Rab12 was identified as a key modulator of LRRK2-dependent Rab phosphorylation that mediates the recruitment of LRRK2 to lysosomes in response to damage.

A combination of spatial proteomic and autophagic flux approaches was used to reveal the landscape of turnover of damaged lysosomes, demonstrating a key role for the autophagy receptor TAX1BP1 and its associated kinase TBK1 in both HeLa cells and iNeurons.

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.

The so far uncharacterized lysosomal transporter protein MFSD1 is essential for liver homeostasis and needs the highly glycosylated GLMP protein as an accessory subunit for stability.

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

Multi-omic profiling of gene expression in response to reduced insulin/IGF-like-signalling reveals tissue-specific regulation of DNA damage and lysosomal mannosidase regulation of tissue homeostasis as pro-longevity responses.

A decline in iron-recycling functions of the splenic red pulp macrophages early during aging is driven by iron loading and involves their damage and a loss in red blood cell clearance capacity.

Mitophagy occurs in Drosophila flight muscle and dopaminergic neurons in vivo and increases with aging in a PINK1/parkin-dependent fashion.

Sterol kinetics and cell-based assays reveal a heretofore unknown step in cholesterol trafficking through the endolysosomal compartment, involving a direct functional interaction between NPC2 and lysosbisphosphatidic acid.

Cell biological and genetic studies reveal age-associated alterations of lysosomes and modulation of lysosomal activity by longevity pathways.