RapamycinFungusV1, Main, Exploration, bibRecord, 000276

Modelling of Neuronal Ceroid Lipofuscinosis Type 2 in Dictyostelium discoideum Suggests That Cytopathological Outcomes Result from Altered TOR Signalling.

Identifieur interne : 000276 ( Main/Exploration ); précédent : 000275; suivant : 000277

Modelling of Neuronal Ceroid Lipofuscinosis Type 2 in Dictyostelium discoideum Suggests That Cytopathological Outcomes Result from Altered TOR Signalling.

Auteurs : Paige K. Smith [Australie] ; Melodi G. Sen [Australie] ; Paul R. Fisher [Australie] ; Sarah J. Annesley [Australie]

Source :

Cells [ 2073-4409 ] ; 2019.

RBID : pubmed:31100984

Descripteurs français

KwdFr :
- ADN antisens (MeSH), ADN des protozoaires (MeSH), ARN messager (génétique), Aminopeptidases (génétique), Céroïdes-lipofuscinoses neuronales (métabolisme), Dictyostelium (cytologie), Dictyostelium (génétique), Dictyostelium (métabolisme), Dipeptidyl-Peptidases and Tripeptidyl-Peptidases (génétique), Expression des gènes (MeSH), Imagerie optique (MeSH), Lignée cellulaire (MeSH), Lysosomes (enzymologie), Mutation (MeSH), Phagocytose (effets des médicaments et des substances chimiques), Phototaxie (MeSH), Phénotype (MeSH), Prolifération cellulaire (effets des médicaments et des substances chimiques), Protéases à sérine (génétique), Protéine homologue de Ras enrichie dans le cerveau (génétique), Protéine homologue de Ras enrichie dans le cerveau (métabolisme), Sirolimus (pharmacologie), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (métabolisme), Techniques de knock-down de gènes (MeSH).
MESH :
- antagonistes et inhibiteurs : Sérine-thréonine kinases TOR.
- cytologie : Dictyostelium.
- effets des médicaments et des substances chimiques : Phagocytose, Prolifération cellulaire.
- enzymologie : Lysosomes.
- génétique : ARN messager, Aminopeptidases, Dictyostelium, Dipeptidyl-Peptidases and Tripeptidyl-Peptidases, Protéases à sérine, Protéine homologue de Ras enrichie dans le cerveau.
- métabolisme : Céroïdes-lipofuscinoses neuronales, Dictyostelium, Protéine homologue de Ras enrichie dans le cerveau, Sérine-thréonine kinases TOR.
- pharmacologie : Sirolimus.
- ADN antisens, ADN des protozoaires, Expression des gènes, Imagerie optique, Lignée cellulaire, Mutation, Phototaxie, Phénotype, Techniques de knock-down de gènes.

English descriptors

KwdEn :
- Aminopeptidases (genetics), Cell Line (MeSH), Cell Proliferation (drug effects), DNA, Antisense (MeSH), DNA, Protozoan (MeSH), Dictyostelium (cytology), Dictyostelium (genetics), Dictyostelium (metabolism), Dipeptidyl-Peptidases and Tripeptidyl-Peptidases (genetics), Gene Expression (MeSH), Gene Knockdown Techniques (MeSH), Lysosomes (enzymology), Mutation (MeSH), Neuronal Ceroid-Lipofuscinoses (metabolism), Optical Imaging (MeSH), Phagocytosis (drug effects), Phenotype (MeSH), Phototaxis (MeSH), RNA, Messenger (genetics), Ras Homolog Enriched in Brain Protein (genetics), Ras Homolog Enriched in Brain Protein (metabolism), Serine Proteases (genetics), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (metabolism).
MESH :
- chemical , antagonists & inhibitors : TOR Serine-Threonine Kinases.
- chemical , genetics : Aminopeptidases, Dipeptidyl-Peptidases and Tripeptidyl-Peptidases, RNA, Messenger, Ras Homolog Enriched in Brain Protein, Serine Proteases.
- cytology : Dictyostelium.
- drug effects : Cell Proliferation, Phagocytosis.
- enzymology : Lysosomes.
- genetics : Dictyostelium.
- metabolism : Dictyostelium, Neuronal Ceroid-Lipofuscinoses, Ras Homolog Enriched in Brain Protein, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Sirolimus.
- Cell Line, DNA, Antisense, DNA, Protozoan, Gene Expression, Gene Knockdown Techniques, Mutation, Optical Imaging, Phenotype, Phototaxis.

