Cited by 195T-cell and B-cell ImmunologyDevelopmental Biology and Gene RegulationGenomics and Chromatin Dynamics

Mast cell lineage diversion of T lineage precursors by the essential T cell transcription factor GATA-3

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Taghon, Tom, Yui, Mary A, Rothenberg, Ellen V·2007·Nature Immunology

Abstract

GATA-3 is essential for T cell development from the earliest stages. However, abundant GATA-3 can drive T lineage precursors to a non-T cell fate, depending on Notch signaling and developmental stage. Here, overexpression of GATA-3 blocked the survival of pro-T cells when Notch-Delta signals were present but enhanced viability in their absence. In fetal thymocytes at the double-negative 1 (DN1) stage and DN2 stage but not those at the DN3 stage, overexpression of GATA-3 rapidly induced respecification to the mast cell lineage with high frequency by direct transcriptional 'reprogramming'. Normal DN2 thymocytes also showed mast cell potential when interleukin 3 and stem cell factor were added in the absence of Notch signaling. Our results suggest a close relationship between the pro-T cell and mast cell programs and a previously unknown function for Notch in T lineage fidelity.

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Crossref · 10.1038/ni1486

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  • The best current candidates for this silencing activity include GATA-3, TCF-1 or LEF-1, and especially Runx1, probably working in a dose-dependent combination, although the mechanism through which they finally achieve the ability to repress PU.1 has not yet been reported.

    “The best current candidates for this silencing activity include GATA-3 (104, 105), TCF-1 or LEF-1 (37), and especially Runx1 (80, 150–152), probably working in a dose-dependent combination, although the mechanism through which they finally achieve the ability to repress PU.1 has not yet been reported.”

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Authors
Taghon, T., Yui, M. A., & Rothenberg, E. V.
Affiliations
  • Ghent University Hospital (BE)
  • California Institute of Technology (US)
Corresponding author
Rothenberg, Ellen V
Venue
Nature Immunology
Published
2007-07-01
Volume
8
Issue
8
Pages
845-855
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
OpenAlex
W1989604593
Cited by
195
References
49
Citations by year
2026: 7 · 2025: 1 · 2024: 5 · 2023: 4 · 2022: 5 · 2021: 11 · 2020: 9 · 2019: 13 · 2018: 4 · 2017: 10 · 2016: 9 · 2015: 11 · 2014: 19 · 2013: 16 · 2012: 10
FWCI
5.83
Type
journal article
Language
en
Open access
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • CaltechAUTHORS (California Institute of Technology) (submittedVersion)
  • Ghent University Academic Bibliography (Ghent University) (submittedVersion)
Funders
  • National Cancer Institute (R01CA98925, R01CA90233, R01CA090233, R01CA098925)
  • National Institute of Allergy and Infectious Diseases (R01AI064590)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords
GATA3, T cell development, pro-T cells, Notch signaling, lineage reprogramming, transcriptional reprogramming, interleukin-3, stem cell factor, thymocyte survival
MeSH terms
Animals, Cell Differentiation, Cells, Cultured, Flow Cytometry, Mast Cells, Mice, Transgenic, T-Lymphocytes, Cell Lineage, Reverse Transcriptase Polymerase Chain Reaction, GATA3 Transcription Factor, Mice, Receptors, Notch

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