Sox11 regulates survival and axonal growth of embryonic sensory neurons

Authors

  • L. Lin,

    1. Department of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, Texas
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    • Drs. Lin, Lee, and Wang contributed equally to this work.

  • V.M. Lee,

    1. Division of Developmental Biology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin
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    • Drs. Lin, Lee, and Wang contributed equally to this work.

  • Y. Wang,

    1. Department of Biology and Center for Excellence in the Neurosciences, University of New England, Biddeford, Maine
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    • Drs. Lin, Lee, and Wang contributed equally to this work.

  • J.S. Lin,

    1. Department of Neurosurgery, Medical College of Wisconsin, Milwaukee, Wisconsin
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  • E. Sock,

    1. Institut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany
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  • M. Wegner,

    1. Institut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany
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  • L. Lei

    Corresponding author
    1. Department of Biology and Center for Excellence in the Neurosciences, University of New England, Biddeford, Maine
    • Department of Biology and Center for Excellence in the Neurosciences, University of New England, Biddeford, ME 04005
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Abstract

Sensory neurons transduce various stimuli including temperature, pain, and touch from the periphery to the central nervous system. Sensory neuron development is governed by a combination of extracellular cues and specific gene expression. We demonstrated that the transcription factor Sox11 was highly expressed in the developing sensory neurons. To test the function of Sox11, we used a knockin mouse model where the entire coding region of Sox11 was replaced by a LacZ reporter. The ablation of Sox11 caused severe reduction in sensory neuron survival in the trigeminal and dorsal root ganglia, although it did not affect migration of neural crest cells or acquisition of major sensory neuron subtypes. We further demonstrated that ablating Sox11 caused an arrest of axonal outgrowth in vivo and in vitro. This defect could not be fully rescued by blocking cell death. Our data suggest that Sox11 is a key regulator of sensory neuron development. Developmental Dynamics, 2011. © 2010 Wiley-Liss, Inc.

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