Lysosomes serve as the important intracellular function of
compartmentalizing pH-dependent degradation. They receive
extracellular components via endocytosis and intracellular
material through autophagy or the biosynthetic pathway.1,2
These catabolic functions are essential regulators of cellular
homeostasis, and lysosomal dysfunction is implicated in
various pathological processes including neurodegenerative
diseases.3 Being part of a highly dynamic endocytic system
that implicates constant exchange of incoming and outgoing
membranes and multiple fusion events, cellular mechanisms
regulating lysosomal maturation and activity remain incompletely
understood.2 Growing evidence indicates that lysosome
positioning in cells can modulate lysosomal function.4–6
For instance, their clustering in the perinuclear area facilitates
autophagy,6 probably because of the spatially-restricted
increased concentration of lysosomes available for fusion
with autophagosomes.