Loss of porin function in dopaminergic neurons of Drosophila is suppressed by Buffy.
Identifieur interne : 000216 ( PubMed/Checkpoint ); précédent : 000215; suivant : 000217Loss of porin function in dopaminergic neurons of Drosophila is suppressed by Buffy.
Auteurs : P Githure M'Angale [Canada] ; Brian E. Staveley [Canada]Source :
- Journal of biomedical science [ 1423-0127 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Dopaminergic Neurons (metabolism), Dopaminergic Neurons (pathology), Drosophila Proteins (biosynthesis), Drosophila Proteins (genetics), Drosophila melanogaster (genetics), Gene Expression Regulation, Humans, Mitochondria (genetics), Mitochondria (pathology), Parkinson Disease (genetics), Parkinson Disease (pathology), Porins (genetics), Proto-Oncogene Proteins c-bcl-2 (biosynthesis), Proto-Oncogene Proteins c-bcl-2 (genetics).
- MESH :
- chemical , biosynthesis : Drosophila Proteins, Proto-Oncogene Proteins c-bcl-2.
- chemical , genetics : Drosophila Proteins, Porins, Proto-Oncogene Proteins c-bcl-2.
- genetics : Drosophila melanogaster, Mitochondria, Parkinson Disease.
- metabolism : Dopaminergic Neurons.
- pathology : Dopaminergic Neurons, Mitochondria, Parkinson Disease.
- Animals, Disease Models, Animal, Gene Expression Regulation, Humans.
Abstract
Mitochondrial porin, also known as the voltage-dependent anion channel (VDAC), is a multi-functional channel protein that shuttles metabolites between the mitochondria and the cytosol and implicated in cellular life and death decisions. The inhibition of porin under the control of neuronal Ddc-Gal4 result in short lifespan and in an age-dependent loss in locomotor function, phenotypes that are strongly associated with Drosophila models of Parkinson disease.
DOI: 10.1186/s12929-016-0300-1
PubMed: 27881168
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:27881168Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Loss of porin function in dopaminergic neurons of Drosophila is suppressed by Buffy.</title><author><name sortKey="M Angale, P Githure" sort="M Angale, P Githure" uniqKey="M Angale P" first="P Githure" last="M'Angale">P Githure M'Angale</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9</wicri:regionArea><wicri:noRegion>A1B 3X9</wicri:noRegion></affiliation></author><author><name sortKey="Staveley, Brian E" sort="Staveley, Brian E" uniqKey="Staveley B" first="Brian E" last="Staveley">Brian E. Staveley</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9, Canada. bestave@mun.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9</wicri:regionArea><wicri:noRegion>A1B 3X9</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27881168</idno><idno type="pmid">27881168</idno><idno type="doi">10.1186/s12929-016-0300-1</idno><idno type="wicri:Area/PubMed/Corpus">000119</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000119</idno><idno type="wicri:Area/PubMed/Curation">000119</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000119</idno><idno type="wicri:Area/PubMed/Checkpoint">000119</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000119</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Loss of porin function in dopaminergic neurons of Drosophila is suppressed by Buffy.</title><author><name sortKey="M Angale, P Githure" sort="M Angale, P Githure" uniqKey="M Angale P" first="P Githure" last="M'Angale">P Githure M'Angale</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9</wicri:regionArea><wicri:noRegion>A1B 3X9</wicri:noRegion></affiliation></author><author><name sortKey="Staveley, Brian E" sort="Staveley, Brian E" uniqKey="Staveley B" first="Brian E" last="Staveley">Brian E. Staveley</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9, Canada. bestave@mun.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9</wicri:regionArea><wicri:noRegion>A1B 3X9</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of biomedical science</title><idno type="eISSN">1423-0127</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>Disease Models, Animal</term><term>Dopaminergic Neurons (metabolism)</term><term>Dopaminergic Neurons (pathology)</term><term>Drosophila Proteins (biosynthesis)</term><term>Drosophila Proteins (genetics)</term><term>Drosophila melanogaster (genetics)</term><term>Gene Expression Regulation</term><term>Humans</term><term>Mitochondria (genetics)</term><term>Mitochondria (pathology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Porins (genetics)</term><term>Proto-Oncogene Proteins c-bcl-2 (biosynthesis)</term><term>Proto-Oncogene Proteins c-bcl-2 (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Drosophila Proteins</term><term>Proto-Oncogene Proteins c-bcl-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Drosophila Proteins</term><term>Porins</term><term>Proto-Oncogene Proteins c-bcl-2</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Drosophila melanogaster</term><term>Mitochondria</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dopaminergic Neurons</term><term>Mitochondria</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Gene Expression Regulation</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mitochondrial porin, also known as the voltage-dependent anion channel (VDAC), is a multi-functional channel protein that shuttles metabolites between the mitochondria and the cytosol and implicated in cellular life and death decisions. The inhibition of porin under the control of neuronal Ddc-Gal4 result in short lifespan and in an age-dependent loss in locomotor function, phenotypes that are strongly associated with Drosophila models of Parkinson disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27881168</PMID><DateCreated><Year>2016</Year><Month>11</Month><Day>24</Day></DateCreated><DateCompleted><Year>2017</Year><Month>03</Month><Day>09</Day></DateCompleted><DateRevised><Year>2017</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1423-0127</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>1</Issue><PubDate><Year>2016</Year><Month>Nov</Month><Day>24</Day></PubDate></JournalIssue><Title>Journal of biomedical science</Title><ISOAbbreviation>J. Biomed. Sci.