
@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}
}
@article {73034,
	title = {Association of  With the Apical Domain of Hepatocytes Is Necessary for the Parasite{\textquoteright}s Liver Stage Development.},
	journal = {Front Cell Infect Microbiol},
	volume = {9},
	year = {2020},
	month = {2019},
	pages = {451},
	abstract = {<p>parasites undergo a dramatic transformation during the liver stage of their life cycle, amplifying over 10,000-fold inside infected hepatocytes within a few days. Such a rapid growth requires large-scale interactions with, and manipulations of, host cell functions. Whereas hepatocyte polarity is well-known to be critical for liver function, little is presently known about its involvement during the liver stage of development. Apical domains of hepatocytes are critical components of their polarity machinery and constitute the bile canalicular network, which is central to liver function. Here, we employed high resolution 3-D imaging and advanced image analysis of -infected liver tissues to show that the parasite associates preferentially with the apical domain of hepatocytes and induces alterations in the organization of these regions, resulting in localized changes in the bile canalicular architecture in the liver tissue. Pharmacological perturbation of the bile canalicular network by modulation of AMPK activity reduces the parasite{\textquoteright}s association with bile canaliculi and arrests the parasite development. Our findings using -infected liver tissues reveal a host- interaction at the level of liver tissue organization. We demonstrate for the first time a role for bile canaliculi, a central component of the hepatocyte polarity machinery, during the liver stage of development.</p>
},
	issn = {2235-2988},
	doi = {10.3389/fcimb.2019.00451},
	author = {Balasubramanian, Lakshmi and Zuzarte-Lu{\'\i}s, Vanessa and Syed, Tabish and Mullick, Debakshi and Deb, Saptarathi and Ranga-Prasad, Harish and Meissner, Jana and Almeida, Ana and Furstenhaupt, Tobias and Siddiqi, Kaleem and Prud{\^e}ncio, Miguel and Rodrigues, Cecilia M P and Mota, Maria and Sundaramurthy, Varadharajan}
}
