Role of Toxoplasma gondii p24δ in Regulating the Transition from Tachyzoite to Bradyzoite Development

TL;DR

This study explores how a protein called p24δ in Toxoplasma gondii affects the parasite's life cycle stages and its ability to infect mice.

Contribution

The study identifies Tgp24δ as a key regulator of tachyzoite-to-bradyzoite transition in T. gondii.

Findings

Loss of p24δ in T. gondii reduces proliferation and virulence in mice.

TgΔp24δ tachyzoites express bradyzoite-specific genes under normal conditions.

TgΔp24δ tachyzoites can differentiate into bradyzoites in vitro.

Abstract

Toxoplasma gondii is an obligate intracellular parasite capable of infecting warm-blooded vertebrates, including humans. In its intermediate hosts, T. gondii can transition between two life stages: the rapidly replicating tachyzoite and the quiescent bradyzoite. In Saccharomyces cerevisiae, the p24 protein acts as a cargo receptor, cycling between the ER and Golgi in the early secretory pathway to recruit cargo proteins into nascent vesicles. However, the function of p24 in T. gondii remains undefined. In this study, we identified four p24 proteins in T. gondii, with Tgp24δ specifically localizing to the ER–Golgi system. Loss of p24δ in a type Ι strain (RHΔku80) significantly reduced proliferation and virulence in mice. Transcriptome and proteomic analyses showed that TgΔp24δ tachyzoites expressed high levels of bradyzoite-specific genes, including bag1, ldh2, and bpk1, under standard culture conditions. Additional data indicate that TgΔp24δ tachyzoites can differentiate and form bradyzoites in vitro. This suggests that Tgp24δ is important for the parasite’s growth.

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