Evidence map›Paper›PMID 40022213›Full record

ArticleGenome biology2025

CTCF is selectively required for maintaining chromatin accessibility and gene expression in human erythropoiesis.

Xue Yang, Li Cheng, Ye Xin, Jianxiang Zhang, Xinfeng Chen, Jinchao Xu, Mengli Zhang, Ruopeng Feng, Judith Hyle, Wenjie Qi and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genome biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The Biological Function of Genome Organization.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Article
  8. Review
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

14 authors.

Xue Yang *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, Jiangsu Province, 215123, China.
Li Cheng *Department of Hematology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Ye Xin *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, Jiangsu Province, 215123, China.
Jianxiang Zhang *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, Jiangsu Province, 215123, China.
Xinfeng ChenCyrus 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, Jiangsu Province, 215123, China.
Jinchao XuCyrus 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, Jiangsu Province, 215123, China.
Mengli ZhangCyrus 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, Jiangsu Province, 215123, China.
Ruopeng FengDepartment of Hematology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Judith HyleDepartment of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Wenjie QiCenter for Applied Bioinformatics, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Wojciech RosikiewiczCenter for Applied Bioinformatics, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Beisi XuCenter for Applied Bioinformatics, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA. beisi.xu@stjude.org.
Chunliang LiDepartment of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA. chunliang.li@stjude.org.
Peng XuCyrus 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, Jiangsu Province, 215123, China. pengxu@suda.edu.cn.

Funding

Jiangsu Province National Science and Technology grant BK20210714National Natural Science Foundation of China 82170119Suzhou Municipality Gusu Leading Talents grant ZXL2022443
6 · The paper itself

Abstract

backgroundCTCF is considered as the most essential transcription factor regulating chromatin architecture and gene expression. However, genome-wide impact of CTCF on erythropoiesis has not been extensively investigated.

resultsUsing a state-of-the-art human erythroid progenitor cell model (HUDEP-2 and HEL cell lines), we systematically investigate the effects of acute CTCF loss by an auxin-inducible degron system on transcriptional programs, chromatin accessibility, CTCF genome occupancy, and genome architecture. By integrating multi-omics datasets, we reveal that acute CTCF loss notably disrupts genome-wide chromatin accessibility and the transcription network. We detect over thousands of decreased chromatin accessibility regions but only a few hundred increased regions after CTCF depletion in HUDEP-2 and HEL lines, suggesting the role of CTCF in maintaining proper chromatin openness in the erythroid lineage. CTCF depletion in the erythroid context notably disrupts the boundary integrity of topologically associating domains and chromatin loops but does not affect nuclear compartmentalization. We find erythroid lineage-specific genes, including some metabolism-related genes, are suppressed at immature and mature stages. Notably, we find a subset of genes whose transcriptional levels increase upon CTCF depletion, accompanied by decreased chromatin accessibility regions enriched with the GATA motif. We further decipher the molecular mechanism underlying the CTCF/GATA2 repression axis through distal non-coding chromatin regions. These results suggest a suppressive role of CTCF in gene expression during erythroid lineage specification.

conclusionsOur study reveals a novel role of CTCF in regulating erythroid differentiation by maintaining its proper chromatin openness and gene expression network, which extends our understanding of CTCF biology.

Indexed as

CCCTC-Binding FactorChromatinErythropoiesisGene Expression RegulationCell LineErythroid Precursor CellsHumansCCCTC-Binding FactorChromatinCTCF protein, humanChromatin accessibilityCTCFErythropoiesisGenome editingHematopoiesisTranscription regulation

Identifiers

PMID40022213
PMCPMC11869676

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LicenceCC BY
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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.