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

<i>Toxoplasma gondii</i> is an obligate intracellular parasite capable of infecting warm-blooded vertebrates, including humans. In its intermediate hosts, <i>T. gondii</i> can transition between two life stages: the rapidly replicating tachyzoite and the quiescent bradyzoite. In <i>Saccharomyces cerevisiae</i>, 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 <i>T. gondii</i> remains undefined. In this study, we identified four p24 proteins in <i>T. gondii</i>, with Tgp24δ specifically localizing to the ER-Golgi system. Loss of p24δ in a type Ι strain (RH<i>Δku80</i>) significantly reduced proliferation and virulence in mice. Transcriptome and proteomic analyses showed that Tg<i>Δp24δ</i> tachyzoites expressed high levels of bradyzoite-specific genes, including <i>bag1</i>, <i>ldh2</i>, and <i>bpk1</i>, under standard culture conditions. Additional data indicate that Tg<i>Δp24δ</i> tachyzoites can differentiate and form bradyzoites in vitro. This suggests that Tgp24δ is important for the parasite's growth.