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Secreted effector proteins of Toxoplasma gondii parasites create a supportive immune environment in mice, allowing individually less fit mutants to thrive and evade detection by in vivo CRISPR screens.

Time-resolved phosphoproteomics and thermal proteome profiling reveal the Ca²⁺-responsive proteome of the model apicomplexan Taxoplasma gondii, identifying PP1 as a Ca²⁺-responsive enzyme that regulates Ca²⁺ uptake to promote parasite motility.

The gene RARRES3 uses an unexpected strategy to eliminate the parasite Toxoplasma gondii from human cells.

The proteins found in the mitochondria of apicomplexan parasites, including key proteins involved in energy generation, are very different from mitochondrial proteins of the animals these parasites infect.

Upon Toxoplasma gondii infection, IL-33 plays a critical role in driving early anti-parasite responses by innate lymphoid cells rendered responsive to its effects by infection.

A transient receptor channel in Toxoplasma gondii that conducts calcium represents the first molecular element that initiates upstream calcium signals that activate parasite pathogenic pathways.

Toxoplasma gondii formins have several non-overlapping roles including generating an apico-basal flux of F-actin that is controlled by phosphorylation and methylation and is essential for motility.

ATG9-dependent autophagy is an essential pathway for long-term survival within the cyst in the parasite Toxoplasma gondii and could be exploited in future studies seeking interventions against persistent Toxoplasma infection.

In the setting of CNS infection, meningeal lymphatic drainage promotes dendritic cell and T cell responses in the deep cervical lymph nodes but is not necessary for maintaining control of parasite in the brain.

Parasites constrict as they propel themselves through the extracellular matrix one body length at a time, in a process highly reminiscent of host cell invasion.