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XB-ART-12160
Genes Dev October 1, 1999; 13 (19): 2538-48.

Peripheral nervous system defects in erbB2 mutants following genetic rescue of heart development.

Woldeyesus MT , Britsch S , Riethmacher D , Xu L , Sonnenberg-Riethmacher E , Abou-Rebyeh F , Harvey R , Caroni P , Birchmeier C .


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 alpha-AChR, AChE, epsilon-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.

PubMed ID: 10521398
PMC ID: PMC317072
Article link: Genes Dev

Genes referenced: ache egf erbb2 erbb3 erbb4 il6st

References [+] :
Altiok, ErbB3 and ErbB2/neu mediate the effect of heregulin on acetylcholine receptor gene expression in muscle: differential expression at the endplate. 1995, Pubmed


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