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First published online 24 July 2008
doi: 10.1242/dev.023960

Development 135, 2949-2957 (2008)
Published by The Company of Biologists 2008
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Abnormal sympathetic nervous system development and physiological dysautonomia in Egr3-deficient mice

Laurie C. Eldredge1, Xiaoguang M. Gao1, David H. Quach1, Lin Li1, Xiaoqiang Han1, Jon Lomasney1 and Warren G. Tourtellotte1,2,3,*

1 Department of Pathology, Northwestern University, Chicago, IL 60611, USA.
2 Department of Neurology, Northwestern University, Chicago, IL 60611, USA.
3 Division of Neuropathology, Northwestern University, Chicago, IL 60611, USA.

* Author for correspondence (e-mail: warren{at}northwestern.edu)

Accepted 23 June 2008

Sympathetic nervous system development depends upon many factors that mediate neuron migration, differentiation and survival. Target tissue-derived nerve growth factor (NGF) signaling-induced gene expression is required for survival, differentiation and target tissue innervation of post-migratory sympathetic neurons. However, the transcriptional regulatory mechanisms mediated by NGF signaling are very poorly defined. Here, we identify Egr3, a member of the early growth response (Egr) family of transcriptional regulators, as having an important role in sympathetic nervous system development. Egr3 is regulated by NGF signaling and it is expressed in sympathetic neurons during development when they depend upon NGF for survival and target tissue innervation. Egr3-deficient mice have severe sympathetic target tissue innervation abnormalities and profound physiological dysautonomia. Unlike NGF, which is essential for sympathetic neuron survival and for axon branching within target tissues, Egr3 is required for normal terminal axon extension and branching, but not for neuron survival. The results indicate that Egr3 is a novel NGF signaling effector that regulates sympathetic neuron gene expression required for normal target tissue innervation and function. Egr3-deficient mice have a phenotype that is remarkably similar to humans with sympathetic nervous system disease, raising the possibility that it may have a role in some forms of human dysautonomia, most of which have no known cause.

Key words: Egr3, Sympathetic, Ptosis, Neurotrophin, Physiology, Mouse


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