F-actin production in rat's cataracts is best understood when the structure is considered in terms of tensegrity. The authors speculate that the rapid alteration of fiber end migration paths results in the F-actin being reorganized into configurations that help support and maintain the shape of the fiber ends, thus preventing their complete breakdown.
Similar to the concept of tensegrity in architecture, to balance the combined compressive and tensile forces that could potentially be acting on these fiber ends during phases of misdirected and/or uncontrolled migration, the F-actin could be rearranging itself into a structure that is tensegral. It is possible that the ‘rosette’ arrangement of F-actin seen during the initial cataract formation closely mimics a tensegral structure, rendering some semblance of stability to a rapidly deteriorating system. This would be especially advantageous in the fiber ends that are excessively enlarged and domed and could be the initial step that leads to the internalization and recovery of the lens previously documented in this animal model. Our studies indicate that lenses that develop dilated fiber ends stabilized by F-actin adopting tensegral configurations go on to recover by internalizing the cataract.The authors are drawing on the growing body of evidence collected by Ingber and his colleagues. A decade ago they described the role of actin in this way
Established engineering and biological models of cell mechanics assume that the dense cortical microfilament network that lies directly beneath the cell membrane is the primary load-bearing element in the cell. In contrast, the cellular tensegrity model predicts that mechanical loads are borne by discrete molecular networks composed of interconnected actin microfilaments, microtubules, and intermediate filaments that extend through the cytoplasm and link to adhesion receptors, such as integrins, that span the cell surface. [1]
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From "Abnormal fiber end migration in Royal College of Surgeons rats during posterior subcapsular cataract formation" By Anita Joy, Tabraiz A. Mohammed, Kristin J. Al-Ghoul.
Anita Joy is at the Department of Anatomy & Cell Biology, Rush University Medical Center, Chicago, IL; Tabraiz A. Mohammed is at the Department of Ophthalmology, Rush University Medical Center, Chicago, IL; he is currently at the Department of Medicine, University of Wisconsin Hospitals and Clinics, Madison, WI.
For more info, contact: Kristin J. Al-Ghoul, Ph.D., Department of Anatomy and Cell Biology, Rush University Medical Center, 600 S. Paulina St., Ste 507, Chicago, IL, 60612; Phone: (312) 563-2672; FAX: (312) 942-5744; email: kristin_j_al-ghoul -at- rush.edu
References:
[1] Mechanical behavior in living cells consistent with the tensegrity model by Wang et. al. www.pnas.orgycgiydoiy10.1073ypnas.141199598
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