Verslag – Rapport – Bericht – Report - GSKE - FMRE

In summary we show an essential role for b-actin in neural crest cell ontogeny. The observed NCC
migration defect is likely due to both altered post-transcriptional signaling (at least in the Rho pathway
that is connected to cadherin signaling) and an improper EMT in the NCC cells resulting in aberrant
cadherin expression. These data are consistent with an upstream regulatory role of b-actin suggesting
again that its nuclear function, and not its cytoskeletal function, is the more important one.
This work is part of the PhD doctoral thesis of Davina Tondeleir, submitted January 7 th , defense foreseen
end of March.
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