Arkadia enhances nodal-related signalling to induce mesendoderm

Christiane Niederländer, James J. Walsh, Vasso Episkopou and C. Michael Jones ()
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Christiane Niederländer: Section of Gene Function and Regulation, Chester Beatty Laboratories, Institute of Cancer Research
James J. Walsh: Mammalian Neurogenesis Group, MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital
Vasso Episkopou: Mammalian Neurogenesis Group, MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital
C. Michael Jones: Section of Gene Function and Regulation, Chester Beatty Laboratories, Institute of Cancer Research

Nature, 2001, vol. 410, issue 6830, 830-834

Abstract: Abstract Nodal-related members of the transforming growth factor (TGF)-β family regulate the induction of mesoderm, endoderm, and mesendoderm, a tissue specific to the Spemann organizer1,2,3,4,5,6,7. How these different tissues form in response to the same signalling molecules is not completely understood. It has been suggested that concentration-dependent effects, mediated by extracellular cofactors and antagonists, are responsible for the differences1,8,9,10. Here we show that the nuclear protein Arkadia specifically potentiates the mesendoderm-inducing activity of a subset of TGF-β family members. The combined activities of Arkadia and Xenopus nodal-related-1 are sufficient to induce mesendoderm and suppress mesoderm. Arkadia dorsalizes ventral tissues, resulting in the induction of organizer-specific gene expression. Blocking nodal signalling extracellularly inhibits these effects. Arkadia influences nodal activity when co-expressed and can function in cells adjacent to those producing the nodal signal. Our findings, together with the observation that Arkadia mutant mice lack a node and node-derived mesendoderm, identify Arkadia as an essential modulator of the nodal signalling cascade that leads to induction of Spemann's organizer.

Date: 2001
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DOI: 10.1038/35071103

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