The Plasmodium translocon of exported proteins component EXP2 is critical for establishing a patent malaria infection in mice.
Identifieur interne : 001608 ( Main/Exploration ); précédent : 001607; suivant : 001609The Plasmodium translocon of exported proteins component EXP2 is critical for establishing a patent malaria infection in mice.
Auteurs : Ming Kalanon [Australie] ; Daniel Bargieri [France] ; Angelika Sturm [Australie] ; Kathryn Matthews [Australie] ; Sreejoyee Ghosh [Australie] ; Christopher D. Goodman [Australie] ; Sabine Thiberge [France] ; Vanessa Mollard [Australie] ; Geoffrey I. Mcfadden [Australie] ; Robert Ménard [France] ; Tania F. De Koning-Ward [Australie]Source :
- Cellular microbiology [ 1462-5822 ] ; 2016.
Descripteurs français
- KwdFr :
- Animal génétiquement modifié, Animaux, Foie (parasitologie), Interactions hôte-parasite, Paludisme (parasitologie), Plasmodium berghei (génétique), Plasmodium berghei (pathogénicité), Protéines de protozoaire (génétique), Protéines de protozoaire (métabolisme), Protéines du choc thermique (métabolisme), Protéines à fluorescence verte (génétique), Protéines à fluorescence verte (métabolisme), Régulation de l'expression des gènes (), Souris, Techniques de knock-down de gènes, Transport de protéines (génétique), Tétracyclines (pharmacologie).
- MESH :
- génétique : Plasmodium berghei, Protéines de protozoaire, Protéines à fluorescence verte, Transport de protéines.
- métabolisme : Protéines de protozoaire, Protéines du choc thermique, Protéines à fluorescence verte.
- parasitologie : Foie, Paludisme.
- pathogénicité : Plasmodium berghei.
- pharmacologie : Tétracyclines.
- Animal génétiquement modifié, Animaux, Interactions hôte-parasite, Régulation de l'expression des gènes, Souris, Techniques de knock-down de gènes.
English descriptors
- KwdEn :
- Animals, Animals, Genetically Modified, Gene Expression Regulation (drug effects), Gene Knockdown Techniques, Green Fluorescent Proteins (genetics), Green Fluorescent Proteins (metabolism), Heat-Shock Proteins (metabolism), Host-Parasite Interactions, Liver (parasitology), Malaria (parasitology), Mice, Plasmodium berghei (genetics), Plasmodium berghei (pathogenicity), Protein Transport (genetics), Protozoan Proteins (genetics), Protozoan Proteins (metabolism), Tetracyclines (pharmacology).
- MESH :
- chemical , genetics : Green Fluorescent Proteins, Protozoan Proteins.
- drug effects : Gene Expression Regulation.
- genetics : Plasmodium berghei, Protein Transport.
- chemical , metabolism : Green Fluorescent Proteins, Heat-Shock Proteins, Protozoan Proteins.
- parasitology : Liver, Malaria.
- pathogenicity : Plasmodium berghei.
- chemical , pharmacology : Tetracyclines.
- Animals, Animals, Genetically Modified, Gene Knockdown Techniques, Host-Parasite Interactions, Mice.
Abstract
Export of most malaria proteins into the erythrocyte cytosol requires the Plasmodium translocon of exported proteins (PTEX) and a cleavable Plasmodium export element (PEXEL). In contrast, the contribution of PTEX in the liver stages and export of liver stage proteins is unknown. Here, using the FLP/FRT conditional mutatagenesis system, we generate transgenic Plasmodium berghei parasites deficient in EXP2, the putative pore-forming component of PTEX. Our data reveal that EXP2 is important for parasite growth in the liver and critical for parasite transition to the blood, with parasites impaired in their ability to generate a patent blood-stage infection. Surprisingly, whilst parasites expressing a functional PTEX machinery can efficiently export a PEXEL-bearing GFP reporter into the erythrocyte cytosol during a blood stage infection, this same reporter aggregates in large accumulations within the confines of the parasitophorous vacuole membrane during hepatocyte growth. Notably HSP101, the putative molecular motor of PTEX, could not be detected during the early liver stages of infection, which may explain why direct protein translocation of this soluble PEXEL-bearing reporter or indeed native PEXEL proteins into the hepatocyte cytosol has not been observed. This suggests that PTEX function may not be conserved between the blood and liver stages of malaria infection.