Abstract

The neuronal ceroid lipofuscinoses comprise a group of neurodegenerative disorders with similar clinical manifestations whose precise mechanisms of disease are presently unknown. We created multiple cell lines each with different levels of reduction of expression of the gene coding for the type 2 variant of the disease, Tripeptidyl peptidase (Tpp1), in the cellular slime mould Dictyostelium discoideum. Knocking down Tpp1 in Dictyostelium resulted in the accumulation of autofluorescent material, a characteristic trait of Batten disease. Phenotypic characterisation of the mutants revealed phenotypic deficiencies in growth and development, whilst endocytic uptake of nutrients was enhanced. Furthermore, the severity of the phenotypes correlated with the expression levels of Tpp1. We propose that the phenotypic defects are due to altered Target of Rapamycin (TOR) signalling. We show that treatment of wild type Dictyostelium cells with rapamycin (a specific TOR complex inhibitor) or antisense inhibition of expression of Rheb (Ras homologue enriched in the brain) (an upstream TOR complex activator) phenocopied the Tpp1 mutants. We also show that overexpression of Rheb rescued the defects caused by antisense inhibition of Tpp1. These results suggest that the TOR signalling pathway is responsible for the cytopathological outcomes in the Dictyostelium Tpp1 model of Batten disease.

DOI: 10.3390/cells8050469
PubMed: 31100984
PubMed Central: PMC6562681

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000271
to stream Main, to step Curation: 000271

