Xantivin suppresses the activity of EGF-CFC genes to regulate nodal signaling

Kousuke Tanegashima1, Yoshikazu Haramoto, Chika Yokota

  • 1Department of Life Sciences (Biology), University of Tokyo, Komaba, Tokyo, Japan.

Insights

Xenopus antivin (Xantivin) antagonizes nodal signaling by inhibiting EGF-CFC co-receptors. Depleting Xantivin expands mesodermal tissue and head defects, confirming its role in feedback inhibition during embryogenesis.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Nodal signaling is crucial for vertebrate embryonic development.
  • Lefty and antivin family genes regulate nodal signaling through feedback inhibition.
  • Understanding Xantivin's role in Xenopus embryogenesis is essential.

Purpose of the Study:

  • To investigate the function of Xantivin, a feedback inhibitor of nodal signaling, in Xenopus embryos.
  • To elucidate the interaction between Xantivin and nodal signaling components, including EGF-CFC genes.

Main Methods:

  • Morpholino antisense oligonucleotide (XatvMO) injection to deplete Xantivin in Xenopus embryos.
  • Analysis of mesodermal marker gene expression (Xbra, Xwnt8, Xnot, Chordin).
  • Animal cap assays and co-immunoprecipitation to study gene interactions.

Main Results:

  • XatvMO injection led to mesodermal tissue expansion and head defects.
  • Depletion of Xantivin up-regulated nodal signaling targets.
  • Xantivin was found to interact with EGF-CFC proteins (FRL-1, Cripto) and suppress their activity.

Conclusions:

  • Xantivin acts as a feedback inhibitor of nodal signaling in Xenopus.
  • Xantivin antagonizes nodal signaling by opposing the activity of EGF-CFC co-receptors.
  • These findings provide insights into the regulation of nodal signaling during vertebrate embryogenesis.

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