DOI: 10.1111/cmi.12520
PubMed: 26347246
Affiliations:
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Goodman</name><affiliation wicri:level="4"><nlm:affiliation>School of BioSciences, The University of Melbourne, Parkville, Victoria, 3010, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of BioSciences, The University of Melbourne, Parkville, Victoria, 3010</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation></author><author><name sortKey="Thiberge, Sabine" sort="Thiberge, Sabine" uniqKey="Thiberge S" first="Sabine" last="Thiberge">Sabine Thiberge</name><affiliation wicri:level="3"><nlm:affiliation>Unité de Biologie et Génétique du Paludisme, Institut Pasteur, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unité de Biologie et Génétique du Paludisme, Institut Pasteur, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Mollard, Vanessa" sort="Mollard, Vanessa" uniqKey="Mollard V" first="Vanessa" last="Mollard">Vanessa Mollard</name><affiliation wicri:level="4"><nlm:affiliation>School of BioSciences, The University of Melbourne, Parkville, Victoria, 3010, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of BioSciences, The University of Melbourne, Parkville, Victoria, 3010</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation></author><author><name sortKey="Mcfadden, Geoffrey I" sort="Mcfadden, Geoffrey I" uniqKey="Mcfadden G" first="Geoffrey I" last="Mcfadden">Geoffrey I. Mcfadden</name><affiliation wicri:level="4"><nlm:affiliation>School of BioSciences, The University of Melbourne, Parkville, Victoria, 3010, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of BioSciences, The University of Melbourne, Parkville, Victoria, 3010</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation></author><author><name sortKey="Menard, Robert" sort="Menard, Robert" uniqKey="Menard R" first="Robert" last="Ménard">Robert Ménard</name><affiliation wicri:level="3"><nlm:affiliation>Unité de Biologie et Génétique du Paludisme, Institut Pasteur, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unité de Biologie et Génétique du Paludisme, Institut Pasteur, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="De Koning Ward, Tania F" sort="De Koning Ward, Tania F" uniqKey="De Koning Ward T" first="Tania F" last="De Koning-Ward">Tania F. De Koning-Ward</name><affiliation wicri:level="1"><nlm:affiliation>Molecular and Medical Research Unit, School of Medicine, Deakin University, Waurn Ponds, Geelong, Victoria, 3216, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Molecular and Medical Research Unit, School of Medicine, Deakin University, Waurn Ponds, Geelong, Victoria, 3216</wicri:regionArea><wicri:noRegion>3216</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cellular microbiology</title><idno type="eISSN">1462-5822</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Animals, Genetically Modified</term><term>Gene Expression Regulation (drug effects)</term><term>Gene Knockdown Techniques</term><term>Green Fluorescent Proteins (genetics)</term><term>Green Fluorescent Proteins (metabolism)</term><term>Heat-Shock Proteins (metabolism)</term><term>Host-Parasite Interactions</term><term>Liver (parasitology)</term><term>Malaria (parasitology)</term><term>Mice</term><term>Plasmodium berghei (genetics)</term><term>Plasmodium berghei (pathogenicity)</term><term>Protein Transport (genetics)</term><term>Protozoan Proteins (genetics)</term><term>Protozoan Proteins (metabolism)</term><term>Tetracyclines (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animal génétiquement modifié</term><term>Animaux</term><term>Foie (parasitologie)</term><term>Interactions hôte-parasite</term><term>Paludisme (parasitologie)</term><term>Plasmodium berghei (génétique)</term><term>Plasmodium berghei (pathogénicité)</term><term>Protéines de protozoaire (génétique)</term><term>Protéines de protozoaire (métabolisme)</term><term>Protéines du choc thermique (métabolisme)</term><term>Protéines à fluorescence verte (génétique)</term><term>Protéines à fluorescence verte (métabolisme)</term><term>Régulation de l'expression des gènes ()</term><term>Souris</term><term>Techniques de knock-down de gènes</term><term>Transport de protéines (génétique)</term><term>Tétracyclines (pharmacologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Green Fluorescent Proteins</term><term>Protozoan Proteins</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Plasmodium berghei</term><term>Protein Transport</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Plasmodium berghei</term><term>Protéines de protozoaire</term><term>Protéines à fluorescence verte</term><term>Transport de protéines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Green