Le document en format XML

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 Suggests That Cytopathological Outcomes Result from Altered TOR Signalling.</title>
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 Suggests That Cytopathological Outcomes Result from Altered TOR Signalling.</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aminopeptidases (genetics)</term>
<term>Cell Line (MeSH)</term>
<term>Cell Proliferation (drug effects)</term>
<term>DNA, Antisense (MeSH)</term>
<term>DNA, Protozoan (MeSH)</term>
<term>Dictyostelium (cytology)</term>
<term>Dictyostelium (genetics)</term>
<term>Dictyostelium (metabolism)</term>
<term>Dipeptidyl-Peptidases and Tripeptidyl-Peptidases (genetics)</term>
<term>Gene Expression (MeSH)</term>
<term>Gene Knockdown Techniques (MeSH)</term>
<term>Lysosomes (enzymology)</term>
<term>Mutation (MeSH)</term>
<term>Neuronal Ceroid-Lipofuscinoses (metabolism)</term>
<term>Optical Imaging (MeSH)</term>
<term>Phagocytosis (drug effects)</term>
<term>Phenotype (MeSH)</term>
<term>Phototaxis (MeSH)</term>
<term>RNA, Messenger (genetics)</term>
<term>Ras Homolog Enriched in Brain Protein (genetics)</term>
<term>Ras Homolog Enriched in Brain Protein (metabolism)</term>
<term>Serine Proteases (genetics)</term>
<term>Sirolimus (pharmacology)</term>
<term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ADN antisens (MeSH)</term>
<term>ADN des protozoaires (MeSH)</term>
<term>ARN messager (génétique)</term>
<term>Aminopeptidases (génétique)</term>
<term>Céroïdes-lipofuscinoses neuronales (métabolisme)</term>
<term>Dictyostelium (cytologie)</term>
<term>Dictyostelium (génétique)</term>
<term>Dictyostelium (métabolisme)</term>
<term>Dipeptidyl-Peptidases and Tripeptidyl-Peptidases (génétique)</term>
<term>Expression des gènes (MeSH)</term>
<term>Imagerie optique (MeSH)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lysosomes (enzymologie)</term>
<term>Mutation (MeSH)</term>
<term>Phagocytose (effets des médicaments et des substances chimiques)</term>
<term>Phototaxie (MeSH)</term>
<term>Phénotype (MeSH)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Protéases à sérine (génétique)</term>
<term>Protéine homologue de Ras enrichie dans le cerveau (génétique)</term>
<term>Protéine homologue de Ras enrichie dans le cerveau (métabolisme)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Techniques de knock-down de gènes (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Aminopeptidases</term>
<term>Dipeptidyl-Peptidases and Tripeptidyl-Peptidases</term>
<term>RNA, Messenger</term>
<term>Ras Homolog Enriched in Brain Protein</term>
<term>Serine Proteases</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Dictyostelium</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Dictyostelium</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Proliferation</term>
<term>Phagocytosis</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Phagocytose</term>
<term>Prolifération cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dictyostelium</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term>
<term>Aminopeptidases</term>
<term>Dictyostelium</term>
<term>Dipeptidyl-Peptidases and Tripeptidyl-Peptidases</term>
<term>Protéases à sérine</term>
<term>Protéine homologue de Ras enrichie dans le cerveau</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dictyostelium</term>
<term>Neuronal Ceroid-Lipofuscinoses</term>
<term>Ras Homolog Enriched in Brain Protein</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Céroïdes-lipofuscinoses neuronales</term>
<term>Dictyostelium</term>
<term>Protéine homologue de Ras enrichie dans le cerveau</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line</term>
<term>DNA, Antisense</term>
<term>DNA, Protozoan</term>
<term>Gene Expression</term>
<term>Gene Knockdown Techniques</term>
<term>Mutation</term>
<term>Optical Imaging</term>
<term>Phenotype</term>
<term>Phototaxis</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>ADN antisens</term>
<term>ADN des protozoaires</term>
<term>Expression des gènes</term>
<term>Imagerie optique</term>
<term>Lignée cellulaire</term>
<term>Mutation</term>
<term>Phototaxie</term>
<term>Phénotype</term>
<term>Techniques de knock-down de gènes</term>
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<front><div type="abstract" xml:lang="en">The neuronal ceroid lipofuscinoses comprise a group of neurodegenerative disorders with similar clinical manifestations whose precise mechanisms of disease are presently unknown. We created multiple cell lines each with different levels of reduction of expression of the gene coding for the type 2 variant of the disease, Tripeptidyl peptidase (Tpp1), in the cellular slime mould <i>Dictyostelium discoideum.</i>
 Knocking down Tpp1 in <i>Dictyostelium</i>
 resulted in the accumulation of autofluorescent material, a characteristic trait of Batten disease. Phenotypic characterisation of the mutants revealed phenotypic deficiencies in growth and development, whilst endocytic uptake of nutrients was enhanced. Furthermore, the severity of the phenotypes correlated with the expression levels of Tpp1. We propose that the phenotypic defects are due to altered Target of Rapamycin (TOR) signalling. We show that treatment of wild type <i>Dictyostelium</i>
