Peripheral nervous system defects in erbB2 mutants following genetic rescue of heart development
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Date
1999
Authors
Woldeyesus, Masresha T.
Britsch, Stefan
Riethmacher, Dieter
Xu, Lan
Sonnenberg-Riethmacher, Eva
Abou-Rebyeh, Faikah
Harvey, Richard
Caroni, Pico
Birchmeier, Carmen
Journal Title
Journal ISSN
Volume Title
Publisher
Cold Spring Harbor Laboratory Press
Abstract
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 a-AChR, AChE, e-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
Description
Keywords
Motoneuron loss, neuromuscular synapse, coreceptor, neuregulin, AChR
Citation
Masresha T. Woldeyesus, Stefan Britsch, Dieter Riethmacher, Lan Xu, Eva Sonnenberg-Riethmacher, Faikah Abou-Rebyeh, Richard Harvey, Pico Caroni, Carmen Birchmeier; 1999; Peripheral nervous system defects in erbB2 mutants following genetic rescue of heart development; GENES & DEVELOPMENT