Impaired lysosomal acidification results in retention of iron inside lysosomes, triggering functional iron deficiency, dysfunctional mitochondria (especially mtDNA loss), and inflammation in vivo in a mouse model of lysosomal disease.

A whole-genome genetic screen links new aspects of oocyte maturation to proteostasis renewal in the immortal Caenorhabditis elegans germ-cell lineage and reveals similarities to somatic cell maintenance during aging.

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.

Emerin, a protein that plays key roles in nuclear organization, can be dynamically degraded in response to environmental stimuli such as ER stress.

A novel, inexpensive, easy-to-use method to analyse traffic along the endosomal pathway in mammalian cells shows that there is coordination between Rab conversion and acidification, but almost none between Rab conversion and recycling.

The endoplasmic reticulum serves as a direct and primary source of calcium ions for the lysosome.

The phagocytic receptor CED-1 is kept at the appropriate level by E3 ligase trim-21-mediated ubiquitination-proteasomal degradation for apoptotic cell clearance, which is independent of retromer-dependent recycling and lysosomal degradation.

The AAA-ATPase VCP sustains sarcoplasmic proteostasis, in part, by controlling autophagosome-lysosome fusion and the integrity of a dynamic tubular lysosomal network.

An unbiased genome-wide human forward genetic screen identifies the vacuolar ATPase complex and assembly factors as regulators of HIF stability through their actions on intracellular iron metabolism.

Inhibiyiton of the lysosomal chloride-proton antiporter ClC-7 by the signaling lipid PI(3,5)P2 is important for lysosomal pH maintenance and is disrupted by a disease-causing gain-of-function mutation.