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RalA and RalB function as the critical GTP sensors for GTP-dependent exocytosis.

J. Neurosci.2007 Jan 03;27(1):190-202
Gang Li 1 , Liping Han , Ting-Chieh Chou , Yoshihito Fujita , Lakshmanan Arunachalam , Ainan Xu , Aaron Wong , Soon-Kwang Chiew , Qi Wan , Li Wang , Shuzo Sugita
Gang Li 1 , Liping Han , Ting-Chieh Chou , Yoshihito Fujita , Lakshmanan Arunachalam , Ainan Xu , Aaron Wong , Soon-Kwang Chiew , Qi Wan , Li Wang , Shuzo Sugita
+ et al

[No authors listed]

Author information
  • 1 Division of Cellular and Molecular Biology, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada M5T 2S8.

摘要


Although it has been established that the activation of GTPases by non-hydrolyzable GTP stimulates neurotransmitter release from many different secretory cell types, the underlying mechanisms remain unclear. In the present study we aimed to elucidate the functional role(s) for endogenous Ras-like protein A (RalA) and RalB GTPases in GTP-dependent exocytosis. For this purpose stable neuroendocrine pheochromocytoma 12 (PC12) cell lines were generated in which the expressions of both RalA and RalB were strongly downregulated. In these double knock-down cells GTP-dependent exocytosis was reduced severely and was restored after the expression of RalA or RalB was reintroduced by transfection. In contrast, Ca2+-dependent exocytosis and the docking of dense core vesicles analyzed by electron microscopy remained unchanged in the double knock-down cells. Furthermore, the transfected RalA and RalB appeared to be localized primarily on the dense core vesicles in undifferentiated and nerve growth factor-differentiated PC12 cells. Our results indicate that endogenous RalA and RalB function specifically as GTP sensors for the GTP-dependent exocytosis of dense core vesicles, but they are not required for the general secretory pathways, including tethering of vesicles to the plasma membrane and Ca2+-dependent exocytosis.