Expression of Pink1 with α-synuclein in the dopaminergic neurons of Drosophila leads to increases in both lifespan and healthspan.
Identifieur interne : 000A67 ( PubMed/Curation ); précédent : 000A66; suivant : 000A68Expression of Pink1 with α-synuclein in the dopaminergic neurons of Drosophila leads to increases in both lifespan and healthspan.
Auteurs : A M Todd [Canada] ; B E StaveleySource :
- Genetics and molecular research : GMR [ 1676-5680 ] ; 2012.
English descriptors
- KwdEn :
- Animals, Animals, Genetically Modified (genetics), Animals, Genetically Modified (metabolism), Animals, Genetically Modified (physiology), Dopaminergic Neurons (metabolism), Drosophila (genetics), Drosophila (metabolism), Drosophila (physiology), Drosophila Proteins (genetics), Drosophila Proteins (metabolism), Longevity (genetics), Longevity (physiology), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (metabolism), alpha-Synuclein (genetics), alpha-Synuclein (metabolism).
- MESH :
- chemical , genetics : Drosophila Proteins, Protein-Serine-Threonine Kinases, alpha-Synuclein.
- genetics : Animals, Genetically Modified, Drosophila, Longevity.
- metabolism : Animals, Genetically Modified, Dopaminergic Neurons, Drosophila, Drosophila Proteins, Protein-Serine-Threonine Kinases, alpha-Synuclein.
- physiology : Animals, Genetically Modified, Drosophila, Longevity.
- Animals.
Abstract
Overexpression of the gene coding for α-synuclein has been shown to be an inherited cause of Parkinson disease. Our laboratory has previously co-expressed the parkin and Pink1 genes to rescue α-synuclein-induced phenotypes within a Drosophila model. To further investigate the effect of Pink1 in this model, we performed longevity and behavioral studies using several drivers to express the α-synuclein and Pink1 genes. Our findings showed that overexpression of Pink1 and overexpression of Pink1 with α-synuclein resulted in an increased lifespan when driven with the TH-Gal4 transgene. This increase in longevity was accompanied by an increased healthspan, as measured by mobility over time, suggesting that this is an example of improved functional aging. Our results indicate that, in the dopaminergic cells targeted by TH-Gal4, increased expression of α-synuclein and Pink1 together have a synergistic effect, allowing for enhanced protection and increased survival of the organism.
DOI: 10.4238/2012.May.21.6
PubMed: 22653599
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Our laboratory has previously co-expressed the parkin and Pink1 genes to rescue α-synuclein-induced phenotypes within a Drosophila model. To further investigate the effect of Pink1 in this model, we performed longevity and behavioral studies using several drivers to express the α-synuclein and Pink1 genes. Our findings showed that overexpression of Pink1 and overexpression of Pink1 with α-synuclein resulted in an increased lifespan when driven with the TH-Gal4 transgene. This increase in longevity was accompanied by an increased healthspan, as measured by mobility over time, suggesting that this is an example of improved functional aging. Our results indicate that, in the dopaminergic cells targeted by TH-Gal4, increased expression of α-synuclein and Pink1 together have a synergistic effect, allowing for enhanced protection and increased survival of the organism.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22653599</PMID><DateCreated><Year>2012</Year><Month>06</Month><Day>01</Day></DateCreated><DateCompleted><Year>2012</Year><Month>09</Month><Day>27</Day></DateCompleted><DateRevised><Year>2012</Year><Month>06</Month><Day>01</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1676-5680</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>2</Issue><PubDate><Year>2012</Year><Month>May</Month><Day>21</Day></PubDate></JournalIssue><Title>Genetics and molecular research : GMR</Title><ISOAbbreviation>Genet. Mol. Res.</ISOAbbreviation></Journal><ArticleTitle>Expression of Pink1 with α-synuclein in the dopaminergic neurons of Drosophila leads to increases in both lifespan and healthspan.</ArticleTitle><Pagination><MedlinePgn>1497-502</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4238/2012.May.21.6</ELocationID><Abstract><AbstractText>Overexpression of the gene coding for α-synuclein has been shown to be an inherited cause of Parkinson disease. Our laboratory has previously co-expressed the parkin and Pink1 genes to rescue α-synuclein-induced phenotypes within a Drosophila model. To further investigate the effect of Pink1 in this model, we performed longevity and behavioral studies using several drivers to express the α-synuclein and Pink1 genes. Our findings showed that overexpression of Pink1 and overexpression of Pink1 with α-synuclein resulted in an increased lifespan when driven with the TH-Gal4 transgene. This increase in longevity was accompanied by an increased healthspan, as measured by mobility over time, suggesting that this is an example of improved functional aging. Our results indicate that, in the dopaminergic cells targeted by TH-Gal4, increased expression of α-synuclein and Pink1 together have a synergistic effect, allowing for enhanced protection and increased survival of the organism.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Todd</LastName><ForeName>A M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Department of Biology, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Staveley</LastName><ForeName>B E</ForeName><Initials>BE</Initials></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>2012</Year><Month>05</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Brazil</Country><MedlineTA>Genet Mol Res</MedlineTA><NlmUniqueID>101169387</NlmUniqueID><ISSNLinking>1676-5680</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029721">Drosophila Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C534484">PINK1 protein, Drosophila</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D017346">Protein-Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D030801" MajorTopicYN="N">Animals, Genetically Modified</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059290" MajorTopicYN="N">Dopaminergic Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004330" MajorTopicYN="N">Drosophila</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029721" MajorTopicYN="N">Drosophila Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008136" MajorTopicYN="N">Longevity</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051844" MajorTopicYN="N">alpha-Synuclein</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>6</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>6</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>9</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22653599</ArticleId><ArticleId IdType="pii">gmr1547</ArticleId><ArticleId IdType="doi">10.4238/2012.May.21.6</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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