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