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4. Apolipoprotein-L Functions in Membrane Remodeling.

Author

Pays, Etienne

Subjects
*BACTERIAL cell walls, *FISSION (Asexual reproduction), *MEMBRANE fusion, *ANTIGEN processing, *DENDRITIC cells, *LYSOSOMES
Abstract

The mammalian Apolipoprotein-L families (APOLs) contain several isoforms of membrane-interacting proteins, some of which are involved in the control of membrane dynamics (traffic, fission and fusion). Specifically, human APOL1 and APOL3 appear to control membrane remodeling linked to pathogen infection. Through its association with Non-Muscular Myosin-2A (NM2A), APOL1 controls Golgi-derived trafficking of vesicles carrying the lipid scramblase Autophagy-9A (ATG9A). These vesicles deliver APOL3 together with phosphatidylinositol-4-kinase-B (PI4KB) and activated Stimulator of Interferon Genes (STING) to mitochondrion–endoplasmic reticulum (ER) contact sites (MERCSs) for the induction and completion of mitophagy and apoptosis. Through direct interactions with PI4KB and PI4KB activity controllers (Neuronal Calcium Sensor-1, or NCS1, Calneuron-1, or CALN1, and ADP-Ribosylation Factor-1, or ARF1), APOL3 controls PI(4)P synthesis. PI(4)P is required for different processes linked to infection-induced inflammation: (i) STING activation at the Golgi and subsequent lysosomal degradation for inflammation termination; (ii) mitochondrion fission at MERCSs for induction of mitophagy and apoptosis; and (iii) phagolysosome formation for antigen processing. In addition, APOL3 governs mitophagosome fusion with endolysosomes for mitophagy completion, and the APOL3-like murine APOL7C is involved in phagosome permeabilization linked to antigen cross-presentation in dendritic cells. Similarly, APOL3 can induce the fusion of intracellular bacterial membranes, and a role in membrane fusion can also be proposed for endothelial APOLd1 and adipocyte mAPOL6, which promote angiogenesis and adipogenesis, respectively, under inflammatory conditions. Thus, different APOL isoforms play distinct roles in membrane remodeling associated with inflammation. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Apolipoprotein-L1 (APOL1): From Sleeping Sickness to Kidney Disease.

Author

Pays, Etienne

Subjects
*HUMAN cloning, *INTRACELLULAR membranes, *ARTIFICIAL membranes, *CELL membranes, *CHRONIC kidney failure
Abstract

Apolipoprotein-L1 (APOL1) is a membrane-interacting protein induced by inflammation, which confers human resistance to infection by African trypanosomes. APOL1 kills Trypanosoma brucei through induction of apoptotic-like parasite death, but two T. brucei clones acquired resistance to APOL1, allowing them to cause sleeping sickness. An APOL1 C-terminal sequence alteration, such as occurs in natural West African variants G1 and G2, restored human resistance to these clones. However, APOL1 unfolding induced by G1 or G2 mutations enhances protein hydrophobicity, resulting in kidney podocyte dysfunctions affecting renal filtration. The mechanism involved in these dysfunctions is debated. The ability of APOL1 to generate ion pores in trypanosome intracellular membranes or in synthetic membranes was provided as an explanation. However, transmembrane insertion of APOL1 strictly depends on acidic conditions, and podocyte cytopathology mainly results from secreted APOL1 activity on the plasma membrane, which occurs under non-acidic conditions. In this review, I argue that besides inactivation of APOL3 functions in membrane dynamics (fission and fusion), APOL1 variants induce inflammation-linked podocyte toxicity not through pore formation, but through plasma membrane disturbance resulting from increased interaction with cholesterol, which enhances cation channels activity. A natural mutation in the membrane-interacting domain (N264K) abrogates variant APOL1 toxicity at the expense of slightly increased sensitivity to trypanosomes, further illustrating the continuous mutual adaptation between host and parasite. [ABSTRACT FROM AUTHOR]

