Direct evidence of involvement of glycosylphosphatidylinositol‐anchored proteins in the heavy metal‐mediated signal delivery into T lymphocytes

FEBS Letters

Taguchi, Ryo²  Ikezawa, Hiroh²  Ma, Li³  Isobe, Ken-Ichi³  Ohkusu, Kozo³  Hamaguchi, Michinari¹  Nakashima, Izumi³  Pu, Meiyi³ 

[1] Institute of Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya 466, Japan;Faculty of Pharmaceutical Sciences, Nagoya City University, Nagoya 467, Japan;Department of Immunology, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan

关键词: Glycosylphosphatidylinositol (GPI)-anchored protein;    Mercuric chloride;    Signal transduction;    Phosphatidylinositol-specific phospholipase C (PIPLC);    Phosphatidylinositol glycan-class A gene (PIG-A);    GPI;    glycosylphosphatidylinositol;    PIPLC;    phosphatidylinositol-specific phospholipase C;    PIG-A;    phosphatidylinositol glycan-class A gene;    PTYR;    phosphotyrosine;   

DOI  :  10.1016/0014-5793(95)00193-D

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The biological significance of the action of glycosylphosphatidylinositol (GPI)-anchored proteins in cell physiology and pathology when stimulated with their natural agonists is not known. Here we provide evidence that GPI-anchored proteins play a crucial role in the recently defined heavy metal (HgCl₂)-triggered signal delivery to T lymphocytes. Thiol-reactive HgCl₂, a multi-potent crosslinker of cell membrane proteins, induced heavy aggregation of Thy-1, a representative GPI-anchored protein, on murine thymocytes, and delivered a signal to induce heavy tyrosine phosphorylation of cellular proteins. This rather unusual signal delivery by HgCl₂ is diminished by the pre-treatment of cells with phosphatidylinositol-specific phospholipase C, which partially cleaved GPI-anchored proteins from the cell surface. Direct evidence for the involvement of GPI or GPI-anchored proteins in the HgCl₂-mediated signaling is provided by the loss of signaling in a mutant thymoma cell line defective in the phosphatidylinositol glycan-class A gene (PIG-A), and its restoration in a transfectant with PIG-A.

【 授权许可】

Unknown