Evidence map›Paper›PMID 25550471›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

Setd1a regulates progenitor B-cell-to-precursor B-cell development through histone H3 lysine 4 trimethylation and Ig heavy-chain rearrangement.

Betsabeh Khoramian Tusi, Changwang Deng, Tal Salz, Leilani Zeumer, Yangqiu Li, Chi Wai Eric So, Laurence M Morel, Yi Qiu, Suming Huang

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  3. Observational
  4. Article
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  9. Wdr5 is essential for fetal erythropoiesis and hematopoiesis.Experimental hematology & oncology · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. The MLL/SET family and haematopoiesis.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020
    Review
  17. Histone lysine methyltransferases in biology and disease.Nature structural & molecular biology · 2019
    Review
  18. Review
  19. Review
  20. 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

9 authors at 4 institutions in 3 countries.

Betsabeh Khoramian TusiDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom.
Changwang DengDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom.
Tal SalzDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom.
Leilani ZeumerDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom.
Yangqiu LiDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom.
Chi Wai Eric SoDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom.
Laurence M MorelDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom.
Yi QiuDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom qiuy@ufl.edu sumingh@ufl.edu.
Suming HuangDepartments of *Biochemistry & Molecular Biology, Pathology, Immunology & Laboratory Medicine, and Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, Florida, USA; Institute of Hematology, Jinan University Medical College, ShiPai, Guangzhou, China; and Department of Haematological Medicine, King's College London, London, United Kingdom qiuy@ufl.edu sumingh@ufl.edu.
University of Florida · USFlorida College · USJinan University · CNKing's College London · GB

Funding

B Cell Development Defects in Murine LupusR01AI058150 · NIAID · UNIVERSITY OF FLORIDA · PI MOREL, LAURENCE · 2004 to 2014
$3.7M
Regulation of insulator function and globin gene expression by USF and associatedR01HL091929 · NHLBI · UNIVERSITY OF FLORIDA · PI HUANG, SUMING · 2009 to 2013
$2.0M
Transcriptional regulation of TAL1/SCL in normal and malignant hematopoiesisR01HL090589 · NHLBI · UNIVERSITY OF FLORIDA · PI HUANG, SUMING · 2008 to 2012
$1.9M
The role of HDAC1 acetylation on corepressor complex activity and hematopoiesisR01HL095674 · NHLBI · UNIVERSITY OF FLORIDA · PI QIU, YI · 2010 to 2013
$1.4M
Cancer Research UK 16753NHLBI NIH HHS R01 HL090589NHLBI NIH HHS R01HL090589NHLBI NIH HHS R01 HL091929NHLBI NIH HHS R01HL091929NHLBI NIH HHS R01 HL095674NHLBI NIH HHS R01HL095674NIAID NIH HHS R01 AI058150
6 · The paper itself

Abstract

SETD1A is a member of trithorax-related histone methyltransferases that methylate lysine 4 at histone H3 (H3K4). We showed previously that Setd1a is required for mesoderm specification and hematopoietic lineage differentiation in vitro. However, it remains unknown whether or not Setd1a controls specific hematopoietic lineage commitment and differentiation during animal development. Here, we reported that homozygous Setd1a knockout (KO) mice are embryonic lethal. Loss of the Setd1a gene in the hematopoietic compartment resulted in a blockage of the progenitor B-cell-to-precursor B-cell development in bone marrow (BM) and B-cell maturation in spleen. The Setd1a-cKO (conditional knockout) mice exhibited an enlarged spleen with disrupted spleen architecture and leukocytopenia. Mechanistically, Setd1a deficiency in BM reduced the levels of H3K4me3 at critical B-cell gene loci, including Pax5 and Rag1/2, which are critical for the IgH (Ig heavy-chain) locus contractions and rearrangement. Subsequently, the differential long-range looped interactions of the enhancer Eμ with proximal 5' DH region and 3' regulatory regions as well as with Pax5-activated intergenic repeat elements and 5' distal VH genes were compromised by the Setd1a-cKO. Together, our findings revealed a critical role of Setd1a and its mediated epigenetic modifications in regulating the IgH rearrangement and B-cell development.

Indexed as

Gene Rearrangement, B-Lymphocyte, Heavy ChainAnimalsCell DifferentiationDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseHistonesHomeodomain ProteinsIon ChannelsLeukopoiesisMiceMice, Inbred C57BLMice, KnockoutPAX5 Transcription FactorPrecursor Cells, B-LymphoidDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseHistonesHomeodomain ProteinsIon ChannelsNsccn1 protein, mousePax5 protein, mousePAX5 Transcription FactorRAG-1 proteinRag2 protein, mouseB-cell differentiationlong-range chromatin loopspromoter H3K4me3Setd1a KO micetranscriptional regulation

Identifiers

PMID25550471
PMCPMC4396605
OpenAlexW1994531727

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.