Targeted expression of an oncogenic adaptor protein v-Crk potentiates axonal growth in dorsal root ganglia and motor neurons in vivo.
Brain Res Dev Brain Res
; 116(1): 29-39, 1999 Aug 05.
Article
de En
| MEDLINE
| ID: mdl-10446344
ABSTRACT
The ability of neurons to survive and to target axonal growth requires a coordinated series of cell extrinsic and intrinsic events. Previously, in a cellular model for neuronal differentiation, we showed that pheochromocytoma (PC12) cells expressing v-Crk, an oncogenic form of the SH2/SH3-containing c-Crk adaptor protein, potentiates axonal growth and prolongs nerve growth factor (NGF)-independent survival. In the present study, we have generated transgenic mice that express v-Crk in sensory, motor, and enteric neurons by placing v-crk under the control of the neuron-specific peripherin promoter. In contrast to wild-type (wt) mice, dorsal root ganglia (DRG) neurons explanted from post-natal day 1 transgenic mice demonstrated a reduced dependence on trophic factors for both survival and axonogenesis. v-Crk also caused an increase in the number of surviving spinal motor neurons (SMN), and interestingly, upon staining of sternomastoid muscle fibers with rhodamine conjugated alpha-bungarotoxin, many muscle fibers displayed an apparent increase in volume of motor end plates, and an increase in complexity of neuromuscular junctions (NMJ). Our data suggest that v-Crk may be involved in transducing extracellular signals to regulate cytoskeletal organization, and may act on an intrinsic determinant for axonal growth in a variety of neural types including sensory and motor neurons during development.
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Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Axones
/
Protéines oncogènes des retroviridae
/
Ganglions sensitifs des nerfs spinaux
/
Motoneurones
Type d'étude:
Prognostic_studies
Limites:
Animals
Langue:
En
Journal:
Brain Res Dev Brain Res
Sujet du journal:
CEREBRO
/
NEUROLOGIA
Année:
1999
Type de document:
Article
Pays d'affiliation:
États-Unis d'Amérique