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Notch signaling is necessary for GATA3 function in the initiation of T cell development.

Authors
  • Hozumi, Katsuto1
  • Negishi, Naoko
  • Tsuchiya, Izumi
  • Abe, Natsumi
  • Hirano, Ken-ichi
  • Suzuki, Daisuke
  • Yamamoto, Masayuki
  • Engel, James D
  • Habu, Sonoko
  • 1 Department of Immunology, and Research Center for Embryogenesis and Organogenesis, Tokai University School of Medicine, Isehara, Japan. [email protected] , (Japan)
Type
Published Article
Journal
European journal of immunology
Publication Date
Apr 01, 2008
Volume
38
Issue
4
Pages
977–985
Identifiers
DOI: 10.1002/eji.200737688
PMID: 18383037
Source
Medline
License
Unknown

Abstract

GATA3 and Notch1 are essential for T cell development at the earliest stage, but their mutual roles in this process remain to be clarified. In this study, we demonstrated that impairment of T lymphopoiesis in hematopoietic progenitor cells (HPC) of GATA3-deficient fetal liver (FL) on day 11.5 of gestation (E11.5) was rescued only by introduction of both GATA3 and the intracellular region of Notch1 but not by either alone. However, the introduction of GATA3 only was sufficient for T cell induction in GATA3-deficient FL cells at the advanced stage, where Notch signaling is well detectable. This indicates that Notch signaling is necessary for GATA3 to function for T cell fate specification but is not sufficient without GATA3. On the other hand, Notch signaling is sufficient for blockage of B cell development without GATA3, suggesting that T cell fate specification at the branching point does not result simply from the developmental arrest of B cell lineage by Notch signaling.

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