Sox10 participates in the early development of neural crest by controlling its specification and survival

HONORÉ S. M.; AYBAR M. J.; MAYOR R.

Marriott Copley, Boston, MA, USA.

Congreso; Society for Developmental Biology 62nd Annual Meeting; 2003

Society for Developmental Biology

The Sox family of transcription factors has been implicated in the development of different tissues during embryogenesis. Several mutations in humans and mice and zebrafish have shown that depletion of Sox10 activity produces defects in the development of neural crest derivatives. We have isolated the Xenopus homologue of the Sox10 gene and shown that is expressed in prospective neural crest and otic placode regions from the earliest stages of neural crest specification. Loss of function experiments using morpholino antisense oligos against Sox10 produce a loss of neural crest precursors as cell as an increase in apoptosis and a decrease in cell proliferation in the neural folds, suggesting that Sox10 could work as a survival factor in neural crest precursors in premigratory stages. An additional role of Sox10 on neural crest derivatives was studied in experiments where the development of melanocytes and ganglia induced in vivo and in vitro were blocked by inhibiting Sox10 activity. We also show that Sox10 expression is dependent on FGF and Wnt activity. Finally, we used inducible forms of the wild-type and dominant negatives for the Snail and Slug genes to establish the position of Sox10 in the hierarchical cascade of gene activation required for neural crest specification. Our results indicate that Sox10 may lie between Snail and Slug in the genetic cascade of transcription factors that controls neural crest development