Actors of the tyrosine kinase receptor downstream signaling pathways in amphioxus

One of the major goals of evo-developmentalists is to understand how the genetic mechanisms controlling embryonic development have evolved to create the current diversity of bodyplans that we encounter in the animal kingdom. Tyrosine kinase receptors (RTKs) are transmembrane receptors present in all...

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Veröffentlicht in:Evolution & development 2009, Vol.11 (1), p.13-26
Hauptverfasser: Bertrand, Stéphanie, Campo-Paysaa, Florent, Camasses, Alain, García-Fernàndez, Jordi, Escrivà, Héctor
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Sprache:eng
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Zusammenfassung:One of the major goals of evo-developmentalists is to understand how the genetic mechanisms controlling embryonic development have evolved to create the current diversity of bodyplans that we encounter in the animal kingdom. Tyrosine kinase receptors (RTKs) are transmembrane receptors present in all metazoans known to control several developmental processes. They act via the activation of various cytoplasmic signaling cascades, including the mitogen-activated protein kinase (MAPK), the PI3K/Akt, and the phospholipase C-γ (PLCγ)/protein kinase C (PKC) pathways. In order to address the evolution of these three pathways and their involvement during embryogenesis in chordates, we took advantage of the complete genome sequencing of a key evolutionarily positioned species, the cephalochordate amphioxus, and searched for the complete gene set of the three signaling pathways. We found that the amphioxus genome contains all of the most important modules of the RTK-activated cascades, and looked at the embryonic expression of two genes selected from each cascade. Our data suggest that although the PI3K/Akt pathway may have ubiquitous functions, the MAPK and the PLCγ/PKC cascades may play specific roles in amphioxus development. Together with data known in vertebrates, the expression pattern of PKC in amphioxus suggests that the PLCγ/PKC cascade was implicated in neural development in the ancestor of all chordates.
ISSN:1520-541X
1525-142X
DOI:10.1111/j.1525-142X.2008.00299.x