Sox10-iCreERT2: A mouse line to inducibly trace the neural crest and oligodendrocyte lineage

Authors

  • Christiane Simon,

    1. Physiological Genomics, Institute of Physiology, Ludwig-Maximilians University, Munich, Germany
    2. Institute for Stem Cell Research, HelmholtzZentrum münchen, Neuherberg, Germany
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  • Heiko Lickert,

    1. Institute for Stem Cell Research, HelmholtzZentrum münchen, Neuherberg, Germany
    2. Institute of Diabetes and Regeneration Research, HelmholtzZentrum münchen, Neuherberg, Germany
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  • Magdalena Götz,

    1. Physiological Genomics, Institute of Physiology, Ludwig-Maximilians University, Munich, Germany
    2. Institute for Stem Cell Research, HelmholtzZentrum münchen, Neuherberg, Germany
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  • Leda Dimou

    Corresponding author
    1. Physiological Genomics, Institute of Physiology, Ludwig-Maximilians University, Munich, Germany
    2. Institute for Stem Cell Research, HelmholtzZentrum münchen, Neuherberg, Germany
    • Physiological Genomics, Institute of Physiology, Ludwig-Maximilians University, 80336 Munich, Germany
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Abstract

SOX10 is a well-conserved and widely expressed transcription factor involved in the regulation of embryonic development and in the determination of cell fate. As it is expressed in neural crest cells, their derivatives and the oligodendrocyte lineage, mutations of the protein contribute to a variety of diseases like neurocristopathies, peripheral demyelinating neuropathies, and melanoma. Here, we report the generation of an inducible Sox10-iCreERT2 BAC transgenic mouse line that labels, depending on the timepoint of induction, distinct derivatives of the otic placode and the neural crest as well as cells of the oligodendrocyte lineage. Surprisingly, we could show a neural crest origin of pericytes in the brain. Besides its use for fate-mapping, the Sox10-iCreERT2 mouse line is a powerful tool to conditionally inactivate genes in the neural crest cells, their progeny and/or the oligodendrocyte lineage in a time-dependent fashion to gain further insights into their function and contribution to diseases. genesis 50:506–515, 2012. © 2011 Wiley Periodicals, Inc.

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