NDLI: Full length talin stimulates integrin activation and axon regeneration

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Full length talin stimulates integrin activation and axon regeneration

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Full length talin stimulates integrin activation and axon regeneration

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tan, Chin Lik Kwok, Jessica C. F. Heller, Janosch P. D. Zhao, Rongrong Eva, Richard Fawcett, James W.
Description	Country affiliation: United kingdom Author Affiliation: Tan CL ( John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK.); Kwok JC ( John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK.); Heller JP ( John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK.); Zhao R ( John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK.); Eva R ( John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK.); Fawcett JW ( John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK. Electronic address: jf108@cam.ac.uk.)
Abstract	Integrin function is regulated by activation involving conformational changes that modulate ligand-binding affinity and downstream signaling. Activation is regulated through inside-out signaling which is controlled by many signaling pathways via a final common pathway through kindlin and talin, which bind to the intracellular tail of beta integrins. Previous studies have shown that the axon growth inhibitory molecules NogoA and chondroitin sulfate proteoglycans (CSPGs) inactivate integrins. Overexpressing kindlin-1 in dorsal root ganglion (DRG) neurons activates integrins, enabling their axons to overcome inhibitory molecules in the environment, and promoting regeneration in vivo following dorsal root crush. Other studies have indicated that expression of the talin head alone or with kindlin can enhance integrin activation. Here, using adult rat DRG neurons, we investigate the effects of overexpressing various forms of talin on axon growth and integrin signaling. We found that overexpression of the talin head activated axonal integrins but inhibited downstream signaling via FAK, and did not promote axon growth. Similarly, co-expression of the talin head and kindlin-1 prevented the growth-promoting effect of kindlin-1, suggesting that the talin head acts as a form of dominant negative for integrin function. Using full-length talin constructs in PC12 cells we observed that neurite growth was enhanced by the expression of wild-type talin and more so by two ‘activated’ forms of talin produced by point mutation (on laminin and aggrecan–laminin substrates). Nevertheless, co-expression of full-length talin with kindlin did not promote neurite growth more than either molecule alone. In vivo, we find that talin is present in PNS axons (sciatic nerve), and also in CNS axons of the corticospinal tract.
File Format	HTM / HTML
ISSN	10447431
e-ISSN	10959327
DOI	10.1016/j.mcn.2015.03.011
Journal	Molecular and Cellular Neuroscience
Volume Number	68
Language	English
Publisher	Elsevier
Publisher Date	2015-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Discipline Molecular Biology Discipline Neurology Integrins Metabolism Neurons Drug Effects Talin Aggrecans Animals Axons Physiology Cells, Cultured Ganglia, Spinal Cytology Green Fluorescent Proteins Genetics Laminin Nerve Tissue Proteins Peptides Rats, Sprague-dawley Sciatic Nerve Spinal Cord Transfection Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology Cellular and Molecular Neuroscience

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