
@article {111547,
	title = {Active APPL1 sequestration by Plasmodium favors liver-stage development.},
	journal = {Cell Rep},
	volume = {39},
	year = {2022},
	month = {2022 May 31},
	pages = {110886},
	abstract = {<p>Intracellular pathogens manipulate host cells to survive and thrive. Cellular sensing and signaling pathways are among the key host machineries deregulated to favor infection. In this study, we show that liver-stage Plasmodium parasites compete with the host to sequester a host endosomal-adaptor protein (APPL1) known to regulate signaling in response to endocytosis. The enrichment of APPL1 at the parasitophorous vacuole membrane (PVM) involves an atypical Plasmodium Rab5 isoform (Rab5b). Depletion of host APPL1 alters neither the infection nor parasite development; however, upon overexpression of a GTPase-deficient host Rab5 mutant (hRab5_Q79L), the parasites are smaller and their PVM is stripped of APPL1. Infection with the GTPase-deficient Plasmodium berghei Rab5b mutant (PbRab5b_Q91L) in this case rescues the PVM APPL1 signal and parasite size. In summary, we observe a robust correlation between the level of APPL1 retention at the PVM and parasite size during exoerythrocytic development.</p>
},
	issn = {2211-1247},
	doi = {10.1016/j.celrep.2022.110886},
	author = {Lahree, Aparajita and Baptista, Sara de Jesus Santos and Marques, Sofia and Perschin, Veronika and Zuzarte-Lu{\'\i}s, Vanessa and Goel, Manisha and Choudhary, Hadi Hasan and Mishra, Satish and Stigloher, Christian and Zerial, Marino and Sundaramurthy, Varadharajan and Mota, Maria M}
}
