When translation stops, cells require intracellular acidification to turn on the conserved heat shock response during stress, and stress-triggered acidification (common in eukaryotes) is adaptive, promoting cell and population fitness.
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.
Parallel measurements of pH gradient and membrane potential at the single vesicle level have revealed that the synaptic vesicle acidification is initiated by removal of its clathrin coat, which blocks vesicular ATPase activity.
Analysis of iconic and gating currents of wild type and mutated BK channels reveals a strong inhibition of this channel by extracellular acidification and elucidates the underlying mechanism that is potentially applicable to other voltage-dependent cation channels.
Cellular carbon accumulation systems are a fundamental prerequisite for biomineralization to stabilize pH and to supply inorganic carbon for CaCO3 precipitation under changing environmental conditions.
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.
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.