Bax-inhibitor-1 knockdown phenotypes are suppressed by Buffy and exacerbate degeneration in a Drosophila model of Parkinson disease.
Identifieur interne : 000100 ( PubMed/Checkpoint ); précédent : 000099; suivant : 000101Bax-inhibitor-1 knockdown phenotypes are suppressed by Buffy and exacerbate degeneration in a Drosophila model of Parkinson disease.
Auteurs : P Githure M'Angale [Canada] ; Brian E. Staveley [Canada]Source :
- PeerJ ; 2017.
Abstract
Bax inhibitor-1 (BI-1) is an evolutionarily conserved cytoprotective transmembrane protein that acts as a suppressor of Bax-induced apoptosis by regulation of endoplasmic reticulum stress-induced cell death. We knocked down BI-1 in the sensitive dopa decarboxylase (Ddc) expressing neurons of Drosophila melanogaster to investigate its neuroprotective functions. We additionally sought to rescue the BI-1-induced phenotypes by co-expression with the pro-survival Buffy and determined the effect of BI-1 knockdown on the neurodegenerative α-synuclein-induced Parkinson disease (PD) model.
DOI: 10.7717/peerj.2974
PubMed: 28243526
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Bax-inhibitor-1 knockdown phenotypes are suppressed by Buffy and exacerbate degeneration in a Drosophila model of Parkinson disease.</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 , Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland , St. John's, NL </wicri:regionArea><wicri:noRegion>NL </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 , Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland , St. John's, NL </wicri:regionArea><wicri:noRegion>NL </wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28243526</idno><idno type="pmid">28243526</idno><idno type="doi">10.7717/peerj.2974</idno><idno type="wicri:Area/PubMed/Corpus">000057</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000057</idno><idno type="wicri:Area/PubMed/Curation">000057</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000057</idno><idno type="wicri:Area/PubMed/Checkpoint">000057</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000057</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Bax-inhibitor-1 knockdown phenotypes are suppressed by Buffy and exacerbate degeneration in a Drosophila model of Parkinson disease.</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 , Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland , St. John's, NL </wicri:regionArea><wicri:noRegion>NL </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 , Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland , St. John's, NL </wicri:regionArea><wicri:noRegion>NL </wicri:noRegion></affiliation></author></analytic><series><title level="j">PeerJ</title><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Bax inhibitor-1 (BI-1) is an evolutionarily conserved cytoprotective transmembrane protein that acts as a suppressor of Bax-induced apoptosis by regulation of endoplasmic reticulum stress-induced cell death. We knocked down BI-1 in the sensitive dopa decarboxylase (Ddc) expressing neurons of Drosophila melanogaster to investigate its neuroprotective functions. We additionally sought to rescue the BI-1-induced phenotypes by co-expression with the pro-survival Buffy and determined the effect of BI-1 knockdown on the neurodegenerative α-synuclein-induced Parkinson disease (PD) model.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">28243526</PMID><DateCreated><Year>2017</Year><Month>02</Month><Day>28</Day></DateCreated><DateRevised><Year>2017</Year><Month>03</Month><Day>03</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><JournalIssue CitedMedium="Print"><Volume>5</Volume><PubDate><Year>2017</Year></PubDate></JournalIssue><Title>PeerJ</Title><ISOAbbreviation>PeerJ</ISOAbbreviation></Journal><ArticleTitle>Bax-inhibitor-1 knockdown phenotypes are suppressed by Buffy and exacerbate degeneration in a Drosophila model of Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>e2974</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.7717/peerj.2974</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Bax inhibitor-1 (BI-1) is an evolutionarily conserved cytoprotective transmembrane protein that acts as a suppressor of Bax-induced apoptosis by regulation of endoplasmic reticulum stress-induced cell death. We knocked down BI-1 in the sensitive dopa decarboxylase (Ddc) expressing neurons of Drosophila melanogaster to investigate its neuroprotective functions. We additionally sought to rescue the BI-1-induced phenotypes by co-expression with the pro-survival Buffy and determined the effect of BI-1 knockdown on the neurodegenerative α-synuclein-induced Parkinson disease (PD) model.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We used organismal assays to assess longevity of the flies to determine the effect of the altered expression of BI-1 in the Ddc-Gal4-expressing neurons by employing two RNAi transgenic fly lines. We measured the locomotor ability of these RNAi lines by computing the climbing indices of the climbing ability and compared them to a control line that expresses the lacZ transgene. Finally, we performed biometric analysis of the developing eye, where we counted the number of ommatidia and calculated the area of ommatidial disruption.