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Calcium negatively regulates secretion from dense granules in Toxoplasma gondii
Author(s) -
Katris Nicholas J.,
Ke Huiling,
McFadden Geoffrey I.,
Dooren Giel G.,
Waller Ross F.
Publication year - 2019
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.13011
Subject(s) - rhoptry , microneme , exocytosis , biology , secretion , microbiology and biotechnology , dense granule , toxoplasma gondii , extracellular , cytosol , granule (geology) , intracellular , second messenger system , apicomplexa , immunology , biochemistry , paleontology , malaria , antibody , plasmodium falciparum , enzyme
Apicomplexan parasites including Toxoplasma gondii and Plasmodium spp. manufacture a complex arsenal of secreted proteins used to interact with and manipulate their host environment. These proteins are organised into three principle exocytotic compartment types according to their functions: micronemes for extracellular attachment and motility, rhoptries for host cell penetration, and dense granules for subsequent manipulation of the host intracellular environment. The order and timing of these events during the parasite's invasion cycle dictates when exocytosis from each compartment occurs. Tight control of compartment secretion is, therefore, an integral part of apicomplexan biology. Control of microneme exocytosis is best understood, where cytosolic intermediate molecular messengers cGMP and Ca 2+ act as positive signals. The mechanisms for controlling secretion from rhoptries and dense granules, however, are virtually unknown. Here, we present evidence that dense granule exocytosis is negatively regulated by cytosolic Ca 2+ , and we show that this Ca 2+ ‐mediated response is contingent on the function of calcium‐dependent protein kinases Tg CDPK1 and Tg CDPK3. Reciprocal control of micronemes and dense granules provides an elegant solution to the mutually exclusive functions of these exocytotic compartments in parasite invasion cycles and further demonstrates the central role that Ca 2+ signalling plays in the invasion biology of apicomplexan parasites.

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