Countervailing, time-dependent effects on host autophagy promotes intracellular survival of Leishmania.
Identifieur interne : 000628 ( Main/Exploration ); précédent : 000627; suivant : 000629Countervailing, time-dependent effects on host autophagy promotes intracellular survival of Leishmania.
Auteurs : Sneha A. Thomas [Canada] ; Devki Nandan [Canada] ; Jennifer Kass [Canada] ; Neil E. Reiner [Canada]Source :
- The Journal of biological chemistry [ 1083-351X ] ; 2018.
Descripteurs français
- KwdFr :
- Autophagie (MeSH), Humains (MeSH), Interactions hôte-parasite (MeSH), Leishmania donovani (croissance et développement), Leishmania donovani (génétique), Leishmania donovani (physiologie), Leishmaniose viscérale (génétique), Leishmaniose viscérale (métabolisme), Leishmaniose viscérale (parasitologie), Leishmaniose viscérale (physiopathologie), Macrophages (cytologie), Macrophages (métabolisme), Macrophages (parasitologie), Phosphoric monoester hydrolases (génétique), Phosphoric monoester hydrolases (métabolisme), Protéine-5 associée à l'autophagie (génétique), Protéine-5 associée à l'autophagie (métabolisme), Protéines associées aux microtubules (génétique), Protéines associées aux microtubules (métabolisme), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme).
- MESH :
- croissance et développement : Leishmania donovani.
- cytologie : Macrophages.
- génétique : Leishmania donovani, Leishmaniose viscérale, Phosphoric monoester hydrolases, Protéine-5 associée à l'autophagie, Protéines associées aux microtubules, Sérine-thréonine kinases TOR.
- métabolisme : Leishmaniose viscérale, Macrophages, Phosphoric monoester hydrolases, Protéine-5 associée à l'autophagie, Protéines associées aux microtubules, Sérine-thréonine kinases TOR.
- parasitologie : Leishmaniose viscérale, Macrophages.
- physiologie : Leishmania donovani.
- physiopathologie : Leishmaniose viscérale.
- Autophagie, Humains, Interactions hôte-parasite.
English descriptors
- KwdEn :
- Autophagy (MeSH), Autophagy-Related Protein 5 (genetics), Autophagy-Related Protein 5 (metabolism), Host-Parasite Interactions (MeSH), Humans (MeSH), Leishmania donovani (genetics), Leishmania donovani (growth & development), Leishmania donovani (physiology), Leishmaniasis, Visceral (genetics), Leishmaniasis, Visceral (metabolism), Leishmaniasis, Visceral (parasitology), Leishmaniasis, Visceral (physiopathology), Macrophages (cytology), Macrophages (metabolism), Macrophages (parasitology), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Phosphoric Monoester Hydrolases (genetics), Phosphoric Monoester Hydrolases (metabolism), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , genetics : Autophagy-Related Protein 5, Microtubule-Associated Proteins, Phosphoric Monoester Hydrolases, TOR Serine-Threonine Kinases.
- chemical , metabolism : Autophagy-Related Protein 5, Microtubule-Associated Proteins, Phosphoric Monoester Hydrolases, TOR Serine-Threonine Kinases.
- cytology : Macrophages.
- genetics : Leishmania donovani, Leishmaniasis, Visceral.
- growth & development : Leishmania donovani.
- metabolism : Leishmaniasis, Visceral, Macrophages.
- parasitology : Leishmaniasis, Visceral, Macrophages.
- physiology : Leishmania donovani.
- physiopathology : Leishmaniasis, Visceral.
- Autophagy, Host-Parasite Interactions, Humans.
