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First published online 21 June 2006
doi: 10.1242/dev.02477


Development 133, 2875-2886 (2006)
Published by The Company of Biologists 2006


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Replacement of the Sox10 transcription factor by Sox8 reveals incomplete functional equivalence

Susanne Kellerer1,*, Silke Schreiner1,*, C. Claus Stolt1, Stefanie Scholz1, Michael R. Bösl2 and Michael Wegner1,{dagger}

1 Institut für Biochemie, Universität Erlangen, Fahrstrasse 17, D-91054 Erlangen, Germany
2 Max-Planck-Institut für Neurobiologie, Martinsried, Germany.

{dagger} Author for correspondence (e-mail: m.wegner{at}biochem.uni-erlangen.de)

Accepted 1 June 2006

Sox8 and Sox10 are two closely related transcription factors of the Sox protein family with overlapping expression patterns during development. They are believed to perform very similar functions because several developmental processes, including enteric nervous system development and oligodendrocyte differentiation, are regulated by both Sox proteins. To analyze the extent of functional equivalence between the two Sox proteins, we employed targeted mutagenesis to replace Sox10 with Sox8 in the mouse. In mice that expressed Sox8 instead of Sox10, Sox10 deficiency was phenotypically rescued to different extents in affected tissues. Whereas development of glial cells and neurons in the sensory and sympathetic parts of the peripheral nervous system was almost normal when Sox10 was replaced by Sox8, melanocyte development was as defective as in Sox10-deficient mice. The ability of Sox8 to rescue the defects in enteric nervous system development and oligodendrocyte differentiation of Sox10-deficient mice was limited. We conclude that the extent of functional equivalence depends on the tissue and that, despite their relatedness, Sox8 and Sox10 have more unique functions than previously appreciated.

Key words: Sry, High-mobility-group, Redundancy, Glia, Oligodendrocyte, Neural crest


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