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Xenopus laevis as a Model to Identify Translation Impairment
10:24

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Published on: September 27, 2015

Eukaryotic initiation factor 6 (eif6) overexpression affects eye development in Xenopus laevis.

N De Marco1, M Tussellino, A Vitale

  • 1Department of Structural and Functional Biology, University of Naples Federico II, Naples, Italy. nademarc@unina.it

Differentiation; Research in Biological Diversity
|May 24, 2011
PubMed
Summary

Overexpression of translation factor eIF6 in Xenopus embryos causes transient eye defects, unrelated to its known roles in ribosome assembly or apoptosis. The eye phenotype is not linked to PKC-dependent phosphorylation or anti-apoptotic functions of eIF6.

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Published on: June 15, 2017

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Cell Signaling

Background:

  • The translation initiation factor eIF6 regulates ribosome assembly, mRNA translation, and apoptosis.
  • eIF6 phosphorylation at Serine 235 by PKC influences its functions.
  • eIF6 overexpression in Xenopus embryos leads to aberrant eye development.

Purpose of the Study:

  • To investigate the transient eye phenotype caused by eIF6 overexpression in Xenopus embryos.
  • To determine the underlying mechanisms of eIF6-induced eye development defects.
  • To assess the link between eye development and eIF6's roles in ribosome assembly and apoptosis.

Main Methods:

  • mRNA injection of eIF6 into Xenopus embryos.
  • Morpholino-mediated knockdown of eIF6 protein synthesis.
  • Analysis of eye development and retinal layer recovery.
  • Assessment of anterior and brain-specific neural markers.
  • Co-injection experiments with Bcl2 and Bax.

Main Results:

  • eIF6 overexpression caused a transient eye phenotype that recovered by stage 42.
  • Other neural regions and anterior/brain markers remained unaffected.
  • Reducing eIF6 protein synthesis with morpholinos did not cause eye defects.
  • The eye phenotype was independent of eIF6's anti-apoptotic role (Bcl2/Bax pathways).
  • PKC-dependent phosphorylation of Ser235 was not required for the eye defect.

Conclusions:

  • The aberrant eye phenotype in eIF6-overexpressing embryos is transient and self-correcting.
  • This phenotype is not directly linked to eIF6's established functions in ribosome biogenesis or its anti-apoptotic activity.
  • The specific pathway mediating eIF6-induced eye development alterations remains to be elucidated.