ArticleNature communications2025
ATF7IP/SETDB1-mediated epigenetic programming regulates thymic homing and T lymphopoiesis of hematopoietic progenitors during embryogenesis.
Wenqi Chen, Jiaxin Wu, Peilu She, Juan Li, Yuying Lan, Xueli Hu, Yangguo Huangfu, Chen Wu, Daqing Jin, Peng Xie and 6 more
Erratum issuedAbstract read
In one paragraphArticle in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
5 · Who and what moneyAuthors and funding
16 authors.
Wenqi Chen *Shanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.ORCID http://orcid.org/0000-0001-8057-4378 Jiaxin Wu *Shanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.
Peilu She *Shanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.ORCID http://orcid.org/0009-0001-1772-4414 Juan Li *Shanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.
Yuying LanShanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.
Xueli HuShanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.
Yangguo HuangfuShanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.
Chen WuSEU-ALLEN Joint Center, Institute for Brain and Intelligence, Southeast University, Nanjing, China.
Daqing JinShanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.
Yuxuan WuShanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China.ORCID http://orcid.org/0000-0002-9155-9883 Ping ZhuGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. tanganqier@163.com.ORCID http://orcid.org/0000-0002-4276-9593 Tao P ZhongShanghai Key Laboratory of Regulatory Biology, Shanghai Frontier Science Center of Genome Editing and Cell Therapy, East China Normal University School of Life Sciences, Shanghai, China. tzhong@bio.ecnu.edu.cn.ORCID http://orcid.org/0000-0003-1159-5487 Funding
Stem cells for therapeutics discovery in genetic blood disordersU01HL134812 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI DALEY, GEORGE Q, LIPTON, JEFFREY M · 2016 to 2022
$8.3MSystems Biology of Bone Marrow Failure and MDS for Precision MedicineRC2DK122533 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI FIGUEROA, MARIA EUGENIA, FLEMING, MARK D · 2019 to 2023
$6.4MFunctional characterization of the endothelial cell niche for hematopoietic stem cellsR01DK140372 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI LEONARD Ira ZON · 2024 to 2026
$2.1MGuangzhou Municipal Science and Technology Project 2024A04J4487Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2018YFA0108700Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2024YFA1803303National Natural Science Foundation of China (National Science Foundation of China) NSFC 82170256National Natural Science Foundation of China (National Science Foundation of China) NSFC82300275Natural Science Foundation of Chongqing (Natural Science Foundation of Chongqing Municipality) CSTB2023NSCQ-MSX0738NHLBI NIH HHS U01 HL134812NIDDK NIH HHS R01 DK140372NIDDK NIH HHS RC2 DK122533
6 · The paper itselfAbstract
T lymphocytes, which are essential for cell-mediated immunity in vertebrates, rely on thymic seeding of lymphoid progenitors for commitment, differentiation and maturation. However, the epigenetic programming of lymphoid-primed progenitor migration and differentiation is incompletely understood. Here, we show that zebrafish embryos lacking the epigenetic modulator Atf7ip or Setdb1 methyltransferase exhibit decreased thymic homing and differentiation of lymphoid progenitor cells. We show that Atf7ip regulates T cell progenitor homing and differentiation via Setdb1-triggered H3K9 trimethylation. Atf7ip interacts with Setdb1 to catalyze H3K9me3 modification of the key immune regulator bach2b to derepress the expression of ccr9a and irf4a, thereby promoting lymphoid progenitor homing and intrathymic differentiation. In the absence of Atf7ip or Setdb1, replenishing irf4a or diminishing bach2b restores the thymic trafficking and differentiation of lymphoid progenitor cells. Notably, depletion of ATF7IP by two complementary cre-recombinase alleles in mice (CAG-CreERT2 and Mx1-iCre) impedes the migration of hematopoietic progenitors to the thymus, resulting in declined T lymphopoiesis. These findings establish the role of ATF7IP/SETDB1-mediated epigenetic programming in governing T lymphoid progenitor trafficking and differentiation, with implications for understanding the pathogenesis of human T lymphoid diseases.
Indexed as
Embryonic DevelopmentEpigenesis, GeneticHematopoietic Stem CellsHistone-Lysine N-MethyltransferaseLymphopoiesisThymus GlandT-LymphocytesZebrafish ProteinsAnimalsBasic-Leucine Zipper Transcription FactorsCell DifferentiationCell MovementGene Expression Regulation, DevelopmentalInterferon Regulatory Factor-4Interferon Regulatory FactorsMiceBasic-Leucine Zipper Transcription FactorsHistone-Lysine N-MethyltransferaseInterferon Regulatory Factor-4Interferon Regulatory FactorsReceptors, CCRZebrafish Proteins
Identifiers
PMID40670340
PMCPMC12267628
What Socratic holds
Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390