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A cholera toxin-sensitive G-protein stimulates exocytosis in sea urchin eggs

Developmental Biology
|April 1, 1987
PubMed

Insights

Cholera toxin (CTX) sensitive G-proteins in sea urchin eggs regulate calcium release and cortical vesicle exocytosis during fertilization. This study identifies specific G-proteins involved in this crucial signal transduction pathway.

Area of Science:

  • Marine Biology
  • Cell Biology
  • Biochemistry

Background:

  • Guanine nucleotide-binding proteins (G-proteins) are key regulators of signal transduction pathways in eukaryotic cells.
  • Understanding G-protein involvement in fertilization is crucial for reproductive biology and developmental processes.
  • Sea urchin eggs serve as a model system for studying fertilization due to their accessibility and well-characterized responses.

Purpose of the Study:

  • To identify G-proteins in sea urchin eggs.
  • To investigate the role of G-proteins in signal transduction during fertilization.
  • To elucidate the mechanism of cortical vesicle exocytosis.

Main Methods:

  • Use of cholera toxin (CTX) and pertussis toxin (PTX) to ADP-ribosylate G-proteins.
  • Preparation of cell surface complexes from Lytechinus variegatus eggs.
  • Incubation with 32P-labeled NAD in the presence of toxins.
  • Microinjection of CTX, CTX subunit A, EGTA, cAMP, and cAMP-S into sea urchin eggs.

Main Results:

  • CTX catalyzed ADP-ribosylation of a 47-kDa polypeptide.
  • PTX catalyzed ADP-ribosylation of a 40-kDa polypeptide.
  • Microinjection of CTX induced cortical vesicle exocytosis, which was blocked by EGTA.
  • cAMP or cAMP-S injection did not induce exocytosis.

Conclusions:

  • A CTX-sensitive G-protein is involved in regulating Ca2+ release in sea urchin eggs.
  • This G-protein plays a role in the exocytosis of cortical vesicles during fertilization.
  • The findings provide insights into the molecular mechanisms of fertilization signal transduction.

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