Published
2024
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7. The Trypanosoma Brucei KIFC1 Kinesin Ensures the Fast Antibody Clearance Required for Parasite Infectivity

Author

Lecordier, Laurence, Uzureau, Sophie, Vanwalleghem, Gilles, Deleu, Magali, Crowet, Jean-Marc, Barry, Paul, Moran, Barry, Voorheis, Paul, Dumitru, Andra-Cristina, Yamaryo-Botté, Yoshiki, Dieu, Marc, Tebabi, Patricia, Vanhollebeke, Benoit, Lins, Laurence, Botté, Cyrille Y., Alsteens, David, Dufrêne, Yves, Pérez-Morga, David, Nolan, Derek P., and Pays, Etienne

Published
2020
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8. APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin

Author

Uzureau, Sophie, Lecordier, Laurence, Uzureau, Pierrick, Hennig, Dorle, Graversen, Jonas H., Homblé, Fabrice, Mfutu, Pepe Ekulu, Oliveira Arcolino, Fanny, Ramos, Ana Raquel, La Rovere, Rita M., Luyten, Tomas, Vermeersch, Marjorie, Tebabi, Patricia, Dieu, Marc, Cuypers, Bart, Deborggraeve, Stijn, Rabant, Marion, Legendre, Christophe, Moestrup, Søren K., Levtchenko, Elena, Bultynck, Geert, Erneux, Christophe, Pérez-Morga, David, and Pays, Etienne

Published
2020
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19. Adenylate Cyclases of Trypanosoma brucei Inhibit the Innate Immune Response of the Host

Author

Salmon, Didier, Vanwalleghem, Gilles, Morias, Yannick, Denoeud, Julie, Krumbholz, Carsten, Lhommé, Frédéric, Bachmaier, Sabine, Kador, Markus, Gossmann, Jasmin, Dias, Fernando Braga Stehling, De Muylder, Géraldine, Uzureau, Pierrick, Magez, Stefan, Moser, Muriel, De Baetselier, Patrick, Van Den Abbeele, Jan, Beschin, Alain, Boshart, Michael, and Pays, Etienne

Published
2012
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20. Association of Trypanolytic ApoL1 Variants with Kidney Disease in African Americans

Author

Genovese, Giulio, Friedman, David J., Ross, Michael D., Lecordier, Laurence, Uzureau, Pierrick, Freedman, Barry I., Bowden, Donald W., Langefeld, Carl D., Oleksyk, Taras K., Knob, Andrea L. Uscinski, Bernhardy, Andrea J., Hicks, Pamela J., Nelson, George W., Vanhollebeke, Benoit, Winkler, Cheryl A., Kopp, Jeffrey B., Pays, Etienne, and Pollak, Martin R.

Published
2010

31. Mechanism of Trypanosoma brucei gambiense resistance to human serum

Author

Uzureau, Pierrick, Uzureau, Sophie, Lecordier, Laurence, Fontaine, Frederic, Tebabi, Patricia, Homble, Fabrice, Grelard, Axelle, Zhendre, Vanessa, Nolan, Derek P., Lins, Laurence, Crowet, Jean-Marc, Pays, Annette, Felu, Cecile, Poelvoorde, Philippe, Vanhollebeke, Benoit, Moestrup, Soren K., Lyngso, Jeppe, Pedersen, Jan Skov, Mottram, Jeremy C., Dufoure, Erick J., Perez-Morga, David, and Pays, Etienne

Subjects
Physiological aspects, Properties, Blood serum -- Properties, Trypanosoma brucei -- Properties, Lipid membranes -- Physiological aspects, Serum -- Properties
Abstract

