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1: Genes Dev. 2006 Oct 1;20(19):2728-38.

FGF signaling delineates the cardiac progenitor field in the simple chordate,
Ciona intestinalis.

Davidson B, Shi W, Beh J, Christiaen L, Levine M.

Department of Molecular and Cellular Biology, Division of Genetics and
Development, Center for Integrative Genomics, University of California, Berkeley,
California 94720, USA. [e-mail]

Comprehensive gene networks in Ciona intestinalis embryos provide a foundation
for characterizing complex developmental processes, such as the initial phases of
chordate heart development. The basic helix-loop-helix regulatory gene Ci-Mesp is
required for activation of cardiac transcription factors. Evidence is presented
that Ci-Ets1/2, a transcriptional effector of receptor tyrosine kinase (RTK)
signaling, acts downstream from Mesp to establish the heart field. Asymmetric
activation of Ets1/2, possibly through localized expression of FGF9, drives heart
specification within this field. During gastrulation, Ets1/2 is expressed in a
group of four cells descended from two Mesp-expressing founder cells (the B7.5
cells). After gastrulation, these cells divide asymmetrically; the smaller
rostral daughters exhibit RTK activation (phosphorylation of ERK) and form the
heart lineage while the larger caudal daughters form the anterior tail muscle
lineage. Inhibition of RTK signaling prevents heart specification. Targeted
inhibition of Ets1/2 activity or FGF receptor function also blocks heart
specification. Conversely, application of FGF or targeted expression of
constitutively active Ets1/2 (EtsVp16) cause both rostral and caudal B7.5
lineages to form heart cells. This expansion produces an unexpected phenotype:
transformation of a single-compartment heart into a functional multicompartment
organ. We discuss these results with regard to the development and evolution of
the multichambered vertebrate heart.

PMID: 17015434 [PubMed - indexed for MEDLINE]

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