</ISOAbbreviation></Journal><ArticleTitle>Loss of porin function in dopaminergic neurons of Drosophila is suppressed by Buffy.</ArticleTitle><Pagination><MedlinePgn>84</MedlinePgn></Pagination><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Mitochondrial porin, also known as the voltage-dependent anion channel (VDAC), is a multi-functional channel protein that shuttles metabolites between the mitochondria and the cytosol and implicated in cellular life and death decisions. The inhibition of porin under the control of neuronal Ddc-Gal4 result in short lifespan and in an age-dependent loss in locomotor function, phenotypes that are strongly associated with Drosophila models of Parkinson disease.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Loss of porin function was achieved through exploitation of RNA interference while derivative lines were generated by homologous recombination and tested by PCR. The UAS/Gal4 expression system was exploited with directed expression in neurons achieved with the use of the Dopa decarboxylase and in the developing eye with the Glass multiple reporter transgenes. Statistical analyses for ageing assay employed Log rank (Mantel-Cox) test, climbing indices were fitted with a non-linear curve and confidence intervals compared at 95%. Biometric analysis of the eye phenotypes was obtained by unpaired student T-test.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The expression of α-synuclein in neuronal populations that include dopamine producing neurons under the control of Ddc-Gal4 produces a robust Parkinson disease model, and results in severely reduced lifespan and locomotor dysfunction. In addition, the porin-induced phenotypes are greatly suppressed when the pro-survival Bcl-2 homologue Buffy is overexpressed in these neurons and in the developing eye adding to the cellular advantages of altered expression of this anti-apoptotic gene. When we co-expressed α-synuclein along with porin, it results in a decrease in lifespan and impaired climbing ability. This enhancement of the α-synuclein-induced phenotypes observed in neurons was demonstrated in the neuron rich eye, where the simultaneous co-expression of porin-RNAi and α-synuclein resulted in an enhanced eye phenotype, marked by reduced number of ommatidia and increased disarray of the ommatidia.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The inhibition of porin in dopaminergic neurons among others result in reduced lifespan and age-dependent loss in climbing ability, phenotypes that are suppressed by the overexpression of the sole pro-survival Bcl-2 homologue Buffy. The inhibition of porin phenocopies Parkinson disease phenotypes in Drosophila, while the overexpression of Buffy can counteract these phenotypes to improve the overall "healthspan" of the organism.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>M'Angale</LastName><ForeName>P Githure</ForeName><Initials>PG</Initials><AffiliationInfo><Affiliation>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Staveley</LastName><ForeName>Brian E</ForeName><Initials>BE</Initials><AffiliationInfo><Affiliation>Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland & Labrador, A1B 3X9, Canada. bestave@mun.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>11</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Biomed Sci</MedlineTA><NlmUniqueID>9421567</NlmUniqueID><ISSNLinking>1021-7770</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C477358">Buffy protein, Drosophila</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029721">Drosophila Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018272">Porins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019253">Proto-Oncogene Proteins c-bcl-2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Curr Biol. 2000 May 4;10(9):547-50</RefSource><PMID 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MajorTopicYN="N">Drosophila Proteins</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004331" MajorTopicYN="N">Drosophila melanogaster</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018272" MajorTopicYN="N">Porins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Buffy</Keyword><Keyword MajorTopicYN="Y">Dopaminergic neurons</Keyword><Keyword MajorTopicYN="Y">Mitochondria</Keyword><Keyword MajorTopicYN="Y">Parkinson disease</Keyword><Keyword MajorTopicYN="Y">Porin</Keyword><Keyword MajorTopicYN="Y">α-synuclein</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>06</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>11</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>11</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>3</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27881168</ArticleId><ArticleId IdType="doi">10.1186/s12929-016-0300-1</ArticleId><ArticleId IdType="pii">10.1186/s12929-016-0300-1</ArticleId><ArticleId IdType="pmc">PMC5122015</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="M Angale, P Githure" sort="M Angale, P Githure" uniqKey="M Angale P" first="P Githure" last="M'Angale">P Githure M'Angale</name></noRegion><name sortKey="Staveley, Brian E" sort="Staveley, Brian E" uniqKey="Staveley B" first="Brian E" last="Staveley">Brian E. 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