Bcl-2 homologue Debcl enhances α-synuclein-induced phenotypes in Drosophila
Identifieur interne : 000463 ( Main/Exploration ); précédent : 000462; suivant : 000464Bcl-2 homologue Debcl enhances α-synuclein-induced phenotypes in Drosophila
Auteurs : P. Githure M Ngale ; Brian E. StaveleySource :
- PeerJ [ 2167-8359 ] ; 2016.
Abstract
Parkinson disease (PD) is a debilitating movement disorder that afflicts 1–2% of the population over 50 years of age. The common hallmark for both sporadic and familial forms of PD is mitochondrial dysfunction. Mammals have at least twenty proapoptotic and antiapoptotic
The directed overexpression of
The overexpression of
Url:
DOI: 10.7717/peerj.2461
PubMed: 27672511
PubMed Central: 5028777
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en"><italic>Bcl-2</italic> homologue <italic>Debcl</italic> enhances <italic>α-synuclein</italic>-induced phenotypes in <italic>Drosophila</italic></title><author><name sortKey="M Ngale, P Githure" sort="M Ngale, P Githure" uniqKey="M Ngale P" first="P. Githure" last="M Ngale">P. Githure M Ngale</name></author><author><name sortKey="Staveley, Brian E" sort="Staveley, Brian E" uniqKey="Staveley B" first="Brian E." last="Staveley">Brian E. Staveley</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">27672511</idno><idno type="pmc">5028777</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5028777</idno><idno type="RBID">PMC:5028777</idno><idno type="doi">10.7717/peerj.2461</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">000B38</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000B38</idno><idno type="wicri:Area/Pmc/Curation">000B38</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000B38</idno><idno type="wicri:Area/Pmc/Checkpoint">000172</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000172</idno><idno type="wicri:source">PubMed</idno><idno type="wicri:Area/PubMed/Corpus">000152</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000152</idno><idno type="wicri:Area/PubMed/Curation">000152</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000152</idno><idno type="wicri:Area/PubMed/Checkpoint">000152</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000152</idno><idno type="wicri:Area/Ncbi/Merge">002097</idno><idno type="wicri:Area/Ncbi/Curation">002097</idno><idno type="wicri:Area/Ncbi/Checkpoint">002097</idno><idno type="wicri:Area/Main/Merge">000464</idno><idno type="wicri:Area/Main/Curation">000463</idno><idno type="wicri:Area/Main/Exploration">000463</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>Bcl-2</italic> homologue <italic>Debcl</italic> enhances <italic>α-synuclein</italic>-induced phenotypes in <italic>Drosophila</italic></title><author><name sortKey="M Ngale, P Githure" sort="M Ngale, P Githure" uniqKey="M Ngale P" first="P. Githure" last="M Ngale">P. Githure M Ngale</name></author><author><name sortKey="Staveley, Brian E" sort="Staveley, Brian E" uniqKey="Staveley B" first="Brian E." last="Staveley">Brian E. Staveley</name></author></analytic><series><title level="j">PeerJ</title><idno type="eISSN">2167-8359</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Parkinson disease (PD) is a debilitating movement disorder that afflicts 1–2% of the population over 50 years of age. The common hallmark for both sporadic and familial forms of PD is mitochondrial dysfunction. Mammals have at least twenty proapoptotic and antiapoptotic <italic>Bcl-2</italic> family members, in contrast, only two <italic>Bcl-2</italic> family genes have been identified in <italic>Drosophila melanogaster</italic>, the proapoptotic mitochondrial localized <italic>Debcl</italic> and the antiapoptotic <italic>Buffy</italic>. The expression of the human transgene <italic>α-synuclein</italic>, a gene that is strongly associated with inherited forms of PD, in dopaminergic neurons (DA) of Drosophila, results in loss of neurons and locomotor dysfunction to model PD in flies. The altered expression of <italic>Debcl</italic> in the DA neurons and neuron-rich eye and along with the expression of <italic>α-synuclein</italic> offers an opportunity to highlight the role of <italic>Debcl</italic> in mitochondrial-dependent neuronal degeneration and death.</p></sec><sec><title>Results</title><p>The directed overexpression of <italic>Debcl</italic> using the <italic>Ddc-Gal4</italic> transgene in the DA of Drosophila resulted in flies with severely decreased survival and a premature age-dependent loss in climbing ability. The inhibition of <italic>Debcl</italic> resulted in enhanced survival and improved climbing ability whereas the overexpression of <italic>Debcl</italic> in the <italic>α-synuclein</italic>-induced Drosophila model of PD resulted in more severe phenotypes. In addition, the co-expression of <italic>Debcl</italic> along with <italic>Buffy</italic> partially counteracts the <italic>Debcl</italic>-induced phenotypes, to improve the lifespan and the associated loss of locomotor ability observed. In complementary experiments, the overexpression of <italic>Debcl</italic> along with the expression of <italic>α-synuclein</italic> in the eye, enhanced the eye ablation that results from the overexpression of <italic>Debcl</italic>. The co-expression of <italic>Buffy</italic> along with <italic>Debcl</italic> overexpression results in the rescue of the moderate developmental eye defects. The co-expression of <italic>Buffy</italic> along with inhibition of <italic>Debcl</italic> partially restores the eye to a roughened eye phenotype.</p></sec><sec><title>Discussion</title><p>The overexpression of <italic>Debcl</italic> in DA neurons produces flies with shortened lifespan and impaired locomotor ability, phenotypes that are strongly associated with models of PD in Drosophila. The co-expression of <italic>Debcl</italic> along with <italic>α-synuclein</italic> enhanced the PD-like phenotypes. The co-expression of <italic>Debcl</italic> along with <italic>Buffy</italic> suppresses these phenotypes. Complementary experiments in the Drosophila eye show similar trends during development. 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M" uniqKey="Qian Z">Z-M Qian</name></author><author><name sortKey="Ke, Y" uniqKey="Ke Y">Y Ke</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="M Ngale, P Githure" sort="M Ngale, P Githure" uniqKey="M Ngale P" first="P. Githure" last="M Ngale">P. Githure M Ngale</name><name sortKey="Staveley, Brian E" sort="Staveley, Brian E" uniqKey="Staveley B" first="Brian E." last="Staveley">Brian E. Staveley</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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