The transcription factor Sox10 is a key regulator of peripheral glial development

Article Abstract:

Sox10, a transcription factor, has been shown to be a vital peripheral glial development regulator. Sox 10 also controls expression of ErbB3 in neural crest cells. Haploinsufficiency of Sox10 can cause pigmentation and megacolon defects also observed in Sox10(super.Dom/+) mice and in Waardenburg-Hirschsprung patients if the disease is caused by heterozygous SOX10 mutations.

Germany, Statistical Data Included, Genetic regulation, Genetic transcription, Transcription (Genetics), Cytochemistry, Neuroglia, Glia, Developmental neurology, Neurogenetics, Melanocytes, Klein-Waardenburg syndrome, Waardenburg's syndrome

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The ErbB2 and ErbB3 receptors and their ligand, neuregulin-1, are essential for development of the sympathetic nervous system

Article Abstract:

A novel phenotype has been found in mice. Targeted mutations in the erbB2, erbB3 or neuregulin-1 genes cause extreme hypoplasia of the primary sympathetic ganglion chain. There are indications that migration of neural crest cells to the mesenchyme lateral of the dorsal aorta depends on neuregulin-1 and receptors for it. At the dorsal aorta the cells differentiate into sympathetic neurons. It can be seen that the ErbB2 and ErbB3 receptors and the ligand neuregulin-1 are necessary for sympathetic nervous system development.

Protein tyrosine kinase, Protein-tyrosine kinase, Nervous system, Sympathetic, Sympathetic nervous system, Catecholamines, Adrenal medulla

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

Article Abstract:

The article focuses on the role of Schwann cells in motoneuron and neuromuscular synapse development. Genetic rescue of erbB2-deficient mice by miocardial expression of erbB2 cDNA allowing mutants' survival to birth and postsynaptic gene expression in rescued mutants are described.

International, Analysis, Gene mutations, Gene mutation, Heart diseases, Nervous system, Neuromuscular diseases, Nerve degeneration, Molecular microbiology

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