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The temporal and spatial regulation of Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    is crucial for the precise activation of key biological processes. In the apicomplexan parasite\n                    <jats:italic>Toxoplasma gondii<\/jats:italic>\n                    , which infects approximately one-third of the global population, Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    signaling governs essential aspects of the parasite\u2019s infection cycle.\n                    <jats:italic>T. gondii<\/jats:italic>\n                    relies on Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    signals to regulate pathogenic traits, with several Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    -signaling components playing critical roles. Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry from the extracellular environment has been demonstrated in\n                    <jats:italic>T. gondii<\/jats:italic>\n                    for both, extracellular parasites, exposed to high Ca\n                    <jats:sup>2+<\/jats:sup>\n                    , and intracellular parasites, which acquire Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    from host cells during host Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    signaling events. Active egress, an essential step of the parasite\u2019s infection cycle, is preceded by a large increase in cytosolic Ca\n                    <jats:sup>2+<\/jats:sup>\n                    , most likely initiated by release from intracellular stores. However, extracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    is also necessary to reach a cytosolic Ca\n                    <jats:sup>2+<\/jats:sup>\n                    threshold required for timely egress. In this study, we investigated the mechanism of intracellular Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    store replenishment and identified a central role for the SERCA-Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -ATPase in maintaining Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    homeostasis within the ER and in other organelles. We demonstrate mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    uptake, which occurs by transfer of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    from the ER, likely through membrane contact sites. Our findings suggest that the\n                    <jats:italic>T. gondii<\/jats:italic>\n                    ER plays a key role in sequestering and redistributing Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    to intracellular organelles following Ca\u00b2\n                    <jats:sup>+<\/jats:sup>\n                    influx at the PM.\n                  <\/jats:p>","DOI":"10.7554\/elife.101894","type":"journal-article","created":{"date-parts":[[2024,12,9]],"date-time":"2024-12-09T10:25:30Z","timestamp":1733739930000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.101894","source":"Crossref","is-referenced-by-count":4,"title":["Calcium transfer from the ER to other organelles for optimal signaling in Toxoplasma 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