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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson’s disease factors Pink1 and Parkin</title><author><name sortKey="Whitworth, Alexander J" sort="Whitworth, Alexander J" uniqKey="Whitworth A" first="Alexander J." last="Whitworth">Alexander J. Whitworth</name><affiliation><nlm:aff wicri:cut=" and" id="af1-0010168">MRC Centre for Developmental and Biomedical Genetics</nlm:aff></affiliation><affiliation><nlm:aff id="af2-0010168">Department of Biomedical Sciences, University of Sheffield, Sheffield, S10 2TN, UK</nlm:aff></affiliation></author><author><name sortKey="Lee, Jeffrey R" sort="Lee, Jeffrey R" uniqKey="Lee J" first="Jeffrey R." last="Lee">Jeffrey R. Lee</name><affiliation><nlm:aff id="af3-0010168">Department of Biochemistry, University of Toronto, M5S 1A8, Canada</nlm:aff></affiliation></author><author><name sortKey="Ho, Venus M W" sort="Ho, Venus M W" uniqKey="Ho V" first="Venus M.-W." last="Ho">Venus M.-W. Ho</name><affiliation><nlm:aff wicri:cut=" and" id="af1-0010168">MRC Centre for Developmental and Biomedical Genetics</nlm:aff></affiliation><affiliation><nlm:aff id="af2-0010168">Department of Biomedical Sciences, University of Sheffield, Sheffield, S10 2TN, UK</nlm:aff></affiliation></author><author><name sortKey="Flick, Robert" sort="Flick, Robert" uniqKey="Flick R" first="Robert" last="Flick">Robert Flick</name><affiliation><nlm:aff id="af3-0010168">Department of Biochemistry, University of Toronto, M5S 1A8, Canada</nlm:aff></affiliation></author><author><name sortKey="Chowdhury, Ruhena" sort="Chowdhury, Ruhena" uniqKey="Chowdhury R" first="Ruhena" last="Chowdhury">Ruhena Chowdhury</name><affiliation><nlm:aff id="af4-0010168">CRUK, London Institute, Lincoln’s Inn Fields, London, WC2A 3PX, UK</nlm:aff></affiliation></author><author><name sortKey="Mcquibban, G Angus" sort="Mcquibban, G Angus" uniqKey="Mcquibban G" first="G. Angus" last="Mcquibban">G. Angus Mcquibban</name><affiliation><nlm:aff id="af3-0010168">Department of Biochemistry, University of Toronto, M5S 1A8, Canada</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">19048081</idno><idno type="pmc">2562193</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562193</idno><idno type="RBID">PMC:2562193</idno><idno type="doi">10.1242/dmm.000109</idno><date when="2008">2008</date><idno type="wicri:Area/Pmc/Corpus">000531</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000531</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson’s disease factors Pink1 and Parkin</title><author><name sortKey="Whitworth, Alexander J" sort="Whitworth, Alexander J" uniqKey="Whitworth A" first="Alexander J." last="Whitworth">Alexander J. Whitworth</name><affiliation><nlm:aff wicri:cut=" and" id="af1-0010168">MRC Centre for Developmental and Biomedical Genetics</nlm:aff></affiliation><affiliation><nlm:aff id="af2-0010168">Department of Biomedical Sciences, University of Sheffield, Sheffield, S10 2TN, UK</nlm:aff></affiliation></author><author><name sortKey="Lee, Jeffrey R" sort="Lee, Jeffrey R" uniqKey="Lee J" first="Jeffrey R." last="Lee">Jeffrey R. Lee</name><affiliation><nlm:aff id="af3-0010168">Department of Biochemistry, University of Toronto, M5S 1A8, Canada</nlm:aff></affiliation></author><author><name sortKey="Ho, Venus M W" sort="Ho, Venus M W" uniqKey="Ho V" first="Venus M.-W." last="Ho">Venus M.