Disruption of pioneer growth cone guidance in vivo by removal of glycosyl-phosphatidylinositol-anchored cell surface proteins.

摘要: Cell surface proteins anchored to membranes via covalently attached glycosyl-phosphatidylinositol (GPI) have been implicated in neuronal adhesion, promotion of neurite outgrowth and directed cell migration. Treatment grasshopper embryos with bacterial phosphatidylinositol-specific phospholipase C (PI-PLC), an enzyme that cleaves the GPI anchor, often induced disruptions highly stereotyped migrations peripheral pioneer growth cones afferent neuron bodies. In distal limb regions treated PI-PLC at early stages axon outgrowth, lost their proximal orientation toward central nervous system (CNS) turned distally. Pioneer limbs also failed make a characteristic ventral turn along trochanter-coxa (Tr-Cx) segment boundary, instead continued grow proximally across boundary. earlier stage development caused pre-axonogenesis Cx1 neurons abandon normal circumferential migration reorient CNS. None these abnormal phenotypes were observed untreated or exposed other phospholipases do not release GPI-anchored proteins. Incubation effectively removed immunoreactivity for fasciclin I, protein expressed on subset surfaces. These results suggest are involved cone guidance bud vivo.