Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila.
Identifieur interne : 000043 ( PubMed/Checkpoint ); précédent : 000042; suivant : 000044Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila.
Auteurs : P Githure M'Angale [Canada] ; Brian E. Staveley [Canada]Source :
- Genome [ 1480-3321 ] ; 2017.
English descriptors
- KwdEn :
- Age of Onset, Animals, Cell Survival, Culture Media, Drosophila Proteins (genetics), Drosophila melanogaster (genetics), Gene Expression Regulation, Genes, Recessive, Genotype, Male, Microscopy, Electron, Scanning, Mitochondria, Movement, Neurons (metabolism), Parkinson Disease (genetics), Phenotype, Photoreceptor Cells, Invertebrate, Proportional Hazards Models, Protein-Serine-Threonine Kinases (genetics), Proto-Oncogene Proteins c-bcl-2 (genetics), RNA Interference, Temperature, Transgenes, Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , genetics : Drosophila Proteins, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins c-bcl-2, Ubiquitin-Protein Ligases.
- chemical : Culture Media.
- genetics : Drosophila melanogaster, Parkinson Disease.
- metabolism : Neurons.
- Age of Onset, Animals, Cell Survival, Gene Expression Regulation, Genes, Recessive, Genotype, Male, Microscopy, Electron, Scanning, Mitochondria, Movement, Phenotype, Photoreceptor Cells, Invertebrate, Proportional Hazards Models, RNA Interference, Temperature, Transgenes.
Abstract
Mutations in parkin (PARK2) and Pink1 (PARK6) are responsible for autosomal recessive forms of early onset Parkinson's disease (PD). Attributed to the failure of neurons to clear dysfunctional mitochondria, loss of gene expression leads to loss of nigrostriatal neurons. The Pink1/parkin pathway plays a role in the quality control mechanism aimed at eliminating defective mitochondria, and the failure of this mechanism results in a reduced lifespan and impaired locomotor ability, among other phenotypes. Inhibition of parkin or Pink1 through the induction of stable RNAi transgene in the Ddc-Gal4-expressing neurons results in such phenotypes to model PD. To further evaluate the effects of the overexpression of the Bcl-2 homologue Buffy, we analysed lifespan and climbing ability in both parkin-RNAi- and Pink1-RNAi-expressing flies. In addition, the effect of Buffy overexpression upon parkin-induced developmental eye defects was examined through GMR-Gal4-dependent expression. Curiously, Buffy overexpression produced very different effects: the parkin-induced phenotypes were enhanced, whereas the Pink1-enhanced phenotypes were suppressed. Interestingly, the overexpression of Buffy along with the inhibition of parkin in the neuron-rich eye results in the suppression of the developmental eye defects.
DOI: 10.1139/gen-2016-0165
PubMed: 28106473
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:28106473Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila.</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, NL A1B 3X9, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, St. John's, NL A1B 3X9</wicri:regionArea><wicri:noRegion>NL 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, NL A1B 3X9, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, St. John's, NL A1B 3X9</wicri:regionArea><wicri:noRegion>NL A1B 3X9</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28106473</idno><idno type="pmid">28106473</idno><idno type="doi">10.1139/gen-2016-0165</idno><idno type="wicri:Area/PubMed/Corpus">000046</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000046</idno><idno type="wicri:Area/PubMed/Curation">000046</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000046</idno><idno type="wicri:Area/PubMed/Checkpoint">000046</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000046</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila.</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, NL A1B 3X9, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, St. John's, NL A1B 3X9</wicri:regionArea><wicri:noRegion>NL 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, NL A1B 3X9, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, St. John's, NL A1B 3X9</wicri:regionArea><wicri:noRegion>NL A1B 3X9</wicri:noRegion></affiliation></author></analytic><series><title level="j">Genome</title><idno type="eISSN">1480-3321</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age of Onset</term><term>Animals</term><term>Cell Survival</term><term>Culture Media</term><term>Drosophila Proteins (genetics)</term><term>Drosophila melanogaster (genetics)</term><term>Gene Expression Regulation</term><term>Genes, Recessive</term><term>Genotype</term><term>Male</term><term>Microscopy, Electron, Scanning</term><term>Mitochondria</term><term>Movement</term><term>Neurons (metabolism)</term><term>Parkinson Disease (genetics)</term><term>Phenotype</term><term>Photoreceptor Cells, Invertebrate</term><term>Proportional Hazards Models</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>Proto-Oncogene Proteins c-bcl-2 (genetics)</term><term>RNA Interference</term><term>Temperature</term><term>Transgenes</term><term>Ubiquitin-Protein Ligases (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Drosophila Proteins</term><term>Protein-Serine-Threonine Kinases</term><term>Proto-Oncogene Proteins c-bcl-2</term><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Culture Media</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Drosophila melanogaster</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age of Onset</term><term>Animals</term><term>Cell Survival</term><term>Gene Expression Regulation</term><term>Genes, Recessive</term><term>Genotype</term><term>Male</term><term>Microscopy, Electron, Scanning</term><term>Mitochondria</term><term>Movement</term><term>Phenotype</term><term>Photoreceptor Cells, Invertebrate</term><term>Proportional Hazards Models</term><term>RNA Interference</term><term>Temperature</term><term>Transgenes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mutations in parkin (PARK2) and Pink1 (PARK6) are responsible for autosomal recessive forms of early onset Parkinson's disease (PD). Attributed to the failure of neurons to clear dysfunctional mitochondria, loss of gene expression leads to loss of nigrostriatal neurons. The Pink1/parkin pathway plays a role in the quality control mechanism aimed at eliminating defective mitochondria, and the failure of this mechanism results in a reduced lifespan and impaired locomotor ability, among other phenotypes. Inhibition of parkin or Pink1 through the induction of stable RNAi transgene in the Ddc-Gal4-expressing neurons results in such phenotypes to model PD. To further evaluate the effects of the overexpression of the Bcl-2 homologue Buffy, we analysed lifespan and climbing ability in both parkin-RNAi- and Pink1-RNAi-expressing flies. In addition, the effect of Buffy overexpression upon parkin-induced developmental eye defects was examined through GMR-Gal4-dependent expression. Curiously, Buffy overexpression produced very different effects: the parkin-induced phenotypes were enhanced, whereas the Pink1-enhanced phenotypes were suppressed. Interestingly, the overexpression of Buffy along with the inhibition of parkin in the neuron-rich eye results in the suppression of the developmental eye defects.