Calcium transfer from the ER to other organelles for optimal signaling in .

Ca signaling in cells begins with the opening of Ca channels in either the plasma membrane (PM) or the endoplasmic reticulum (ER) and results in a dramatic increase in the physiologically low (<100 nM) cytosolic Ca level. The temporal and spatial Ca levels are well regulated to enable precise and specific activation of critical biological processes. Ca signaling regulates pathogenic features of apicomplexan parasites like which infects approximately one-third of the world's population. relies on Ca signals to stimulate traits of its infection cycle and several Ca signaling elements play essential roles in its parasitic cycle. Active egress, an essential step for the infection cycle of is preceded by a large increase in cytosolic Ca most likely by release from intracellular stores. Intracellular parasites take up Ca from the host cell during host Ca signaling events to replenish intracellular stores. In this work, we investigated the mechanism by which intracellular stores are replenished with Ca and demonstrated a central role for the SERCA-Ca-ATPase in keeping not only the ER filled with Ca but also other stores. We show mitochondrial Ca uptake, by transfer of Ca from the ER likely through membrane contact sites. We propose a central role for the ER in sequestering and redistributing calcium to other intracellular organelles following influx at the PM.