Excellent paper about stress fibers and focal adhesions from the lab of Margaret Gardel

August 15, 2012 at 1:43 am Leave a comment

Just a week ago, I presented a paper at our weekly literature review (journal club) which I found very interesting.  Many biophysics researchers are studying these complexes called focal adhesions.  Focal adhesions are complexes made of several different proteins that serve as the link between a cell’s actin cytoskeleton and the surrounding extracellular matrix (ECM).  It is thought that these complexes generate the tension necessary to pull a cell forward during migration.  Deficiencies in mechanotransduction of these complexes are implicated in numerous diseases, such as cardiomyopathies and cancer.

This paper, titled “Tension is required but not sufficient for focal adhesion maturation without a stress fiber template” is from the lab of Margaret Gardel at the University of Chicago.  The authors show that cellular tension and traction forces are still present even after disruption of the stress fiber template at adhesion sites.  The impaired stress fiber assembly also impeded focal adhesion compositional maturation and ECM remodeling.  Finally they showed that focal adhesion maturation can still proceed even when disrupting myosin II-dependent cellular tension up to 80%.  This study therefore argues against the current hypothesis that stress fibers induce focal adhesion maturation primarily by exerting myosin II-dependent tension at cell-ECM contacts.  Instead, they claim that the structure of the actin cytoskeleton serves to recruit multiple other proteins that are important to focal adhesion maturation.

What I found interesting about this study is that the authors were able to alter the structural framework of the actin cytoskeleton by disrupting only the radial stress fibers (perpendicular to the cell edge), while leaving the transverse arcs (parallel to the cell edge) unperturbed.

Here’s part of figure 1, which explains this.  Note the radial stress fibers in the wild type (WT) cells (indicated by the yellow arrows) and the transverse arcs (indicated by the red arrows), and then note the disappearance of the radial stress fibers in the subsequent images, all of which are ways to disrupt the radial stress fibers.  Also from the paxillin staining, we can see that the focal adhesions are unchanged (paxillin is a focal adhesion protein).

I find it very clever to change the architecture of the actin cytoskeleton, and then observe the changes in tension generation and focal adhesion maturation.  To be able to come up with this idea is a testament to a very creative group of researchers.


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