Autophagosome–lysosome fusion: PIs to the rescue. (20th July 2016)

• Record Type: Journal Article
• Authors: Li, Linsen; Zhong, Qing
• Is Part Of: EMBO journal. Volume 35:Number 17(2016)
• Page Start: 1845
• Page End: 1847
• Publication Date: 2016-07-20
• Subjects: Molecular biology -- Periodicals; 572.805
• DOI: 10.15252/embj.201695134
• Languages: English
• ISSNs: 0261-4189

Abstract

Abstract : Phosphoinositides (PIs), a small fraction of the cellular lipids, function in almost all cellular physiological processes and especially in intracellular membrane trafficking events. PIs play a critical role in autophagy, but only PI(3)P is well studied. In this issue of The EMBO Journal, Hasegawa et al (2016) identified INPP5E, an inositol polyphosphate 5‐phosphatase, as a novel regulator of autophagy. INPP5E controls the level of PI(3, 5)P2 at the lysosome and thereby locally regulates the actin cytoskeleton and autophagosome–lysosome fusion. Abstract : Phosphoinositide 5‐phosphatase INPP5E, one of the genes responsible for Joubert syndrome, decreases phosphatidylinositol 3, 5‐bisphosphate at lysosomes and thereby regulates autophagosome–lysosome fusion, a process that is disrupted in the presence of disease‐associated INPP5E mutations.