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Live Imaging of Cell Motility and Actin Cytoskeleton of Individual Neurons and Neural Crest Cells in Zebrafish Embryos
Published on: February 3, 2010
A chemical screen in zebrafish embryonic cells establishes that Akt activation is required for neural crest
Christie Ciarlo1,2, Charles K Kaufman3,4, Beste Kinikoglu5,6
1Stem Cell Program and Hematology/Oncology, Children's Hospital Boston, Howard Hughes Medical Institute, Boston, United States.
Abstract:
The neural crest is a dynamic progenitor cell population that arises at the border of neural and non-neural ectoderm. The inductive roles of FGF, Wnt, and BMP at the neural plate border are well established, but the signals required for subsequent neural crest development remain poorly characterized. Here, we conducted a screen in primary zebrafish embryo cultures for chemicals that disrupt neural crest development, as read out by crestin:EGFP expression. We found that the natural product caffeic acid phenethyl ester (CAPE) disrupts neural crest gene expression, migration, and melanocytic differentiation by reducing Sox10 activity. CAPE inhibits FGF-stimulated PI3K/Akt signaling, and neural crest defects in CAPE-treated embryos are suppressed by constitutively active Akt1. Inhibition of Akt activity by constitutively active PTEN similarly decreases crestin expression and Sox10 activity. Our study has identified Akt as a novel intracellular pathway required for neural crest differentiation.
Insights
Caffeic acid phenethyl ester (CAPE) disrupts neural crest development by inhibiting Akt signaling and reducing Sox10 activity. This study identifies Akt as a key pathway for neural crest differentiation.
Area of Science:
- Developmental biology
- Cell signaling
- Molecular genetics
Background:
- Neural crest cells are crucial for development, originating from the neural plate border.
- While FGF, Wnt, and BMP signaling are known inducers, signals for later neural crest development are unclear.
Purpose of the Study:
- To identify novel chemical modulators of neural crest development.
- To elucidate the intracellular signaling pathways governing neural crest differentiation.
Main Methods:
- Screening of chemical compounds in zebrafish embryos using crestin:EGFP expression.
- Investigating the effects of caffeic acid phenethyl ester (CAPE) on neural crest gene expression, migration, and differentiation.
- Analyzing the role of PI3K/Akt signaling and Sox10 activity.
Main Results:
- Caffeic acid phenethyl ester (CAPE) was identified as a disruptor of neural crest development.
- CAPE reduces Sox10 activity, impacting gene expression, migration, and melanocytic differentiation.
- The PI3K/Akt pathway is critical for neural crest differentiation, as demonstrated by rescue experiments with active Akt1 and inhibition with PTEN.
Conclusions:
- Akt signaling is a novel intracellular pathway essential for neural crest differentiation.
- Understanding this pathway provides new insights into neural crest development and potential therapeutic targets.
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