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“An asymmetric response to fibroblast growth factor during heart development in the primitive chordate, Ciona intestinalis”
Author(s) -
Davidson Brad
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.387.3
Subject(s) - ciona intestinalis , fibroblast growth factor , chordate , biology , microbiology and biotechnology , ciona , cell division , heart development , cell polarity , signal transduction , asymmetric cell division , basic fibroblast growth factor , embryonic stem cell , cell , growth factor , gene , genetics , receptor , vertebrate
Fibroblast growth factors (FGFs) impact many aspects of cell behavior, playing critical roles in normal development and cancer biology. However, FGF signaling has not been linked to cell polarity. Modifications of cell polarity often direct asymmetric cell division resulting in differential specification of embryonic cell lineages. Here we employ the simple chordate, Ciona intestinalis , to investigate the role of fibroblast growth factor (FGF) in an asymmetric cell division closely tied to differential cardiac specification. Midway through embryogenesis, FGF signaling causes four founder cells to undergo an asymmetric division, generating four small heart precursor cells and four large tail muscle precursors. Targeted expression of a dominant negative FGF receptor blocks both asymmetric division and heart specification. However, application of the MAP kinase pathway inhibitor U0126 blocks heart specification, but does not appear to block asymmetric division. We are currently investigating this apparent uncoupling of specification and asymmetry downstream of FGF. Additionally, we have employed comparative microarray analysis of gene expression from sorted heart cells to identify the primary transcriptional changes mediated by FGF signaling. We are currently investigating the potential role of these target genes in signal modulation, cell polarity and heart specification.