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Updated: Aug 27, 2026

RhoC GTPase Activation Assay
09:58

RhoC GTPase Activation Assay

Published on: August 22, 2010

Tenascin-C suppresses Rho activation

M B Wenk1, K S Midwood, J E Schwarzbauer

  • 1Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA.

The Journal of Cell Biology
|August 23, 2000
PubMed

Insights

Tenascin-C alters cell shape by suppressing RhoA activation, a key regulator of the actin cytoskeleton. This extracellular matrix protein acts as a switch, reversing fibronectin

Area of Science:

  • Cell biology
  • Extracellular matrix (ECM) research
  • Cytoskeletal dynamics

Background:

  • Cell adhesion to extracellular matrix (ECM) components influences cytoskeletal organization via Rho family GTPases.
  • Tenascin-C is a developmentally regulated matrix protein that modulates cellular responses to other ECM proteins like fibronectin (FN).

Purpose of the Study:

  • To investigate the effect of Tenascin-C on cell phenotype and RhoA activation within a three-dimensional fibrin-fibronectin matrix.
  • To elucidate the regulatory role of Tenascin-C in cytoskeletal organization and Rho GTPase signaling.

Main Methods:

  • Culturing cells on a 3D fibrin matrix containing fibronectin.
  • Analyzing cell morphology, specifically actin stress fibers and filopodia formation.
  • Assessing RhoA activation status.
  • Utilizing enforced RhoA activation and a Rho inhibitor (C3 transferase) to study functional effects.

Main Results:

  • Tenascin-C induced a distinct cell phenotype characterized by suppressed actin stress fibers and increased actin-rich filopodia.
  • This morphological change was correlated with a complete suppression of RhoA activation.
  • Enforced RhoA activation rescued the tenascin-C-induced phenotype, while Rho inhibition reversed the effects of active Rho.

Conclusions:

  • Tenascin-C acts as a regulatory switch, suppressing RhoA activation and reversing the effects of adhesive proteins on Rho function.
  • This study presents a novel paradigm for how ECM components regulate cytoskeletal organization through GTPase signaling.
  • Understanding Tenascin-C's role offers new insights into cell adhesion and matrix-mediated cellular responses.

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