 cells with rapamycin (a specific TOR complex inhibitor) or antisense inhibition of expression of Rheb (Ras homologue enriched in the brain) (an upstream TOR complex activator) phenocopied the Tpp1 mutants. We also show that overexpression of Rheb rescued the defects caused by antisense inhibition of Tpp1. These results suggest that the TOR signalling pathway is responsible for the cytopathological outcomes in the <i>Dictyostelium</i>
 Tpp1 model of Batten disease.</div>
</front>
</TEI>
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<DateCompleted><Year>2020</Year>
<Month>01</Month>
<Day>06</Day>
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<DateRevised><Year>2020</Year>
<Month>03</Month>
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<Day>16</Day>
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<Title>Cells</Title>
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<ArticleTitle>Modelling of Neuronal Ceroid Lipofuscinosis Type 2 in <i>Dictyostelium discoideum</i>
 Suggests That Cytopathological Outcomes Result from Altered TOR Signalling.</ArticleTitle>
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<Abstract><AbstractText>The neuronal ceroid lipofuscinoses comprise a group of neurodegenerative disorders with similar clinical manifestations whose precise mechanisms of disease are presently unknown. We created multiple cell lines each with different levels of reduction of expression of the gene coding for the type 2 variant of the disease, Tripeptidyl peptidase (Tpp1), in the cellular slime mould <i>Dictyostelium discoideum.</i>
 Knocking down Tpp1 in <i>Dictyostelium</i>
 resulted in the accumulation of autofluorescent material, a characteristic trait of Batten disease. Phenotypic characterisation of the mutants revealed phenotypic deficiencies in growth and development, whilst endocytic uptake of nutrients was enhanced. Furthermore, the severity of the phenotypes correlated with the expression levels of Tpp1. We propose that the phenotypic defects are due to altered Target of Rapamycin (TOR) signalling. We show that treatment of wild type <i>Dictyostelium</i>
 cells with rapamycin (a specific TOR complex inhibitor) or antisense inhibition of expression of Rheb (Ras homologue enriched in the brain) (an upstream TOR complex activator) phenocopied the Tpp1 mutants. We also show that overexpression of Rheb rescued the defects caused by antisense inhibition of Tpp1. These results suggest that the TOR signalling pathway is responsible for the cytopathological outcomes in the <i>Dictyostelium</i>
 Tpp1 model of Batten disease.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Smith</LastName>
<ForeName>Paige K</ForeName>
<Initials>PK</Initials>
<Identifier Source="ORCID">0000-0002-0750-0468</Identifier>
<AffiliationInfo><Affiliation>Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora 3086, Melbourne, Australia. paigeksmith81@gmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sen</LastName>
<ForeName>Melodi G</ForeName>
<Initials>MG</Initials>
<AffiliationInfo><Affiliation>Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora 3086, Melbourne, Australia. mgsen@students.latrobe.edu.au.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fisher</LastName>
<ForeName>Paul R</ForeName>
<Initials>PR</Initials>
<AffiliationInfo><Affiliation>Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora 3086, Melbourne, Australia. P.Fisher@latrobe.edu.au.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Annesley</LastName>
<ForeName>Sarah J</ForeName>
<Initials>SJ</Initials>
<Identifier Source="ORCID">0000-0002-7604-3985</Identifier>
<AffiliationInfo><Affiliation>Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora 3086, Melbourne, Australia. S.Annesley@latrobe.edu.au.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>05</Month>
<Day>16</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Switzerland</Country>
<MedlineTA>Cells</MedlineTA>
<NlmUniqueID>101600052</NlmUniqueID>
<ISSNLinking>2073-4409</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016373">DNA, Antisense</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016054">DNA, Protozoan</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000076205">Ras Homolog Enriched in Brain Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.-</RegistryNumber>
<NameOfSubstance UI="D057057">Serine Proteases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.11.-</RegistryNumber>
<NameOfSubstance UI="D000626">Aminopeptidases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.-</RegistryNumber>
<NameOfSubstance UI="D004152">Dipeptidyl-Peptidases and Tripeptidyl-Peptidases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.9</RegistryNumber>
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Modelling of Neuronal Ceroid Lipofuscinosis Type 2 in Dictyostelium discoideum Suggests That Cytopathological Outcomes Result from Altered TOR Signalling.

Modelling of Neuronal Ceroid Lipofuscinosis Type 2 in Dictyostelium discoideum Suggests That Cytopathological Outcomes Result from Altered TOR Signalling.

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