TY - JOUR
T1 - Overexpression of a neural-specific Rho family GTPase, cRac1B, selectively induces enhanced neuritogenesis and neurite branching in primary neurons
AU - Albertinazzi, Chiara
AU - Gilardelli, Daniela
AU - Paris, Simona
AU - Longhi, Renato
AU - De Curtis, Ivan
PY - 1998/8/10
Y1 - 1998/8/10
N2 - Rho family GTPases have been implicated in cytoskeletal reorganization during neuritogenesis. We have recently identified a new gene of this family, cRac1B, specifically expressed in the chicken developing nervous system. This GTPase was overexpressed in primary neurons to study the role of cRac1B in the development of the neuronal phenotype. Overexpression of cRac1B induced an increment in the number of neurites per neuron, and dramatically increased neurite branching, whereas overexpression of the highly related and ubiquitous cRac1A GTPase did not evidently affect neuronal morphology. Furthermore, expression of an inactive form of cRac1B strikingly inhibited neurite formation. The specificity of cRac1B action observed in neurons was not observed in fibroblasts, where both GTPases produced similar effects on cell morphology and actin organization, indicating the existence of a cell type-dependent specificity of cRac1B function. Molecular dissection of cRac1B function by analysis of the effects of chimetic cRac1A/cRacZ1B proteins showed that the COOH-terminal portion of cRac1B is essential to induce increased neuritogenesis and neurite branching. Considering the distinctive regulation of cRaclB expression during neural development, our data strongly support an important role of cRaclB during neuritogenesis, and they uncover new mechanisms underlying the functional specificity of distinct Rho family GTPases.
AB - Rho family GTPases have been implicated in cytoskeletal reorganization during neuritogenesis. We have recently identified a new gene of this family, cRac1B, specifically expressed in the chicken developing nervous system. This GTPase was overexpressed in primary neurons to study the role of cRac1B in the development of the neuronal phenotype. Overexpression of cRac1B induced an increment in the number of neurites per neuron, and dramatically increased neurite branching, whereas overexpression of the highly related and ubiquitous cRac1A GTPase did not evidently affect neuronal morphology. Furthermore, expression of an inactive form of cRac1B strikingly inhibited neurite formation. The specificity of cRac1B action observed in neurons was not observed in fibroblasts, where both GTPases produced similar effects on cell morphology and actin organization, indicating the existence of a cell type-dependent specificity of cRac1B function. Molecular dissection of cRac1B function by analysis of the effects of chimetic cRac1A/cRacZ1B proteins showed that the COOH-terminal portion of cRac1B is essential to induce increased neuritogenesis and neurite branching. Considering the distinctive regulation of cRaclB expression during neural development, our data strongly support an important role of cRaclB during neuritogenesis, and they uncover new mechanisms underlying the functional specificity of distinct Rho family GTPases.
KW - Actin
KW - Cytoskeleton
KW - Development
KW - Neurites
KW - Small GTPases
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U2 - 10.1083/jcb.142.3.815
DO - 10.1083/jcb.142.3.815
M3 - Article
C2 - 9700168
AN - SCOPUS:0031852652
VL - 142
SP - 815
EP - 825
JO - Journal of Cell Biology
JF - Journal of Cell Biology
SN - 0021-9525
IS - 3
ER -