Glucose-induced calcium influx in budding yeast involves a novel calcium transport system and can activate calcineurin.

Glucose addition to glucose-starved Saccharomyces cerevisiae cells triggers a quick and transient influx of calcium from the extracellular environment. In yeast at leasttwodifferent carrier systems were identified: a high affinity system, requiring Cch1 channel, and a low affinity system. Here we report that another calcium transport system exists in yeast, not yet identified, that can substitute the two known systems whenthey are inactivated. This systemwascalled GIC (for Glucose Induced Calcium) system and it is a high affinity calcium transport system, magnesium-sensitive but nickel-resistant. Moreover, GIC transport is sensitive to gadolinium and nifedipine, but it is not sensitive to inhibition by verapamil, which conversely behaves as an agonist on glucose response. GIC transport is fully functional in conditions when calcineurin is active, a serine/threonine specificity phosphatase involved in the regulation of calcium homeostasis and in many other cellular phenomena such as tolerance to high concentrations of Na+ and Li+, response to pheromones and gene transcription regulation. Here it is reported for the first time that calcineurin can also be activated by nutrients: the activation of Crz1 transcription factor by calcineurin was observed in derepressed cells after addition of glucose in the presence of extracellular calcium