<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fu Y</submitter><funding>NIAID NIH HHS</funding><funding>National Institutes of Health</funding><pagination>e73011</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8683080</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10</volume><pubmed_abstract>&lt;i>Toxoplasma gondii&lt;/i> has evolved different developmental stages for disseminating during acute infection (i.e., tachyzoites) and establishing chronic infection (i.e., bradyzoites). Calcium ion (Ca&lt;sup>2+&lt;/sup>) signaling tightly regulates the lytic cycle of tachyzoites by controlling microneme secretion and motility to drive egress and cell invasion. However, the roles of Ca&lt;sup>2+&lt;/sup> signaling pathways in bradyzoites remain largely unexplored. Here, we show that Ca&lt;sup>2+&lt;/sup> responses are highly restricted in bradyzoites and that they fail to egress in response to agonists. Development of dual-reporter parasites revealed dampened Ca&lt;sup>2+&lt;/sup> responses and minimal microneme secretion by bradyzoites induced in vitro or harvested from infected mice and tested ex vivo. Ratiometr</pubmed_abstract><journal>eLife</journal><pubmed_title>&lt;i>Toxoplasma&lt;/i> bradyzoites exhibit physiological plasticity of calcium and energy stores controlling motility and egress.</pubmed_title><pmcid>PMC8683080</pmcid><funding_grant_id>R01 AI034036</funding_grant_id><funding_grant_id>R01 AI164473</funding_grant_id><funding_grant_id>R01 AI162749</funding_grant_id><funding_grant_id>R01 AI128356</funding_grant_id><funding_grant_id>R01 AI143857</funding_grant_id><funding_grant_id>R21 AI162033</funding_grant_id><funding_grant_id>AI143857</funding_grant_id><funding_grant_id>R01 AI118426</funding_grant_id><funding_grant_id>AI034036</funding_grant_id><funding_grant_id>AI128356</funding_grant_id><pubmed_authors>Brown KM</pubmed_authors><pubmed_authors>Jones NG</pubmed_authors><pubmed_authors>Sibley LD</pubmed_authors><pubmed_authors>Fu Y</pubmed_authors><pubmed_authors>Moreno SN</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>Toxoplasma&lt;/i> bradyzoites exhibit physiological plasticity of calcium and energy stores controlling motility and egress.</name><description>&lt;i>Toxoplasma gondii&lt;/i> has evolved different developmental stages for disseminating during acute infection (i.e., tachyzoites) and establishing chronic infection (i.e., bradyzoites). Calcium ion (Ca&lt;sup>2+&lt;/sup>) signaling tightly regulates the lytic cycle of tachyzoites by controlling microneme secretion and motility to drive egress and cell invasion. However, the roles of Ca&lt;sup>2+&lt;/sup> signaling pathways in bradyzoites remain largely unexplored. Here, we show that Ca&lt;sup>2+&lt;/sup> responses are highly restricted in bradyzoites and that they fail to egress in response to agonists. Development of dual-reporter parasites revealed dampened Ca&lt;sup>2+&lt;/sup> responses and minimal microneme secretion by bradyzoites induced in vitro or harvested from infected mice and tested ex vivo. Ratiometr</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2026-05-09T12:01:54.809Z</modification><creation>2022-02-11T15:48:03.772Z</creation></dates><accession>S-EPMC8683080</accession><cross_references><pubmed>34860156</pubmed><doi>10.7554/eLife.73011</doi></cross_references></HashMap>