The transcription/migration interface in heart precursors of Ciona intestinalis

Science. 2008 Jun 6;320(5881):1349-52. doi: 10.1126/science.1158170.

Abstract

Gene regulatory networks direct the progressive determination of cell fate during embryogenesis, but how they control cell behavior during morphogenesis remains largely elusive. Cell sorting, microarrays, and targeted molecular manipulations were used to analyze cardiac cell migration in the ascidian Ciona intestinalis. The heart network regulates genes involved in most cellular activities required for migration, including adhesion, cell polarity, and membrane protrusions. We demonstrated that fibroblast growth factor signaling and the forkhead transcription factor FoxF directly upregulate the small guanosine triphosphatase RhoDF, which synergizes with Cdc42 to contribute to the protrusive activity of migrating cells. Moreover, RhoDF induces membrane protrusions independently of other cellular activities required for migration. We propose that transcription regulation of specific effector genes determines the coordinated deployment of discrete cellular modules underlying migration.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Actin Cytoskeleton / metabolism
  • Actin Cytoskeleton / ultrastructure
  • Animals
  • Cell Lineage
  • Cell Movement*
  • Cell Surface Extensions / ultrastructure
  • Ciona intestinalis / cytology
  • Ciona intestinalis / embryology*
  • Ciona intestinalis / genetics*
  • Ciona intestinalis / metabolism
  • Fibroblast Growth Factors / metabolism
  • GTP Phosphohydrolases / metabolism
  • Gene Expression Profiling
  • Gene Expression Regulation, Developmental
  • Gene Regulatory Networks*
  • Heart / embryology*
  • Models, Animal
  • Morphogenesis
  • Muscle Cells / cytology
  • Myocardium / cytology
  • Oligonucleotide Array Sequence Analysis
  • Oligonucleotides, Antisense
  • Signal Transduction
  • Transcription, Genetic*
  • Up-Regulation
  • cdc42 GTP-Binding Protein / metabolism

Substances

  • Oligonucleotides, Antisense
  • Fibroblast Growth Factors
  • GTP Phosphohydrolases
  • cdc42 GTP-Binding Protein