-W. Ho</name><affiliation><nlm:aff wicri:cut=" and" id="af1-0010168">MRC Centre for Developmental and Biomedical Genetics</nlm:aff></affiliation><affiliation><nlm:aff id="af2-0010168">Department of Biomedical Sciences, University of Sheffield, Sheffield, S10 2TN, UK</nlm:aff></affiliation></author><author><name sortKey="Flick, Robert" sort="Flick, Robert" uniqKey="Flick R" first="Robert" last="Flick">Robert Flick</name><affiliation><nlm:aff id="af3-0010168">Department of Biochemistry, University of Toronto, M5S 1A8, Canada</nlm:aff></affiliation></author><author><name sortKey="Chowdhury, Ruhena" sort="Chowdhury, Ruhena" uniqKey="Chowdhury R" first="Ruhena" last="Chowdhury">Ruhena Chowdhury</name><affiliation><nlm:aff id="af4-0010168">CRUK, London Institute, Lincoln’s Inn Fields, London, WC2A 3PX, UK</nlm:aff></affiliation></author><author><name sortKey="Mcquibban, G Angus" sort="Mcquibban, G Angus" uniqKey="Mcquibban G" first="G. Angus" last="Mcquibban">G. Angus Mcquibban</name><affiliation><nlm:aff id="af3-0010168">Department of Biochemistry, University of Toronto, M5S 1A8, Canada</nlm:aff></affiliation></author></analytic><series><title level="j">Disease Models & Mechanisms</title><idno type="ISSN">1754-8403</idno><idno type="eISSN">1754-8411</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>SUMMARY</title><p>Parkinson’s disease (PD) is a common neurodegenerative disorder caused by loss of midbrain dopaminergic neurons, the pathogenetic mechanisms of which remain unclear. Mitochondrial dysfunction, which has long been implicated in sporadic PD, has recently been highlighted as a key pathological cause, particularly with the identification of mutations in the <italic>PTEN-induced putative kinase (pink1)</italic>, <italic>parkin</italic> and <italic>htrA2 (also known as omi)</italic> genes that are linked to PD. Studies in <italic>Drosophila melanogaster</italic> have shown that <italic>pink1</italic> and <italic>parkin</italic> act in a common genetic pathway that maintains mitochondrial integrity, but other upstream or downstream components of this pathway are currently unknown. Using ectopic expression in the Drosophila eye as an assay, we have investigated the involvement of the mitochondrial protease encoded by <italic>omi</italic> in the Pink1/Parkin pathway and found that it acts genetically downstream of <italic>pink1</italic> but functions independently of Parkin. Using the same approach, we also found that Rhomboid-7, a mitochondrial protease not previously implicated in PD, acts as an upstream component of this pathway, and showed that it is required to cleave the precursor forms of both Pink1 and Omi. These data further elucidate the composition of the Pink1 pathway and suggest that regulated intramembrane proteolysis is involved in its regulation.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Dis Model Mech</journal-id><journal-id journal-id-type="hwp">dmm</journal-id><journal-id journal-id-type="publisher-id">DMM</journal-id><journal-title-group><journal-title>Disease Models & Mechanisms</journal-title></journal-title-group><issn pub-type="ppub">1754-8403</issn><issn pub-type="epub">1754-8411</issn><publisher><publisher-name>The Company of Biologists Limited</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">19048081</article-id><article-id pub-id-type="pmc">2562193</article-id><article-id pub-id-type="doi">10.1242/dmm.000109</article-id><article-id pub-id-type="publisher-id">0010168</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Report</subject></subj-group></article-categories><title-group><article-title>Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson’s disease factors Pink1 and Parkin</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Whitworth</surname><given-names>Alexander J.</given-names></name><xref ref-type="aff" rid="af1-0010168">1</xref><xref ref-type="aff" rid="af2-0010168">2</xref><xref ref-type="corresp" rid="c1-0010168">*</xref><xref ref-type="author-notes" rid="fn1-0010168">‡</xref></contrib><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Jeffrey R.</given-names></name><xref ref-type="aff" rid="af3-0010168">3</xref><xref ref-type="author-notes" rid="fn1-0010168">‡</xref></contrib><contrib contrib-type="author"><name><surname>Ho</surname><given-names>Venus M.-W.