2025-10-09 ミュンヘン大学(LMU)
Web要約 の発言:
<関連情報>
- https://www.lmu.de/en/newsroom/news-overview/news/toxoplasmosis-how-the-pathogen-exploits-its-own-envelope.html
- https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3003415
トキソプラズマ・ゴンディの細胞内複製中に細胞膜のリサイクルがリザーバー形成を促進する Plasma membrane recycling drives reservoir formation during Toxoplasma gondii intracellular replication
Julia von Knoerzer-Suckow ,Eva-Helena Aden ,Romuald Haase,Andreas Klingl,Ignasi Forné,Simon Gras
PLOS Biology Published: September 30, 2025
DOI:https://doi.org/10.1371/journal.pbio.3003415
Abstract
During intracellular development, apicomplexan parasites reside within a parasitophorous vacuole largely derived from the host plasma membrane (PM) and rendered nonfusogenic with the host endolysosomal system. 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 Toxoplasma gondii. 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 Plasmodium falciparum, Rab5b is dispensable for the lytic cycle of T. gondii. 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. Perturbation of the endo-exocytic balance disrupts PMR formation, leading to increased number and size of PMRs and, ultimately, to a complete loss of membrane organization directly linking endocytosis to the regulation of PMR formation.