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The knockdown of BI-1 in these neurons was achieved under the direction of the Ddc-Gal4 transgene and resulted in shortened lifespan and precocious loss of locomotor ability. The co-expression of Buffy, the Drosophila anti-apoptotic Bcl-2 homologue, with BI-1-RNAi resulted in suppression of the reduced lifespan and impaired climbing ability. Expression of human α-synuclein in Drosophila dopaminergic neurons results in neuronal degeneration, accompanied by the age-dependent loss in climbing ability. We exploited this neurotoxic system to investigate possible BI-1 neuroprotective function. The co-expression of α-synuclein with BI-1-RNAi results in a slight decrease in lifespan coupled with an impairment in climbing ability. In supportive experiments, we employed the neuron-rich Drosophila compound eye to investigate subtle phenotypes that result from altered gene expression. The knockdown of BI-1 in the Drosophila developing eye under the direction of the GMR-Gal4 transgene results in reduced ommatidia number and increased disruption of the ommatidial array. Similarly, the co-expression of BI-1-RNAi with Buffy results in the suppression of the eye phenotypes. The expression of α-synuclein along with the knockdown of BI-1 resulted in reduction of ommatidia number and more disruption of the ommatidial array.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Knockdown of BI-1 in the dopaminergic neurons of Drosophila results in a shortened lifespan and premature loss in climbing ability, phenotypes that appear to be strongly associated with models of PD in Drosophila, and which are suppressed upon overexpression of Buffy and worsened by co-expression with α-synuclein. This suggests that BI-1 is neuroprotective and its knockdown can be counteracted by the overexpression of the pro-survival Bcl-2 homologue.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>M'Angale</LastName><ForeName>P Githure</ForeName><Initials>PG</Initials><Identifier Source="ORCID">0000-0002-5044-6196</Identifier><AffiliationInfo><Affiliation>Department of Biology, Memorial University of Newfoundland , St. John's, NL , 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 , Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PeerJ</MedlineTA><NlmUniqueID>101603425</NlmUniqueID></MedlineJournalInfo><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Curr Biol. 2000 May 4;10(9):547-50</RefSource><PMID Version="1">10801447</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2000 Sep 1;275(35):27303-6</RefSource><PMID Version="1">10811653</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell. 2009 Mar 27;33(6):679-91</RefSource><PMID Version="1">19328063</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucleic Acids Res. 2010 Jul;38(Web Server issue):W695-9</RefSource><PMID Version="1">20439314</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Syst Biol. 2011 Oct 11;7:539</RefSource><PMID Version="1">21988835</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell. 1998 Feb;1(3):337-46</RefSource><PMID Version="1">9660918</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>BMC Bioinformatics. 2009 Sep 01;10:274</RefSource><PMID Version="1">19723330</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Death Differ. 2016 Feb;23 (2):358-68</RefSource><PMID Version="1">26470731</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Development. 1993 Jun;118(2):401-15</RefSource><PMID Version="1">8223268</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2012 Apr;1823(4):876-88</RefSource><PMID Version="1">22309999</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Protoc. 2015 Jun;10(6):845-58</RefSource><PMID Version="1">25950237</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2016 Apr;1862(4):518-25</RefSource><PMID Version="1">26769358</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cell Sci. 2009 Apr 15;122(Pt 8):1126-33</RefSource><PMID Version="1">19339548</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genome. 2017 Jan;60(1):1-7</RefSource><PMID Version="1">27848260</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Calcium. 2011 Sep;50(3):251-60</RefSource><PMID Version="1">21663964</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Apoptosis. 2009 Nov;14(11):1255-65</RefSource><PMID Version="1">19784873</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>EMBO J. 2003 Jul 15;22(14):3568-79</RefSource><PMID Version="1">12853472</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genome. 1990 Dec;33(6):867-72</RefSource><PMID Version="1">1964925</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2002 Feb 1;295(5556):865-8</RefSource><PMID Version="1">11823645</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Mol Med. 2014;14(5):603-15</RefSource><PMID Version="1">24894176</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Apoptosis. 2004 May;9(3):299-307</RefSource><PMID Version="1">15258461</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucleic Acids Res. 2015 Jan;43(Database issue):D222-6</RefSource><PMID Version="1">25414356</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2008 Apr 25;283(17):11477-84</RefSource><PMID Version="1">18299329</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2015 Sep 11;10(9):e0137432</RefSource><PMID Version="1">26361355</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>EMBO J. 2011 Sep 16;30(21):4465-78</RefSource><PMID Version="1">21926971</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>BMC Biol. 2012 Jul 24;10:63</RefSource><PMID Version="1">22824239</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Oncogene. 