PP2Acα-B'/PR61 Holoenzyme of Toxoplasma gondii Is Required for the Amylopectin Metabolism and Proliferation of Tachyzoites.

Here, we report that the inhibition of the PP2A subfamily by okadaic acid results in an accumulation of polysaccharides in the acute infection stage (tachyzoites) of Toxoplasma gondii, which is a protozoan of global zoonotic importance and a model for the apicomplexan parasites. The loss of the catalytic subunit α of PP2A (Δ) in RHΔ leads to the polysaccharide accumulation phenotype in the base of tachyzoites as well as residual bodies and significantly compromises the intracellular growth and the virulence . A metabolomic analysis revealed that the accumulated polysaccharides in Δ are derived from interrupted glucose metabolism, which affects the production of ATP and energy homeostasis in the T.

Host autophagy limits proliferation in the absence of IFN-γ by affecting the hijack of Rab11A-positive vesicles.

Introduction: Autophagy has been recognized as a bona fide immunological process. Evidence has shown that this process in IFN-γ stimulated cells controls proliferation or eliminates its infection. However, little is known about the effect of infection on the host cell autophagy in the absence of IFN-γ.

DNA double-strand breaks in the Toxoplasma gondii-infected cells by the action of reactive oxygen species.

Background: Toxoplasma gondii is an obligate parasite of all warm-blooded animals around the globe. Once infecting a cell, it manipulates the host's DNA damage response that is yet to be elucidated. The objectives of the present study were three-fold: (i) to assess DNA damages in T.