The crystal structure of human WIPI2 bound to the ATG16L1 WIPI2-interacting region, combined with in vitro reconstitution and cellular autophagy assays, shows how the LC3 lipidation machinery is recruited in autophagy initiation.

The dynamic phosphorylation of autophagy component WIPI2B is critical to maintain autophagosome biogenesis in neurons, and ectopic expression of WIPI2B can restore rates of autophagosome biogenesis in aged neurons.

The autophagy protein ATG2A tethers membranes and transfers lipids between them, suggesting that autophagosome membranes grow upon the acquisition of lipids from the ER through the ATG2A bridge.

In neuronal mitophagy, Parkin and OPTN induce efficient sequestration of damaged somal mitochondria into autophagosomes, but slow turnover via lysosomal acidification may be a point of vulnerability for the cell.

How the autophagy-related E3 complex localizes to pre-autophagosomal structures and a non-E3 function of the complex were revealed, significantly advancing our understanding of the nucleation step in autophagosome formation.

An image-based multiplex autophagosome RNAi screen targeting all Rab GTPases as well as their GAPs and GEFs identifies the Rab GEF SMCR8 as multifaceted autophagy modulator, which regulates kinase activity and gene expression of ULK1.

The autophagosomal membrane becomes negatively charged during maturation due to the accumulation of PI4P, leading to the recruitment of syntaxin 17, which is required for autophagosome-lysosome fusion.

FACS-based pooled CRISPR screening is a powerful forward genetic tool to interrogate cellular pathways and targets that modulate protein fate.

Keratinocytes are critical for normal innocuous and noxious touch through their mechanically evoked ATP release and subsequent signaling to P2X4 channels on sensory neurons.