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Vol. 13, No. 19, pp. 2538-2548, October 1, 1999
1 Max-Delbrück-Center for Molecular Medicine, 13092 Berlin, Germany; 2 Friedrich Miescher Institut, 4058 Basel,
Switzerland; 3 The Victor Chang Cardiac Research Institute,
Darlinghurst 2010, Australia
The ErbB2 tyrosine kinase functions as coreceptor for the neuregulin
receptors ErbB3 and ErbB4 and can participate in signaling of EGF
receptor (ErbB1), interleukin receptor gp130, and G-protein coupled
receptors. ErbB2
/ mice die at
midgestation because of heart malformation. Here, we report a genetic
rescue of their heart development by myocardial expression of erbB2
cDNA that allows survival of the mutants to birth. In rescued
erbB2 mutants, Schwann cells are lacking. Motoneurons form and
can project to muscle, but nerves are poorly fasciculated and
disorganized. Neuromuscular junctions form, as reflected in clustering
of AChR and postsynaptic expression of the genes encoding the 
-AChR,
AChE, 
-AChR, and the RI subunit of the cAMP protein kinase. However,
a severe loss of motoneurons on cervical and lumbar, but not on
thoracic levels occurs. Our results define the roles of Schwann cells
during motoneuron and synapse development, and reveal different
survival requirements for distinct motoneuron populations.
[Key Words: Motoneuron loss; neuromuscular synapse; coreceptor; neuregulin; AChR]
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