Autophagy, a pathway for lysosomal-mediated cellular degradation, has recently been described as a regulator of cell migration. Although the molecular mechanisms underlying autophagy-dependent motility are only beginning to emerge, new work demonstrates that selective autophagy mediated by the autophagy cargo receptor, NBR1, specifically promotes the dynamic turnover of integrin-based focal adhesion sites during motility. Here, we discuss the detailed mechanisms through which NBR1-dependent selective autophagy supports focal adhesion remodeling, and we describe the interconnections between this pathway and other established regulators of focal adhesion turnover, such as microtubules. We also highlight studies that examine the contribution of autophagy to selective degradation of proteins that mediate cellular tension and to integrin trafficking; these findings hint at further roles for autophagy in supporting adhesion and migration. Given the recently appreciated importance of selective autophagy in diverse cellular processes, we propose that further investigation into autophagy-mediated focal adhesion turnover will not only shed light onto how focal adhesions are regulated but will also unveil new mechanisms regulating selective autophagy.
The authors declare no competing or financial interests.
Grant support includes the National Institutes of Health [grant numbers CA126792 and CA188404 to J.D., and GM079139 to T.W.]; the U.S. Department of Defense Breast Cancer Research Program (BCRP; Congressionally Directed Medical Research Programs) [grant number W81XWH-11-1-0130 to J.D.]; and the Samuel Waxman Cancer Research Foundation (to J.D.). Deposited in PMC for release after 12 months.
- © 2016. Published by The Company of Biologists Ltd