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28106473</PMID><DateCreated><Year>2017</Year><Month>01</Month><Day>20</Day></DateCreated><DateCompleted><Year>2017</Year><Month>03</Month><Day>20</Day></DateCompleted><DateRevised><Year>2017</Year><Month>03</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1480-3321</ISSN><JournalIssue CitedMedium="Internet"><Volume>60</Volume><Issue>3</Issue><PubDate><Year>2017</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Genome</Title><ISOAbbreviation>Genome</ISOAbbreviation></Journal><ArticleTitle>Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila.</ArticleTitle><Pagination><MedlinePgn>241-247</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1139/gen-2016-0165</ELocationID><Abstract><AbstractText>Mutations in parkin (PARK2) and Pink1 (PARK6) are responsible for autosomal recessive forms of early onset Parkinson's disease (PD). Attributed to the failure of neurons to clear dysfunctional mitochondria, loss of gene expression leads to loss of nigrostriatal neurons. The Pink1/parkin pathway plays a role in the quality control mechanism aimed at eliminating defective mitochondria, and the failure of this mechanism results in a reduced lifespan and impaired locomotor ability, among other phenotypes. Inhibition of parkin or Pink1 through the induction of stable RNAi transgene in the Ddc-Gal4-expressing neurons results in such phenotypes to model PD. To further evaluate the effects of the overexpression of the Bcl-2 homologue Buffy, we analysed lifespan and climbing ability in both parkin-RNAi- and Pink1-RNAi-expressing flies. In addition, the effect of Buffy overexpression upon parkin-induced developmental eye defects was examined through GMR-Gal4-dependent expression. Curiously, Buffy overexpression produced very different effects: the parkin-induced phenotypes were enhanced, whereas the Pink1-enhanced phenotypes were suppressed. Interestingly, the overexpression of Buffy along with the inhibition of parkin in the neuron-rich eye results in the suppression of the developmental eye defects.</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, NL A1B 3X9, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biology, Memorial University of Newfoundland, St. John's, NL 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, NL A1B 3X9, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biology, Memorial University of Newfoundland, St. John's, NL A1B 3X9, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>12</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Canada</Country><MedlineTA>Genome</MedlineTA><NlmUniqueID>8704544</NlmUniqueID><ISSNLinking>0831-2796</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C477358">Buffy protein, Drosophila</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003470">Culture Media</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029721">Drosophila Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019253">Proto-Oncogene Proteins c-bcl-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</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><Chemical><RegistryNumber>EC 6.3.2.-</RegistryNumber><NameOfSubstance UI="C487430">parkin protein, Drosophila</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017668" MajorTopicYN="N">Age of Onset</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003470" MajorTopicYN="N">Culture Media</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D029721" MajorTopicYN="N">Drosophila Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004331" MajorTopicYN="N">Drosophila melanogaster</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005808" MajorTopicYN="N">Genes, Recessive</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008855" MajorTopicYN="N">Microscopy, Electron, Scanning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009068" MajorTopicYN="N">Movement</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017956" MajorTopicYN="N">Photoreceptor Cells, Invertebrate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016016" MajorTopicYN="N">Proportional Hazards Models</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D034622" MajorTopicYN="N">RNA Interference</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013696" MajorTopicYN="N">Temperature</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019076" MajorTopicYN="Y">Transgenes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D044767" MajorTopicYN="N">Ubiquitin-Protein Ligases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Buffy</Keyword><Keyword MajorTopicYN="N">Ddc-Gal4</Keyword><Keyword MajorTopicYN="N">GMR-Gal4</Keyword><Keyword MajorTopicYN="N">Parkinson’s disease</Keyword><Keyword MajorTopicYN="N">Pink1</Keyword><Keyword MajorTopicYN="N">maladie de Parkinson</Keyword><Keyword MajorTopicYN="N">parkin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>1</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>3</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>1</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28106473</ArticleId><ArticleId IdType="doi">10.1139/gen-2016-0165</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. Staveley</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PubMed/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000043 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 000043 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Canada
|area= ParkinsonCanadaV1
|flux= PubMed
|étape= Checkpoint
|type= RBID
|clé= pubmed:28106473
|texte= Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i -Sk "pubmed:28106473" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonCanadaV1
| This area was generated with Dilib version V0.6.29. |  |