Abstract
Autophagy is essential for cell survival under stress and has also been implicated in host defense. Here, we investigated the interactions between Leishmania donovani, the main etiological agent of visceral leishmaniasis, and the autophagic machinery of human macrophages. Our results revealed that during early infection-and via activation of the Akt pathway-Leishmania actively inhibits the induction of autophagy. However, by 24 h, Leishmania switched from being an inhibitor to an overall inducer of autophagy. These findings of a dynamic, biphasic response were based on the accumulation of lipidated light chain 3 (LC3), an autophagosome marker, by Western blotting and confocal fluorescence microscopy. We also present evidence that Leishmania induces delayed host cell autophagy via a mechanism independent of reduced activity of the mechanistic target of rapamycin (mTOR). Notably, Leishmania actively inhibited mTOR-regulated autophagy even at later stages of infection, whereas there was a clear induction of autophagy via some other mechanism. In this context, we examined host inositol monophosphatase (IMPase), reduced levels of which have been implicated in mTOR-independent autophagy, and we found that IMPase activity is significantly decreased in infected cells. These findings indicate that Leishmania uses an alternative pathway to mTOR to induce autophagy in host macrophages. Finally, RNAi-mediated down-regulation of host autophagy protein 5 (ATG5) or autophagy protein 9A (ATG9A) decreased parasite loads, demonstrating that autophagy is essential for Leishmania survival. We conclude that Leishmania uses an alternative pathway to induce host autophagy while simultaneously inhibiting mTOR-regulated autophagy to fine-tune the timing and magnitude of this process and to optimize parasite survival.
DOI: 10.1074/jbc.M117.808675
PubMed: 29269416
PubMed Central: PMC5818176
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Thomas</name><affiliation wicri:level="4"><nlm:affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</nlm:affiliation><orgName type="university">Université de la Colombie-Britannique</orgName><country>Canada</country><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique </region></placeName></affiliation></author><author><name sortKey="Nandan, Devki" sort="Nandan, Devki" uniqKey="Nandan D" first="Devki" last="Nandan">Devki Nandan</name><affiliation wicri:level="4"><nlm:affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</nlm:affiliation><orgName type="university">Université de la Colombie-Britannique</orgName><country>Canada</country><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique </region></placeName></affiliation></author><author><name sortKey="Kass, Jennifer" sort="Kass, Jennifer" uniqKey="Kass J" first="Jennifer" last="Kass">Jennifer Kass</name><affiliation wicri:level="4"><nlm:affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</nlm:affiliation><orgName type="university">Université de la Colombie-Britannique</orgName><country>Canada</country><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique </region></placeName></affiliation></author><author><name sortKey="Reiner, Neil E" sort="Reiner, Neil E" uniqKey="Reiner N" first="Neil E" last="Reiner">Neil E. 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Thomas</name><affiliation wicri:level="4"><nlm:affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</nlm:affiliation><orgName type="university">Université de la Colombie-Britannique</orgName><country>Canada</country><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique </region></placeName></affiliation></author><author><name sortKey="Nandan, Devki" sort="Nandan, Devki" uniqKey="Nandan D" first="Devki" last="Nandan">Devki Nandan</name><affiliation wicri:level="4"><nlm:affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</nlm:affiliation><orgName type="university">Université de la Colombie-Britannique</orgName><country>Canada</country><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique </region></placeName></affiliation></author><author><name sortKey="Kass, Jennifer" sort="Kass, Jennifer" uniqKey="Kass J" first="Jennifer" last="Kass">Jennifer Kass</name><affiliation wicri:level="4"><nlm:affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</nlm:affiliation><orgName type="university">Université de la Colombie-Britannique</orgName><country>Canada</country><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique </region></placeName></affiliation></author><author><name sortKey="Reiner, Neil E" sort="Reiner, Neil E" uniqKey="Reiner N" first="Neil E" last="Reiner">Neil E. Reiner</name><affiliation wicri:level="4"><nlm:affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and nreiner@mail.ubc.ca.