The protozoan flagellate Trypanosoma brucei brucei infects many mammals, except some primates including humans, where it is lysed by the trypanolytic protein APOL1 (refs 2, 6, 7). APOL1 is associated [...], The African parasite Trypanosoma bruceigambiense accounts for 97% of human sleeping sickness cases (1). T. b. gambiense resists the specific human innate immunity acting against several other tsetse-fly-transmitted trypanosome species such as T. b. brucei, the causative agent of nagana disease in cattle. Human immunity to some African trypanosomes is due to two serum complexes designated trypanolytic factors (TLF-1 and -2), which both contain haptoglobin-related protein (HPR) and apolipoprotein LI (APOL1) (2-4). Whereas HPR association with haemoglobin (Hb) allows TLF-1 binding and uptake via the trypanosome receptor TbHpHbR (ref. 5), TLF-2 enters trypanosomes independently of TbHpHbR (refs 4, 5). APOL1 kills trypanosomes after insertion into endosomal/lysosomal membranes (2,6,7). Here we report that T. b. gambiense resists TLFs via a hydrophobic β-sheet of the T. b. gambiense-specific glycoprotein (TgsGP) (8), which prevents APOL1 toxicity and induces stiffening of membranes upon interaction with lipids. Two additional features contribute to resistance to TLFs: reduction of sensitivity to APOL1 requiring cysteine protease activity, and TbHpHbR inactivation due to a L210S substitution. According to such a multifactorial defence mechanism, transgenic expression of T. b. brucei TbHpHbR in T. b. gambiense did not cause parasite lysis in normal human serum. However, these transgenic parasites were killed in hypohaptoglobinaemic serum, after high TLF-1 uptake in the absence of haptoglobin (Hp) that competes for Hb and receptor binding. TbHpHbR inactivation preventing high APOL1 loading in hypohaptoglobinaemic serum may have evolved because of the overlapping endemic area of T.b. gambiense infection and malaria, the main cause of haemolysis-induced hypohaptoglobinaemia in western and central Africa (9).

Published
2013

34. Human Trypanosoma evansi infection linked to a lack of apolipoprotein L-I

Author

Vanhollebeke, Benoit, Truc, Philippe, Joshi, Prashant P., Katti, Ravindra, Poelvoorde, Philippe, Pays, Annette, Jannin, Jean G., and Pays, Etienne

Subjects
Trypanosoma -- Development and progression, Trypanosoma -- Risk factors, India -- Health aspects
Abstract

Humans have innate immunity against Trypanosoma brucei brucei that is known to involve apolipoprotein L-I (APOL1), but a case of T. evansi infection in a human was identified in India. The serum of the infected patient was found to have no trypanolytic activity, a finding linked to the lack of APOL1, and activity was restored by the addition of recombinant APOL1.

Published
2006

35. Experimental therapy of African trypanosomiasis with a nanobody-conjugated human trypanolytic factor

Author

Baral, Toya Nath, Magez, Stefan, Stijlemans, Benoit, Conrath, Katja, Vanhollebeke, Benoit, Pays, Etienne, Muyldermans, Serge, and De Baetselier, Patrick

Abstract

Author(s): Toya Nath Baral (corresponding author) [1]; Stefan Magez [1]; Benoît Stijlemans [1]; Katja Conrath [1]; Benoit Vanhollebeke [2]; Etienne Pays [2]; Serge Muyldermans [1]; Patrick De Baetselier [1] High [...]

Published
2006
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38. Apolipoprotein L-I is the trypanosome lytic factor of human serum

Author

Vanhamme, Luc, Paturiaux-Hanocq, Francoise, Poelvoorde, Philippe, Nolan, Derek P., Lins, Laurence, Van Den Abbeele, Jan, Pays, Annette, Tebabi, Patricia, Van Xong, Huang, Jacquet, Alain, Moguilevsky, Nicole, Dieu, Marc, Kane, John P., De Baetselier, Patrick, Brasseur, Robert, and Pays, Etienne

Abstract

Author(s): Luc Vanhamme [1, 2]; Françoise Paturiaux-Hanocq [1, 2]; Philippe Poelvoorde [1, 2]; Derek P. Nolan [1, 3]; Laurence Lins [4]; Jan Van Den Abbeele [5]; Annette Pays [1]; Patricia [...]

Published
2003
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