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Translational control of activin in Xenopus laevis embryos

P S Klein1, D A Melton

  • 1Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.

Developmental Genetics
|January 1, 1995
PubMed

Insights

The 3' untranslated region (UTR) of activin beta B mRNA inhibits activin protein production in Xenopus embryos. This regulation by maternal factors is crucial for controlling mesoderm induction and ectodermal development.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Xenopus laevis Embryology

Background:

  • Activin is a key signaling molecule in embryonic development, inducing mesoderm and inhibiting neural development in Xenopus laevis.
  • The concentration-dependent effects of activin highlight the need to understand mechanisms regulating its levels during embryogenesis.

Purpose of the Study:

  • To investigate the role of the 3' untranslated region (UTR) of activin beta B mRNA in regulating activin protein translation.
  • To identify potential maternal factors controlling activin beta B mRNA translation in Xenopus embryos.

Main Methods:

  • Micro-injection of modified activin beta B mRNA (with and without 3' UTR) into Xenopus embryos.
  • In vitro translation assays.
  • Quantification of mesoderm induction and protein levels.

Main Results:

  • Deletion of the 3' UTR of activin beta B mRNA increased mesoderm induction potency by 8-10 fold.
  • Truncation of the 3' UTR significantly enhanced activin protein levels in embryos, but not in vitro.
  • The 3' UTR conferred translational inhibition on a heterologous mRNA, indicating a conserved regulatory mechanism.

Conclusions:

  • The 3' UTR of activin beta B mRNA acts as a translational repressor in Xenopus embryos.
  • Maternal factors in Xenopus laevis embryos regulate the translation of injected activin beta B mRNA.
  • This translational control mechanism is likely essential for regulating endogenous activin beta B protein levels during key developmental events like mesoderm induction and ectodermal patterning.

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