spargel, the PGC-1α homologue, in models of Parkinson disease in Drosophila melanogaster.
Identifieur interne : 000343 ( PubMed/Checkpoint ); précédent : 000342; suivant : 000344spargel, the PGC-1α homologue, in models of Parkinson disease in Drosophila melanogaster.
Auteurs : Eric M. Merzetti [Canada] ; Brian E. Staveley [Canada]Source :
- BMC neuroscience [ 1471-2202 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Dopaminergic Neurons (metabolism), Drosophila Proteins (genetics), Drosophila Proteins (physiology), Drosophila melanogaster, Locomotion (genetics), Locomotion (physiology), Parkinson Disease (genetics), Positive Transcriptional Elongation Factor B (genetics), Positive Transcriptional Elongation Factor B (physiology).
- MESH :
- chemical , genetics : Drosophila Proteins, Positive Transcriptional Elongation Factor B.
- genetics : Locomotion, Parkinson Disease.
- metabolism : Dopaminergic Neurons.
- chemical , physiology : Drosophila Proteins, Locomotion, Positive Transcriptional Elongation Factor B.
- Animals, Disease Models, Animal, Drosophila melanogaster.
Abstract
Parkinson disease (PD) is a progressive neurodegenerative disorder presenting with symptoms of resting tremor, bradykinesia, rigidity, postural instability and additional severe cognitive impairment over time. These symptoms arise from a decrease of available dopamine in the striatum of the brain resulting from the breakdown and death of dopaminergic (DA) neurons. A process implicated in the destruction of these neurons is mitochondrial breakdown and impairment. Upkeep and repair of mitochondria involves a number of complex and key components including Pink1, Parkin, and the PGC family of genes. PGC-1α has been characterized as a regulator of mitochondria biogenesis, insulin receptor signalling and energy metabolism, mutation of this gene has been linked to early onset forms of PD. The mammalian PGC family consists of three partially redundant genes making the study of full or partial loss of function difficult. The sole Drosophila melanogaster homologue of this gene family, spargel (srl), has been shown to function in similar pathways of mitochondrial upkeep and biogenesis.
DOI: 10.1186/s12868-015-0210-2
PubMed: 26502946
Affiliations:
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Staveley</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Memorial University of Newfoundland, 232 Elizabeth Avenue, St. John's, NL, A1B 3X9, Canada. bestave@mun.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, 232 Elizabeth Avenue, St. John's, NL, A1B 3X9</wicri:regionArea><wicri:noRegion>A1B 3X9</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26502946</idno><idno type="pmid">26502946</idno><idno type="doi">10.1186/s12868-015-0210-2</idno><idno type="wicri:Area/PubMed/Corpus">000382</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000382</idno><idno type="wicri:Area/PubMed/Curation">000382</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000382</idno><idno type="wicri:Area/PubMed/Checkpoint">000382</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000382</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">spargel, the PGC-1α homologue, in models of Parkinson disease in Drosophila melanogaster.</title><author><name sortKey="Merzetti, Eric M" sort="Merzetti, Eric M" uniqKey="Merzetti E" first="Eric M" last="Merzetti">Eric M. Merzetti</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Memorial University of Newfoundland, 232 Elizabeth Avenue, St. John's, NL, A1B 3X9, Canada. emvm45@mun.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, 232 Elizabeth Avenue, St. John's, NL, A1B 3X9</wicri:regionArea><wicri:noRegion>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, 232 Elizabeth Avenue, St. John's, NL, A1B 3X9, Canada. bestave@mun.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biology, Memorial University of Newfoundland, 232 Elizabeth Avenue, St. John's, NL, A1B 3X9</wicri:regionArea><wicri:noRegion>A1B 3X9</wicri:noRegion></affiliation></author></analytic><series><title level="j">BMC neuroscience</title><idno type="eISSN">1471-2202</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Dopaminergic Neurons (metabolism)</term><term>Drosophila Proteins (genetics)</term><term>Drosophila Proteins (physiology)</term><term>Drosophila melanogaster</term><term>Locomotion (genetics)</term><term>Locomotion (physiology)</term><term>Parkinson Disease (genetics)</term><term>Positive Transcriptional Elongation Factor B (genetics)</term><term>Positive Transcriptional Elongation Factor B (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Drosophila Proteins</term><term>Positive Transcriptional Elongation Factor B</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Locomotion</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Drosophila Proteins</term><term>Locomotion</term><term>Positive Transcriptional Elongation Factor B</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Drosophila melanogaster</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson disease (PD) is a progressive neurodegenerative disorder presenting with symptoms of resting tremor, bradykinesia, rigidity, postural instability and additional severe cognitive impairment over time. These symptoms arise from a decrease of available dopamine in the striatum of the brain