The Autophagy Regulator p62 Controls PTEN-Dependent Ciliogenesis

Abstract

Autophagy is a catabolic process required for maintaining intracellular energy homeostasis. It eliminates harmful proteins and recycles functional macromolecules back into the cell via cargo breakdown. Autophagy is generally suppressed under fed conditions and induced by serum starvation; therefore, it is considered to be a nutrientsensing mechanism. Cilia, finger-like organelles harboring multiple receptors along their surface, are energy-sensing structures that are also triggered by serum deprivation. Herein, we verified the effect of autophagy alterations on cilia assembly and the specific underlying mechanisms. Autophagy flux altered either by drugs or autophagy-targeting siRNAs strongly inhibited ciliogenesis, and this inhibition was affected by p62, an autophagy regulator, via Pten/Dvl2/AurKA signaling.

The Roles of Autophagy, Mitophagy, and the Akt/mTOR Pathway in the Pathogenesis of Chronic Rhinosinusitis with Nasal Polyps

“…An autophagy cargo protein, p62, has multiple domains that interact with LC3 and ubiquitin. Because p62 expression is reduced by successful autophagy, p62 labeling is used to track the process [ 9 ]. Autophagy can protect cells and tissues by decreasing inflammation, as well as by removing irritants and invading pathogens.…”