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Pre-existing clusters of the adaptor Lat do not participate in early T cell signaling events.

机译:适配器Lat的预先存在的群集不参与早期T细胞信号事件。

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摘要

Engaged T cell antigen receptors (TCRs) initiate signaling through the adaptor protein Lat. In quiescent T cells, Lat is segregated into clusters on the cell surface, which raises the question of how TCR triggering initiates signaling. Using super-resolution fluorescence microscopy, we found that pre-existing Lat domains were neither phosphorylated nor laterally transported to TCR activation sites, which suggested that these clusters do not participate in TCR signaling. Instead, TCR activation resulted in the recruitment and phosphorylation of Lat from subsynaptic vesicles. Studies of Lat mutants confirmed that recruitment preceded and was essential for phosphorylation and that both processes were independent of surface clustering of Lat. Our data suggest that TCR ligation preconditions the membrane for vesicle recruitment and bulk activation of the Lat signaling network.
机译:订婚的T细胞抗原受体(TCR)通过衔接蛋白Lat启动信号传导。在静止的T细胞中,Lat在细胞表面被隔离成簇,这引发了TCR触发如何启动信号传导的问题。使用超分辨率荧光显微镜,我们发现既存的Lat域既未磷酸化也未横向运输至TCR激活位点,这表明这些簇不参与TCR信号传导。相反,TCR激活导致突触下囊泡中Lat的募集和磷酸化。对Lat突变体的研究证实,募集先于磷酸,对于磷酸化必不可少,并且这两个过程都与Lat的表面簇独立。我们的数据表明,TCR结扎为Lat信号网络的囊泡募集和大量激活预先准备了膜。

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