</nlm:affiliation><country wicri:rule="url">Canada</country><wicri:regionArea>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver</wicri:regionArea><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique</region></placeName><orgName type="university">Université de la Colombie-Britannique</orgName></affiliation><affiliation wicri:level="4"><nlm:affiliation>the Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>the Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia V6T 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(parasitology)</term><term>Leishmaniasis, Visceral (physiopathology)</term><term>Macrophages (cytology)</term><term>Macrophages (metabolism)</term><term>Macrophages (parasitology)</term><term>Microtubule-Associated Proteins (genetics)</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Phosphoric Monoester Hydrolases (genetics)</term><term>Phosphoric Monoester Hydrolases (metabolism)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>TOR Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie (MeSH)</term><term>Humains (MeSH)</term><term>Interactions hôte-parasite (MeSH)</term><term>Leishmania donovani (croissance et développement)</term><term>Leishmania donovani (génétique)</term><term>Leishmania donovani (physiologie)</term><term>Leishmaniose viscérale (génétique)</term><term>Leishmaniose viscérale (métabolisme)</term><term>Leishmaniose viscérale (parasitologie)</term><term>Leishmaniose viscérale (physiopathologie)</term><term>Macrophages (cytologie)</term><term>Macrophages (métabolisme)</term><term>Macrophages (parasitologie)</term><term>Phosphoric monoester hydrolases (génétique)</term><term>Phosphoric monoester hydrolases (métabolisme)</term><term>Protéine-5 associée à l'autophagie (génétique)</term><term>Protéine-5 associée à l'autophagie (métabolisme)</term><term>Protéines associées aux microtubules (génétique)</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Protein 5</term><term>Microtubule-Associated Proteins</term><term>Phosphoric Monoester Hydrolases</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Autophagy-Related Protein 5</term><term>Microtubule-Associated Proteins</term><term>Phosphoric Monoester Hydrolases</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Leishmania donovani</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Leishmania donovani</term><term>Leishmaniasis, Visceral</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Leishmania donovani</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Leishmania donovani</term><term>Leishmaniose viscérale</term><term>Phosphoric monoester hydrolases</term><term>Protéine-5 associée à l'autophagie</term><term>Protéines associées aux microtubules</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Leishmaniasis, Visceral</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Leishmaniose viscérale</term><term>Macrophages</term><term>Phosphoric monoester hydrolases</term><term>Protéine-5 associée à l'autophagie</term><term>Protéines associées aux microtubules</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="parasitologie" xml:lang="fr"><term>Leishmaniose viscérale</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Leishmaniasis, Visceral</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Leishmania donovani</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Leishmania donovani</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Leishmaniose viscérale</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Leishmaniasis, Visceral</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Autophagy</term><term>Host-Parasite Interactions</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Humains</term><term>Interactions hôte-parasite</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy is essential for cell survival under stress and has also been implicated in host defense. Here, we investigated the interactions between <i>Leishmania donovani</i>, the main etiological agent of visceral leishmaniasis, and the autophagic machinery of human macrophages. Our results revealed that during early infection-and via activation of the Akt pathway-<i>Leishmania</i> actively inhibits the induction of autophagy. However, by 24 h, <i>Leishmania</i> switched from being an inhibitor to an overall inducer of autophagy. These findings of a dynamic, biphasic response were based on the accumulation of lipidated light chain 3 (LC3), an autophagosome marker, by Western blotting and confocal fluorescence microscopy. We also present evidence that <i>Leishmania</i> induces delayed host cell autophagy via a mechanism independent of reduced activity of the mechanistic target of rapamycin (mTOR). Notably, <i>Leishmania</i> actively inhibited mTOR-regulated autophagy even at later stages of infection, whereas there was a clear induction of autophagy via some other mechanism. In this context, we examined host inositol monophosphatase (IMPase), reduced levels of which have been implicated in mTOR-independent autophagy, and we found that IMPase activity is significantly decreased in infected cells. These findings indicate that <i>Leishmania</i> uses an alternative pathway to mTOR to induce autophagy in host macrophages. Finally, RNAi-mediated down-regulation of host autophagy protein 5 (ATG5) or autophagy protein 9A (ATG9A) decreased parasite loads, demonstrating that autophagy is essential for <i>Leishmania</i> survival. We conclude that <i>Leishmania</i> uses an alternative pathway to induce host autophagy while simultaneously inhibiting mTOR-regulated autophagy to fine-tune the timing and magnitude of this process and to optimize parasite survival.