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Science 6 June 2008:
Vol. 320. no. 5881, pp. 1349 - 1352
DOI: 10.1126/science.1158170
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Reports

The Transcription/Migration Interface in Heart Precursors of Ciona intestinalis

Lionel Christiaen,1* Brad Davidson,1{dagger} Takeshi Kawashima,2 Weston Powell,1 Hector Nolla,3 Karen Vranizan,4 Michael Levine1*

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.

1 Department of Molecular and Cell Biology, Division of Genetics, Genomics and Development, Center for Integrative Genomics, University of California, Berkeley, CA 94720, USA.
2 Department of Energy Joint Genome Institute, Walnut Creek, CA 94598, USA.
3 Cancer Research Laboratory, University of California, Berkeley, CA 94720, USA.
4 Functional Genomics Laboratory, University of California, Berkeley, CA 94720, USA.

{dagger} Present address: Department of Molecular and Cellular Biology, Molecular Cardiovascular Research Program, University of Arizona, Tucson, AZ 85724, USA.

* To whom correspondence should be addressed. E-mail: lionelchristiaen{at}berkeley.edu (L.C.); mlevine{at}berkeley.edu (M.L.)

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Science. ISSN 0036-8075 (print), 1095-9203 (online)