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Updated: Oct 5, 2026

Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
08:15

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Published on: October 17, 2014

Requirement for C3G-dependent Rap1 activation for cell adhesion and embryogenesis

Y Ohba1, K Ikuta, A Ogura

  • 1Department of Tumor Virology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan.

The EMBO Journal
|July 4, 2001
PubMed

Insights

C3G guanine nucleotide exchange factor (GEF) is essential for early mouse development. Its absence causes embryonic lethality, impacting cell adhesion, spreading, and migration by disrupting Rap1 activation.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • C3G functions as a guanine nucleotide exchange factor (GEF) for Rap1.
  • C3G activation is mediated by the Crk adaptor protein.
  • The physiological role of C3G in mammalian development is largely unknown.

Purpose of the Study:

  • To investigate the essential role of C3G in early mouse embryogenesis.
  • To elucidate the function of C3G in regulating Rap1 activation and cellular processes.

Main Methods:

  • Generation of C3G knockout mice.
  • Rescue of embryonic lethality using a human C3G transgene.
  • Establishment of C3G-deficient fibroblast cell lines (MEF-hC3G) via Cre-mediated excision.
  • Analysis of cell adhesion, spreading, and migration dynamics.

Main Results:

  • C3G knockout mice exhibit embryonic lethality before day 7.5.
  • C3G deficiency in MEF-hC3G cells impairs cell adhesion and spreading, while accelerating cell migration.
  • Rap1 activation is crucial for complementing C3G deficiency, as evidenced by suppressed accelerated migration with active Rap1, Rap2, R-Ras, Epac, and CalDAG-GEFI expression.

Conclusions:

  • C3G-dependent Rap1 activation is indispensable for embryonic fibroblast adhesion and spreading.
  • C3G plays a critical role in early mouse embryogenesis, likely through its regulation of Rap1 signaling.

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