</given-names></name><xref ref-type="aff" rid="af1-0010168">1</xref><xref ref-type="aff" rid="af2-0010168">2</xref></contrib><contrib contrib-type="author"><name><surname>Flick</surname><given-names>Robert</given-names></name><xref ref-type="aff" rid="af3-0010168">3</xref></contrib><contrib contrib-type="author"><name><surname>Chowdhury</surname><given-names>Ruhena</given-names></name><xref ref-type="aff" rid="af4-0010168">4</xref></contrib><contrib contrib-type="author"><name><surname>McQuibban</surname><given-names>G. Angus</given-names></name><xref ref-type="aff" rid="af3-0010168">3</xref><xref ref-type="corresp" rid="c1-0010168">*</xref></contrib></contrib-group><aff id="af1-0010168"><label>1</label>MRC Centre for Developmental and Biomedical Genetics and</aff><aff id="af2-0010168"><label>2</label>Department of Biomedical Sciences, University of Sheffield, Sheffield, S10 2TN, UK</aff><aff id="af3-0010168"><label>3</label>Department of Biochemistry, University of Toronto, M5S 1A8, Canada</aff><aff id="af4-0010168"><label>4</label>CRUK, London Institute, Lincoln’s Inn Fields, London, WC2A 3PX, UK</aff><author-notes><corresp id="c1-0010168"><label>*</label>Authors for correspondence (e-mail:
<email>a.whitworth@sheffield.ac.uk</email>;
<email>angus.mcquibban@utoronto.ca</email>)</corresp><fn id="fn1-0010168"><label>‡</label><p>These authors contributed equally to this work</p></fn></author-notes><pub-date pub-type="ppub"><season>Sep-Oct</season><year>2008</year></pub-date><pub-date pub-type="epub"><day>18</day><month>9</month><year>2008</year></pub-date><volume>1</volume><issue>2-3</issue><fpage>168</fpage><lpage>174</lpage><history><date date-type="received"><day>17</day><month>11</month><year>2007</year></date><date date-type="accepted"><day>16</day><month>6</month><year>2008</year></date></history><permissions><copyright-year>2008</copyright-year></permissions><self-uri content-type="pdf" xlink:type="simple" xlink:href="168.pdf"></self-uri><related-article related-article-type="article-reference" id="d32e158" vol="1" page="173" issue="2-3" ext-link-type="pmc"></related-article><abstract><title>SUMMARY</title><p>Parkinson’s disease (PD) is a common neurodegenerative disorder caused by loss of midbrain dopaminergic neurons, the pathogenetic mechanisms of which remain unclear. Mitochondrial dysfunction, which has long been implicated in sporadic PD, has recently been highlighted as a key pathological cause, particularly with the identification of mutations in the <italic>PTEN-induced putative kinase (pink1)</italic>, <italic>parkin</italic> and <italic>htrA2 (also known as omi)</italic> genes that are linked to PD. Studies in <italic>Drosophila melanogaster</italic> have shown that <italic>pink1</italic> and <italic>parkin</italic> act in a common genetic pathway that maintains mitochondrial integrity, but other upstream or downstream components of this pathway are currently unknown. Using ectopic expression in the Drosophila eye as an assay, we have investigated the involvement of the mitochondrial protease encoded by <italic>omi</italic> in the Pink1/Parkin pathway and found that it acts genetically downstream of <italic>pink1</italic> but functions independently of Parkin. Using the same approach, we also found that Rhomboid-7, a mitochondrial protease not previously implicated in PD, acts as an upstream component of this pathway, and showed that it is required to cleave the precursor forms of both Pink1 and Omi. These data further elucidate the composition of the Pink1 pathway and suggest that regulated intramembrane proteolysis is involved in its regulation.</p></abstract><custom-meta-group><custom-meta><meta-name>cover-date</meta-name><meta-value>September/October 2008</meta-value></custom-meta><custom-meta><meta-name>access-type</meta-name><meta-value>free</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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