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29269416</PMID><DateCompleted><Year>2019</Year><Month>02</Month><Day>05</Day></DateCompleted><DateRevised><Year>2019</Year><Month>02</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN><JournalIssue CitedMedium="Internet"><Volume>293</Volume><Issue>7</Issue><PubDate><Year>2018</Year><Month>02</Month><Day>16</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J Biol Chem</ISOAbbreviation></Journal><ArticleTitle>Countervailing, time-dependent effects on host autophagy promotes intracellular survival of <i>Leishmania</i>.</ArticleTitle><Pagination><MedlinePgn>2617-2630</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.M117.808675</ELocationID><Abstract><AbstractText>Autophagy is essential for cell survival under stress and has also been implicated in host defense. Here, we investigated the interactions between <i>Leishmania donovani</i>, the main etiological agent of visceral leishmaniasis, and the autophagic machinery of human macrophages. Our results revealed that during early infection-and via activation of the Akt pathway-<i>Leishmania</i> actively inhibits the induction of autophagy. However, by 24 h, <i>Leishmania</i> switched from being an inhibitor to an overall inducer of autophagy. These findings of a dynamic, biphasic response were based on the accumulation of lipidated light chain 3 (LC3), an autophagosome marker, by Western blotting and confocal fluorescence microscopy. We also present evidence that <i>Leishmania</i> induces delayed host cell autophagy via a mechanism independent of reduced activity of the mechanistic target of rapamycin (mTOR). Notably, <i>Leishmania</i> actively inhibited mTOR-regulated autophagy even at later stages of infection, whereas there was a clear induction of autophagy via some other mechanism. In this context, we examined host inositol monophosphatase (IMPase), reduced levels of which have been implicated in mTOR-independent autophagy, and we found that IMPase activity is significantly decreased in infected cells. These findings indicate that <i>Leishmania</i> uses an alternative pathway to mTOR to induce autophagy in host macrophages. Finally, RNAi-mediated down-regulation of host autophagy protein 5 (ATG5) or autophagy protein 9A (ATG9A) decreased parasite loads, demonstrating that autophagy is essential for <i>Leishmania</i> survival. We conclude that <i>Leishmania</i> uses an alternative pathway to induce host autophagy while simultaneously inhibiting mTOR-regulated autophagy to fine-tune the timing and magnitude of this process and to optimize parasite survival.</AbstractText><CopyrightInformation>© 2018 by The American Society for Biochemistry and Molecular Biology, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Thomas</LastName><ForeName>Sneha A</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nandan</LastName><ForeName>Devki</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kass</LastName><ForeName>Jennifer</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reiner</LastName><ForeName>Neil E</ForeName><Initials>NE</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia V6H 3Z6 and nreiner@mail.ubc.ca.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>the Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MOP-125879</GrantID><Agency>CIHR</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>12</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071187">Autophagy-Related Protein 5</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008869">Microtubule-Associated Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C466626">light chain 3, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.2</RegistryNumber><NameOfSubstance UI="D010744">Phosphoric Monoester Hydrolases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.25</RegistryNumber><NameOfSubstance UI="C021822">myo-inositol-1 (or 4)-monophosphatase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000071187" MajorTopicYN="N">Autophagy-Related Protein 5</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006790" MajorTopicYN="Y">Host-Parasite Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007893" MajorTopicYN="N">Leishmania donovani</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007898" MajorTopicYN="N">Leishmaniasis, Visceral</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010744" MajorTopicYN="N">Phosphoric Monoester Hydrolases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" 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