Systematic Surveys of Iron Homeostasis Mechanisms Reveal Ferritin Superfamily and Nucleotide Surveillance Regulation to be Modified by PINK1 Absence.
Identifieur interne : 000028 ( Main/Exploration ); précédent : 000027; suivant : 000029Systematic Surveys of Iron Homeostasis Mechanisms Reveal Ferritin Superfamily and Nucleotide Surveillance Regulation to be Modified by PINK1 Absence.
Auteurs : Jana Key [Allemagne] ; Nesli Ece Sen [Allemagne] ; Aleksandar Arsovi [Allemagne] ; Stella Kr Mer [Allemagne] ; Robert Hülse [Allemagne] ; Natasha Nadeem Khan [Allemagne] ; David Meierhofer [Allemagne] ; Suzana Gispert [Allemagne] ; Gabriele Koepf [Allemagne] ; Georg Auburger [Allemagne]Source :
- Cells [ 2073-4409 ] ; 2020.
Abstract
Iron deprivation activates mitophagy and extends lifespan in nematodes. In patients suffering from Parkinson's disease (PD), PINK1-PRKN mutations via deficient mitophagy trigger iron accumulation and reduce lifespan. To evaluate molecular effects of iron chelator drugs as a potential PD therapy, we assessed fibroblasts by global proteome profiles and targeted transcript analyses. In mouse cells, iron shortage decreased protein abundance for iron-binding nucleotide metabolism enzymes (prominently XDH and ferritin homolog RRM2). It also decreased the expression of factors with a role for nucleotide surveillance, which associate with iron-sulfur-clusters (ISC), and are important for growth and survival. This widespread effect included prominently Nthl1-Ppat-Bdh2, but also mitochondrial Glrx5-Nfu1-Bola1, cytosolic Aco1-Abce1-Tyw5, and nuclear Dna2-Elp3-Pold1-Prim2. Incidentally, upregulated Pink1-Prkn levels explained mitophagy induction, the downregulated expression of Slc25a28 suggested it to function in iron export. The impact of PINK1 mutations in mouse and patient cells was pronounced only after iron overload, causing hyperreactive expression of ribosomal surveillance factor Abce1 and of ferritin, despite ferritin translation being repressed by IRP1. This misregulation might be explained by the deficiency of the ISC-biogenesis factor GLRX5. Our systematic survey suggests mitochondrial ISC-biogenesis and post-transcriptional iron regulation to be important in the decision, whether organisms undergo PD pathogenesis or healthy aging.
DOI: 10.3390/cells9102229
PubMed: 33023155
PubMed Central: PMC7650593
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Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation><affiliation wicri:level="3"><nlm:affiliation>Faculty of Biosciences, Goethe-University, Altenhöferallee 1, 60438 Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Faculty of Biosciences, Goethe-University, Altenhöferallee 1, 60438 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author><author><name sortKey="Sen, Nesli Ece" sort="Sen, Nesli Ece" 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nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author><author><name sortKey="Arsovi, Aleksandar" sort="Arsovi, Aleksandar" uniqKey="Arsovi A" first="Aleksandar" last="Arsovi">Aleksandar Arsovi</name><affiliation wicri:level="3"><nlm:affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author><author><name sortKey="Kr Mer, Stella" sort="Kr Mer, Stella" uniqKey="Kr Mer S" first="Stella" last="Kr Mer">Stella Kr Mer</name><affiliation wicri:level="3"><nlm:affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author><author><name sortKey="Hulse, Robert" sort="Hulse, Robert" uniqKey="Hulse R" first="Robert" last="Hülse">Robert Hülse</name><affiliation wicri:level="3"><nlm:affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author><author><name sortKey="Khan, Natasha Nadeem" sort="Khan, Natasha Nadeem" uniqKey="Khan N" first="Natasha Nadeem" last="Khan">Natasha Nadeem Khan</name><affiliation wicri:level="3"><nlm:affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author><author><name sortKey="Meierhofer, David" sort="Meierhofer, David" uniqKey="Meierhofer D" first="David" last="Meierhofer">David Meierhofer</name><affiliation wicri:level="3"><nlm:affiliation>Max Planck Institute for Molecular Genetics, Ihnestraße 63-73, 14195 Berlin, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Max Planck Institute for Molecular Genetics, Ihnestraße 63-73, 14195 Berlin</wicri:regionArea><placeName><region type="land" nuts="3">Berlin</region><settlement type="city">Berlin</settlement></placeName></affiliation></author><author><name sortKey="Gispert, Suzana" sort="Gispert, Suzana" uniqKey="Gispert S" first="Suzana" last="Gispert">Suzana Gispert</name><affiliation wicri:level="3"><nlm:affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author><author><name sortKey="Koepf, Gabriele" sort="Koepf, Gabriele" uniqKey="Koepf