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Acetylation of GATA‐3 affects T‐cell survival and homing to secondary lymphoid organs
Author(s) -
Yamagata Tetsuya,
Mitani Kinuko,
Oda Hideaki,
Suzuki Takahiro,
Honda Hiroaki,
Asai Takashi,
Maki Kazuhiro,
Nakamoto Tetsuya,
Hirai Hisamaru
Publication year - 2000
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/19.17.4676
Subject(s) - biology , acetylation , homing (biology) , gata3 , mutant , gata2 , microbiology and biotechnology , transcription factor , cancer research , immune system , t cell , immunology , gene , genetics , ecology
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.