Affordable Access

FoxF is essential for FGF-induced migration of heart progenitor cells in the ascidian Ciona intestinalis.

Authors
  • Beh, Jeni1
  • Shi, Weiyang
  • Levine, Mike
  • Davidson, Brad
  • Christiaen, Lionel
  • 1 Center for Integrative Genomics, Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, CA 94720, USA.
Type
Published Article
Journal
Development (Cambridge, England)
Publication Date
Sep 01, 2007
Volume
134
Issue
18
Pages
3297–3305
Identifiers
PMID: 17720694
Source
Medline
License
Unknown

Abstract

Heart development requires precise coordination of morphogenetic movements with progressive cell fate specification and differentiation. In ascidian embryos, FGF/MAPK-mediated activation of the transcription factor Ets1/2 is required for heart tissue specification and cell migration. We found that FoxF is one of the first genes to be activated in heart precursors in response to FGF signaling. We identified the FoxF minimal heart enhancer and used a cis-trans complementation test to show that Ets1/2 can interact with the FoxF enhancer in vivo. Next, we found that FoxF function is required downstream and in parallel to the FGF/MAPK/Ets cascade for cell migration. In addition, we demonstrated that targeted expression of a dominant-negative form of FoxF inhibits cell migration but not heart differentiation, resulting in a striking phenotype: a beating heart at an ectopic location within the body cavity of juveniles. Taken together, our results indicate that FoxF is a direct target of FGF signaling and is predominantly involved in the regulation of heart cell migration.

Report this publication

Statistics

Seen <100 times