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  • The EMBO Journal (2000) 19, 4676 - 4687
  • doi:10.1093/emboj/19.17.4676

Acetylation of GATA-3 affects T-cell survival and homing to secondary lymphoid organs

Tetsuya Yamagata1, Kinuko Mitani1, Hideaki Oda2, Takahiro Suzuki1, Hiroaki Honda1, Takashi Asai1, Kazuhiro Maki1, Tetsuya Nakamoto1 and Hisamaru Hirai1

  1. Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan
  2. Department of Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan

Correspondence to:

Hisamaru Hirai, E-mail: hhirai-tky@umin.ac.jp

Received 18 April 2000; Accepted 12 July 2000; Revised 4 July 2000

Acetylation of a transcription factor has recently been shown to play a significant role in gene regulation. Here we show that GATA-3 is acetylated in T cells and that a mutation introduced into amino acids 305–307 (KRR-GATA3) creates local hypoacetylation in GATA-3. Remarkably, KRR-GATA3 possesses the most potent suppressive effect when compared with other mutants that are disrupted in putative acetylation targets. Expressing this mutant in peripheral T cells results in defective T-cell homing to systemic lymphnodes, and prolonged T-cell survival after activation. These findings have significant implications in that the acetylation state of GATA-3 affects its physiological function in the immune system and, more importantly, provides evidence for the novel role of GATA-3 in T-cell survival and homing to secondary lymphoid organs.

  • Keywords:

    • acetylation,
    • AICD,
    • GATA-3,
    • T-cell homing