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The transforming growth factor beta type II receptor can replace the activin type II receptor in inducing mesoderm

A Bhushan1, H Y Lin, H F Lodish

  • 1Molecular Neurobiology Laboratory, Salk Institute, La Jolla, California 92037.

Insights

Adding transforming growth factor beta (TGF-beta) type II receptors to Xenopus embryos revealed TGF-beta 1 can induce mesoderm. This suggests TGF-beta and activin signaling pathways are similar, with differences arising from ligand-binding domains.

Area of Science:

  • Developmental Biology
  • Molecular Signaling
  • Cell Biology

Background:

  • Type II receptors for transforming growth factor beta (TGF-beta) and activin are serine/threonine protein kinases.
  • Activin induces mesodermal cell types in Xenopus animal caps, while TGF-beta 1 has no effect due to absent functional receptors.

Purpose of the Study:

  • To investigate the biological activities of TGF-beta 1 by introducing its type II receptor into Xenopus embryos.
  • To compare the signaling pathways utilized by TGF-beta and activin.

Main Methods:

  • Introduction of RNA encoding the TGF-beta type II receptor into Xenopus embryos.
  • Animal cap assays to assess mesoderm induction by TGF-beta 1 and activin.
  • Utilizing a dominant inhibitory ras mutant (p21(Asn-17)Ha-ras) to block signaling.

Main Results:

  • TGF-beta 1 and activin showed similar potency in inducing mesoderm-specific mRNAs in treated Xenopus embryos.
  • Both growth factors elicited the same types of mesodermal tissues.
  • The response to both TGF-beta 1 and activin was inhibited by the ras mutant.

Conclusions:

  • Activin and TGF-beta type II receptors can utilize similar intracellular signaling pathways.
  • The distinct biological effects of TGF-beta and activin are likely due to differences in their ligand-binding domains and cellular responsiveness.

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