/0000-0003-0099-858X
Yong ChengDepartment of Hematology, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID http://orcid.org/0000-0002-9314-0971
Chunliang LiDepartment of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID http://orcid.org/0000-0002-5938-5510
Hans-Martin HerzDepartment of Hematology, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID http://orcid.org/0000-0003-4780-9176
Mitchell J WeissDepartment of Hematology, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID http://orcid.org/0000-0002-6734-4858
Peng XuDepartment of Blood Transfusion, The First Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, National Clinical Research Center for Hematologic Diseases, State Key Laboratory of Radiation Medicine and Protection, Collaborative Innovation Center of Hematology, Suzhou Medical College, Soochow University, Suzhou, China. pengxu@suda.edu.cn.ORCID http://orcid.org/0000-0002-7573-4813

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene expression during cellular differentiation is coordinated by combinatorial interactions between transcription factors (TFs) and cofactors. Although the TF GATA1 coordinates gene transcription in hematopoiesis, the specific cofactors required for GATA1-driven gene expression are incompletely defined. We identify the H3K4 methyltransferase KMT2D, as a cofactor of GATA1 in erythropoiesis. Loss of KMT2D in human erythroid precursors causes developmental arrest with impaired expression of numerous erythroid genes. Mechanistically, KMT2D colocalizes with GATA1 on more than one thousand erythroid enhancers, and such co-occupancy is associated with stronger transcriptional activity than occupancy by GATA1 alone. Acute depletion of KMT2D in erythroid precursors causes rapid reductions of H3K4me1 and H3K27ac on a subset of GATA1-bound enhancers and impairs their target gene expression. Moreover, acute depletion of GATA1 or KMT2D individually causes downregulation of overlapping gene sets. Our findings demonstrate how a lineage-specific TF cooperates with a ubiquitous epigenetic regulator to drive lineage-specific gene expression.

Indexed as

Enhancer Elements, GeneticErythropoiesisGATA1 Transcription FactorHistone-Lysine N-MethyltransferaseAnimalsErythroid CellsHistonesHumansGATA1 protein, humanGATA1 Transcription FactorHistone-Lysine N-MethyltransferaseHistones

Identifiers

PMID42409830
PMCPMC13473644

What OpenQuestion holds

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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.