resulting from the breakdown and death of dopaminergic (DA) neurons. A process implicated in the destruction of these neurons is mitochondrial breakdown and impairment. Upkeep and repair of mitochondria involves a number of complex and key components including Pink1, Parkin, and the PGC family of genes. PGC-1α has been characterized as a regulator of mitochondria biogenesis, insulin receptor signalling and energy metabolism, mutation of this gene has been linked to early onset forms of PD. The mammalian PGC family consists of three partially redundant genes making the study of full or partial loss of function difficult. The sole Drosophila melanogaster homologue of this gene family, spargel (srl), has been shown to function in similar pathways of mitochondrial upkeep and biogenesis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26502946</PMID><DateCreated><Year>2015</Year><Month>10</Month><Day>27</Day></DateCreated><DateCompleted><Year>2016</Year><Month>07</Month><Day>06</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-2202</ISSN><JournalIssue CitedMedium="Internet"><Volume>16</Volume><PubDate><Year>2015</Year><Month>Oct</Month><Day>26</Day></PubDate></JournalIssue><Title>BMC neuroscience</Title><ISOAbbreviation>BMC Neurosci</ISOAbbreviation></Journal><ArticleTitle>spargel, the PGC-1α homologue, in models of Parkinson disease in Drosophila melanogaster.</ArticleTitle><Pagination><MedlinePgn>70</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12868-015-0210-2</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Parkinson disease (PD) is a progressive neurodegenerative disorder presenting with symptoms of resting tremor, bradykinesia, rigidity, postural instability and additional severe cognitive impairment over time. These symptoms arise from a decrease of available dopamine in the striatum of the brain resulting from the breakdown and death of dopaminergic (DA) neurons. A process implicated in the destruction of these neurons is mitochondrial breakdown and impairment. Upkeep and repair of mitochondria involves a number of complex and key components including Pink1, Parkin, and the PGC family of genes. PGC-1α has been characterized as a regulator of mitochondria biogenesis, insulin receptor signalling and energy metabolism, mutation of this gene has been linked to early onset forms of PD. The mammalian PGC family consists of three partially redundant genes making the study of full or partial loss of function difficult. The sole Drosophila melanogaster homologue of this gene family, spargel (srl), has been shown to function in similar pathways of mitochondrial upkeep and biogenesis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Directed expression of srl-RNAi in the D. melanogaster eye causes abnormal ommatidia and bristle formation while eye specific expression of srl-EY does not produce the minor rough eye phenotype associated with high temperature GMR-Gal4 expression. Ddc-Gal4 mediated tissue specific expression of srl transgene constructs in D. melanogaster DA neurons causes altered lifespan and climbing ability. Expression of a srl-RNAi causes an increase in mean lifespan but a decrease in overall loco-motor ability while induced expression of srl-EY causes a severe decrease in mean lifespan and a decrease in loco-motor ability.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The reduced lifespan and climbing ability associated with a tissue specific expression of srl in DA neurons provides a new model of PD in D. melanogaster which may be used to identify novel therapeutic approaches to human disease treatment and prevention.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Merzetti</LastName><ForeName>Eric M</ForeName><Initials>EM</Initials><AffiliationInfo><Affiliation>Department of Biology, Memorial University of Newfoundland, 232 Elizabeth Avenue, St. John's, NL, A1B 3X9, Canada. emvm45@mun.ca.</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, 232 Elizabeth Avenue, St. John's, NL, A1B 3X9, Canada. bestave@mun.ca.</Affiliation></AffiliationInfo></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>2015</Year><Month>10</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Neurosci</MedlineTA><NlmUniqueID>100966986</NlmUniqueID><ISSNLinking>1471-2202</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029721">Drosophila Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C527201">pgc protein, Drosophila</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.-</RegistryNumber><NameOfSubstance UI="D042925">Positive Transcriptional Elongation Factor B</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Nat Commun. 2014;5:3483</RefSource><PMID Version="1">24662282</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 2009 Mar;66(3):352-61</RefSource><PMID Version="1">19273754</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Development. 1993 Jun;118(2):401-15</RefSource><PMID Version="1">8223268</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Geriatr Psychiatry Neurol. 2010 Dec;23(4):228-42</RefSource><PMID Version="1">20938043</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2008 Aug 15;283(33):22464-72</RefSource><PMID 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Merzetti</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)
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