Fluorescent Proteins</term><term>Heat-Shock Proteins</term><term>Protozoan Proteins</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines de protozoaire</term><term>Protéines du choc thermique</term><term>Protéines à fluorescence verte</term></keywords><keywords scheme="MESH" qualifier="parasitologie" xml:lang="fr"><term>Foie</term><term>Paludisme</term></keywords><keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Liver</term><term>Malaria</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Plasmodium berghei</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Plasmodium berghei</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Tétracyclines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Tetracyclines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Genetically Modified</term><term>Gene Knockdown Techniques</term><term>Host-Parasite Interactions</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animal génétiquement modifié</term><term>Animaux</term><term>Interactions hôte-parasite</term><term>Régulation de l'expression des gènes</term><term>Souris</term><term>Techniques de knock-down de gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Export of most malaria proteins into the erythrocyte cytosol requires the Plasmodium translocon of exported proteins (PTEX) and a cleavable Plasmodium export element (PEXEL). In contrast, the contribution of PTEX in the liver stages and export of liver stage proteins is unknown. Here, using the FLP/FRT conditional mutatagenesis system, we generate transgenic Plasmodium berghei parasites deficient in EXP2, the putative pore-forming component of PTEX. Our data reveal that EXP2 is important for parasite growth in the liver and critical for parasite transition to the blood, with parasites impaired in their ability to generate a patent blood-stage infection. Surprisingly, whilst parasites expressing a functional PTEX machinery can efficiently export a PEXEL-bearing GFP reporter into the erythrocyte cytosol during a blood stage infection, this same reporter aggregates in large accumulations within the confines of the parasitophorous vacuole membrane during hepatocyte growth. Notably HSP101, the putative molecular motor of PTEX, could not be detected during the early liver stages of infection, which may explain why direct protein translocation of this soluble PEXEL-bearing reporter or indeed native PEXEL proteins into the hepatocyte cytosol has not been observed. This suggests that PTEX function may not be conserved between the blood and liver stages of malaria infection.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li></country><region><li>Victoria (État)</li><li>Île-de-France</li></region><settlement><li>Melbourne</li><li>Paris</li></settlement><orgName><li>Université de Melbourne</li></orgName></list><tree><country name="Australie"><noRegion><name sortKey="Kalanon, Ming" sort="Kalanon, Ming" uniqKey="Kalanon M" first="Ming" last="Kalanon">Ming Kalanon</name></noRegion><name sortKey="De Koning Ward, Tania F" sort="De Koning Ward, Tania F" uniqKey="De Koning Ward T" first="Tania F" last="De Koning-Ward">Tania F. De Koning-Ward</name><name sortKey="Ghosh, Sreejoyee" sort="Ghosh, Sreejoyee" uniqKey="Ghosh S" first="Sreejoyee" last="Ghosh">Sreejoyee Ghosh</name><name sortKey="Goodman, Christopher D" sort="Goodman, Christopher D" uniqKey="Goodman C" first="Christopher D" last="Goodman">Christopher D. Goodman</name><name sortKey="Matthews, Kathryn" sort="Matthews, Kathryn" uniqKey="Matthews K" first="Kathryn" last="Matthews">Kathryn Matthews</name><name sortKey="Mcfadden, Geoffrey I" sort="Mcfadden, Geoffrey I" uniqKey="Mcfadden G" first="Geoffrey I" last="Mcfadden">Geoffrey I. Mcfadden</name><name sortKey="Mollard, Vanessa" sort="Mollard, Vanessa" uniqKey="Mollard V" first="Vanessa" last="Mollard">Vanessa Mollard</name><name sortKey="Sturm, Angelika" sort="Sturm, Angelika" uniqKey="Sturm A" first="Angelika" last="Sturm">Angelika Sturm</name></country><country name="France"><region name="Île-de-France"><name sortKey="Bargieri, Daniel" sort="Bargieri, Daniel" uniqKey="Bargieri D" first="Daniel" last="Bargieri">Daniel Bargieri</name></region><name sortKey="Menard, Robert" sort="Menard, Robert" uniqKey="Menard R" first="Robert" last="Ménard">Robert Ménard</name><name sortKey="Thiberge, Sabine" sort="Thiberge, Sabine" uniqKey="Thiberge S" first="Sabine" last="Thiberge">Sabine Thiberge</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|clé= pubmed:26347246
|texte= The Plasmodium translocon of exported proteins component EXP2 is critical for establishing a patent malaria infection in mice.
}}
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