2011 May 26;30(21):2391-400</RefSource><PMID Version="1">21297665</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Methods. 2012 Jul;9(7):671-5</RefSource><PMID Version="1">22930834</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Death Dis. 2012 Aug 09;3:e367</RefSource><PMID Version="1">22875004</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2007 Jul 27;282(30):21618-28</RefSource><PMID Version="1">17526500</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>BMC Neurosci. 2016 May 18;17(1):24</RefSource><PMID Version="1">27192974</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Cycle. 2014;13(24):3903-8</RefSource><PMID Version="1">25483063</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Gene. 2003 Dec 24;323:101-13</RefSource><PMID Version="1">14659883</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):662-7</RefSource><PMID Version="1">10639136</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Death Dis. 2014 Sep 04;5:e1405</RefSource><PMID Version="1">25188515</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res. 2011 Jul 27;1403:19-27</RefSource><PMID Version="1">21718971</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell. 2004 Aug 13;15(3):355-66</RefSource><PMID Version="1">15304216</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Mol Neurosci. 2006;29(1):1-8</RefSource><PMID Version="1">16757804</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurosci. 2007 Dec;26(11):3104-12</RefSource><PMID Version="1">18005066</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2012 Dec;1823(12):2190-200</RefSource><PMID Version="1">22906541</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2012 May 4;287(19):15896-905</RefSource><PMID Version="1">22418439</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Int J Biochem Cell Biol. 2012 Apr;44(4):600-11</RefSource><PMID Version="1">22230367</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Protein Eng Des Sel. 2004 Jun;17(6):527-36</RefSource><PMID Version="1">15314210</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genomics. 1995 Jul 20;28(2):301-4</RefSource><PMID Version="1">8530040</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genesis. 2007 Apr;45(4):184-93</RefSource><PMID Version="1">17417787</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucleic Acids Res. 2014 Jan;42(Database issue):D259-66</RefSource><PMID Version="1">24214962</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucleic Acids Res. 2016 Jan 4;44(D1):D294-300</RefSource><PMID Version="1">26615199</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2000 Mar 23;404(6776):394-8</RefSource><PMID Version="1">10746727</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2010 Dec 17;486(3):235-9</RefSource><PMID Version="1">20887775</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Biol. 2000 Feb 24;10(4):211-4</RefSource><PMID Version="1">10704417</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PeerJ. 2016 Sep 15;4:e2461</RefSource><PMID Version="1">27672511</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuromolecular Med. 2009;11(4):268-80</RefSource><PMID Version="1">19855946</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res. 2011 Jan 25;1370:227-37</RefSource><PMID Version="1">21075086</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genet Mol Res. 2003 Mar 31;2(1):43-7</RefSource><PMID Version="1">12917801</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Mol Med. 2008 Mar;8(2):148-56</RefSource><PMID Version="1">18336295</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2007 Jul 12;448(7150):151-6</RefSource><PMID Version="1">17625558</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell. 1996 Nov 15;87(4):651-60</RefSource><PMID Version="1">8929534</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cell Biol. 2000 Feb 21;148(4):703-14</RefSource><PMID Version="1">10684252</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Cell Biol. 2015 Aug;93(4):351-8</RefSource><PMID Version="1">26008822</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucleic Acids Res. 2012 Jul;40(Web Server issue):W597-603</RefSource><PMID Version="1">22661580</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genet Mol Res. 2016 Oct 24;15(4):</RefSource><PMID Version="1">27813607</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Development. 2011 Jan;138(2):327-38</RefSource><PMID Version="1">21177345</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucleic Acids Res. 2016 Jan 4;44(D1):D786-92</RefSource><PMID Version="1">26467478</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Oncogene. 2015 Jan 15;34(3):269-80</RefSource><PMID Version="1">24561528</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genet Mol Res. 2012 May 21;11(2):1497-502</RefSource><PMID Version="1">22653599</PMID></CommentsCorrections></CommentsCorrectionsList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Bax inhibitor-1</Keyword><Keyword MajorTopicYN="N">Buffy</Keyword><Keyword MajorTopicYN="N">Drosophila melanogaster</Keyword><Keyword MajorTopicYN="N">Model of Parkinson disease</Keyword><Keyword MajorTopicYN="N">α-synuclein</Keyword></KeywordList><CoiStatement>The authors declare that they have no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>10</Month><Day>21</Day></PubMedPubDate><PubMedPubDate 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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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