Toxoplasma bradyzoites exhibit physiological plasticity of calcium and energy stores controlling motility and egress.

ABSTRACT: Toxoplasma gondii has evolved different developmental stages for disseminating during acute infection (i.e., tachyzoites) and establishing chronic infection (i.e., bradyzoites). Calcium ion (Ca²⁺) signaling tightly regulates the lytic cycle of tachyzoites by controlling microneme secretion and motility to drive egress and cell invasion. However, the roles of Ca²⁺ signaling pathways in bradyzoites remain largely unexplored. Here, we show that Ca²⁺ responses are highly restricted in bradyzoites and that they fail to egress in response to agonists. Development of dual-reporter parasites revealed dampened Ca²⁺ responses and minimal microneme secretion by bradyzoites induced in vitro or harvested from infected mice and tested ex vivo. Ratiometr

SUBMITTER: Fu Y 

PROVIDER: S-EPMC8683080 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature