Calcium signaling and the lytic cycle of the Apicomplexan parasite Toxoplasma gondii.

Biochim Biophys Acta Mol Cell Res 2018 11 10;1865(11 Pt B):1846-1856. Epub 2018 Aug 10.

Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, GA 30602, USA; Department of Cellular Biology, University of Georgia, Athens, GA 30602, USA. Electronic address:

Toxoplasma gondii has a complex life cycle involving different hosts and is dependent on fast responses, as the parasite reacts to changing environmental conditions. T. gondii causes disease by lysing the host cells that it infects and it does this by reiterating its lytic cycle, which consists of host cell invasion, replication inside the host cell, and egress causing host cell lysis. Calcium ion (Ca) signaling triggers activation of molecules involved in the stimulation and enhancement of each step of the parasite lytic cycle. Ca signaling is essential for the cellular and developmental changes that support T. gondii parasitism. The characterization of the molecular players and pathways directly activated by Ca signaling in Toxoplasma is sketchy and incomplete. The evolutionary distance between Toxoplasma and other eukaryotic model systems makes the comparison sometimes not informative. The advent of new genomic information and new genetic tools applicable for studying Toxoplasma biology is rapidly changing this scenario. The Toxoplasma genome reveals the presence of many genes potentially involved in Ca signaling, even though the role of most of them is not known. The use of Genetically Encoded Calcium Indicators (GECIs) has allowed studies on the role of novel calcium-related proteins on egress, an essential step for the virulence and dissemination of Toxoplasma. In addition, the discovery of new Ca players is generating novel targets for drugs, vaccines, and diagnostic tools and a better understanding of the biology of these parasites.

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Source
https://linkinghub.elsevier.com/retrieve/pii/S01674889183025
Publisher Site
http://dx.doi.org/10.1016/j.bbamcr.2018.08.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6477927PMC
November 2018
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