Resumen:
n this study, we examined the subcellular distribution and functions of
LIMK1 in developing neurons. Confocal microscopy, subcellular
fractionation, and expression of several epitope-tagged LIMK1 constructs
revealed that LIMK1 is enriched in the Golgi apparatus and growth
cones, with the LIM domain required for Golgi localization and the PDZ
domain for its presence at neuritic tips. Overexpression of wild-type
LIMK1 suppresses the formation of trans-Golgi derived tubules, and
prevents cytochalasin D-induced Golgi fragmentation, whereas that of a
kinase-defective mutant has the opposite effect. Transfection of
wild-type LIMK1 accelerates axon formation and enhances the accumulation
of Par3/Par6, insulin-like growth factor (IGF)1 receptors, and neural
cell adhesion molecule (NCAM) at growth cones, whileinhibiting the
Golgi export of synaptophysin-containing vesicles. These effects were
dependent on the Golgi localization of LIMK1, paralleled by an increas