Extracellular Ca2+ sensing contributes to excess Ca2+ accumulation and vacuolar fragmentation in apmr1Δ mutant ofS. cerevisiae

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Abstract
Previous studies have suggested that yeast strains lacking the Ca2+-ATPase Pmr1p are unable to maintain an adequate level of Ca2+ within the Golgi apparatus. It is thought that this compartmental store depletion induces a signal that causes an increased rate of Ca2+ uptake and accumulation in a manner similar to the capacitative Ca2+ entry (CCE) response in non-excitable mammalian cells. To explore this model further, we examined cellular Ca2+ uptake and accumulation in a pmr1Δ strain grown in the presence of a reduced level of divalent cations. We found that the level of Ca2+ uptake and accumulation in a pmr1Δ strain increased as the concentration of divalent cations in the growth medium decreased. These results are inconsistent with a model in which cellular Ca2+ uptake and accumulation are determined solely by the depletion of Ca2+ in an intracellular compartment. Instead, our results suggest that a second regulatory mechanism couples cellular Ca2+ uptake to the availability of Ca2+ in the extracellular environment. Furthermore, we found that various conditions that increase the level of cytosolic Ca2+ correlate with vacuolar fragmentation in wild-type (WT), pmr1Δ and pmr1Δ/pmc1Δ yeast strains. This suggests that vacuolar fragmentation might function as a normal physiological response to Ca2+ stress that increases the vacuolar surface/volume ratio, thereby maximizing the sequestration of this important signaling molecule.