Apicomplexan parasites belong to a recently recognised group of protozoa referred to as Alveolata. These protists contain membranous sacs (alveoli) beneath the plasma membrane, termed the Inner Membrane Complex (IMC) in the case of Apicomplexa. During parasite replication the IMC is formed de novo within the mother cell in a process described as internal budding. We hypothesized that an alveolate specific factor is involved in the specific transport of vesicles from the Golgi to the IMC and identified the small GTPase Rab11B as an alveolate specific Rab-GTPase that localises to the growing end of the IMC during replication of Toxoplasma gondii. Conditional interference with Rab11B function leads to a profound defect in IMC biogenesis, indicating that Rab11B is required for the transport of Golgi derived vesicles to the nascent IMC of the daughter cell. Curiously, a block in IMC biogenesis did not affect formation of sub-pellicular microtubules, indicating that IMC biogenesis and formation of sub-pellicular microtubules is not mechanistically linked. We propose a model where Rab11B specifically transports vesicles derived from the Golgi to the immature IMC of the growing daughter parasites.
Apicomplexan parasites belong to a group of protists known as alveolata that also includes ciliates and dinoflagellates. One of the few morphological similarities within this group is the presence of membranous sacs beneath the plasma membrane, called alveoli. In the case of apicomplexan parasites, alveoli are well developed and described as the Inner Membrane Complex (IMC) that serves as a scaffold for the machinery driving gliding motility and host cell invasion. Given the unique nature of this organelle we aimed to identify key factors that are involved in its formation. We identified a unique family of Rab11-GTPases in Alveolata. Using Toxoplasma gondii as a model system, we show that this small GTPase is essential for the delivery of vesicles from the Golgi to the nascent IMC of the daughter parasites. Interestingly, biogenesis of the IMC is not linked to the formation of subpellicular microtubules. We propose a model where the action of Rab11B is necessary for IMC formation.