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Yet, the parasite is capable of protein uptake from the host cell via endocytosis, which occurs via a conserved structure, the micropore. Recently the composition of the micropore was characterized and its stability was shown to depend on the presence of the kelch-domain protein K13 which is also central to malarial drug-resistance to artemisinin. Interestingly, depletion of K13 also resulted in an impressive accumulation of PM attached to or between individual parasites, suggesting that the micropore plays a critical role in PM homoeostasis. Here, we characterized the dynamics and recycling of the PM in <jats:italic><jats:italic>Toxoplasma gondii<\/jats:italic><\/jats:italic>. In intracellular parasites, the PM is shared between individual parasites and undergoes a cycle of endocytosis and exocytosis during replication, similar to what has been previously demonstrated for extracellular parasites. This cycle appears to depend on Rab5b and MyoF. Interestingly, in contrast to <jats:italic><jats:italic>Plasmodium falciparum<\/jats:italic><\/jats:italic>, Rab5b is dispensable for the lytic cycle of <jats:italic><jats:italic>T. gondii<\/jats:italic><\/jats:italic>. During replication, parasites establish an extracellular plasma membrane reservoir (PMR) prior to daughter cell formation. The PMR is a dynamic membranous structure that varies in size and position throughout replication and disappears after daughter cell budding. 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