G" first="Gabriele" last="Koepf">Gabriele Koepf</name><affiliation wicri:level="3"><nlm:affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author><author><name sortKey="Auburger, Georg" sort="Auburger, Georg" uniqKey="Auburger G" first="Georg" last="Auburger">Georg Auburger</name><affiliation wicri:level="3"><nlm:affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName></affiliation></author></analytic><series><title level="j">Cells</title><idno type="eISSN">2073-4409</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Iron deprivation activates mitophagy and extends lifespan in nematodes. In patients suffering from Parkinson's disease (PD), PINK1-PRKN mutations via deficient mitophagy trigger iron accumulation and reduce lifespan. To evaluate molecular effects of iron chelator drugs as a potential PD therapy, we assessed fibroblasts by global proteome profiles and targeted transcript analyses. In mouse cells, iron shortage decreased protein abundance for iron-binding nucleotide metabolism enzymes (prominently XDH and ferritin homolog RRM2). It also decreased the expression of factors with a role for nucleotide surveillance, which associate with iron-sulfur-clusters (ISC), and are important for growth and survival. This widespread effect included prominently <i>Nthl1-Ppat-Bdh2</i>, but also mitochondrial <i>Glrx5</i>-<i>Nfu1</i>-<i>Bola1</i>, cytosolic <i>Aco1-Abce1-Tyw5</i>, and nuclear <i>Dna2</i>-<i>Elp3</i>-<i>Pold1</i>-<i>Prim2</i>. Incidentally, upregulated <i>Pink1</i>-<i>Prkn</i> levels explained mitophagy induction, the downregulated expression of <i>Slc25a28</i> suggested it to function in iron export. The impact of PINK1 mutations in mouse and patient cells was pronounced only after iron overload, causing hyperreactive expression of ribosomal surveillance factor <i>Abce1</i> and of ferritin, despite ferritin translation being repressed by IRP1. This misregulation might be explained by the deficiency of the ISC-biogenesis factor GLRX5. Our systematic survey suggests mitochondrial ISC-biogenesis and post-transcriptional iron regulation to be important in the decision, whether organisms undergo PD pathogenesis or healthy aging.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">33023155</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>10</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2073-4409</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>10</Issue><PubDate><Year>2020</Year><Month>Oct</Month><Day>02</Day></PubDate></JournalIssue><Title>Cells</Title><ISOAbbreviation>Cells</ISOAbbreviation></Journal><ArticleTitle>Systematic Surveys of Iron Homeostasis Mechanisms Reveal Ferritin Superfamily and Nucleotide Surveillance Regulation to be Modified by PINK1 Absence.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E2229</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/cells9102229</ELocationID><Abstract><AbstractText>Iron deprivation activates mitophagy and extends lifespan in nematodes. In patients suffering from Parkinson's disease (PD), PINK1-PRKN mutations via deficient mitophagy trigger iron accumulation and reduce lifespan. To evaluate molecular effects of iron chelator drugs as a potential PD therapy, we assessed fibroblasts by global proteome profiles and targeted transcript analyses. In mouse cells, iron shortage decreased protein abundance for iron-binding nucleotide metabolism enzymes (prominently XDH and ferritin homolog RRM2). It also decreased the expression of factors with a role for nucleotide surveillance, which associate with iron-sulfur-clusters (ISC), and are important for growth and survival. This widespread effect included prominently <i>Nthl1-Ppat-Bdh2</i>, but also mitochondrial <i>Glrx5</i>-<i>Nfu1</i>-<i>Bola1</i>, cytosolic <i>Aco1-Abce1-Tyw5</i>, and nuclear <i>Dna2</i>-<i>Elp3</i>-<i>Pold1</i>-<i>Prim2</i>. Incidentally, upregulated <i>Pink1</i>-<i>Prkn</i> levels explained mitophagy induction, the downregulated expression of <i>Slc25a28</i> suggested it to function in iron export. The impact of PINK1 mutations in mouse and patient cells was pronounced only after iron overload, causing hyperreactive expression of ribosomal surveillance factor <i>Abce1</i> and of ferritin, despite ferritin translation being repressed by IRP1. This misregulation might be explained by the deficiency of the ISC-biogenesis factor GLRX5. Our systematic survey suggests mitochondrial ISC-biogenesis and post-transcriptional iron regulation to be important in the decision, whether organisms undergo PD pathogenesis or healthy aging.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Key</LastName><ForeName>Jana</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Faculty of Biosciences, Goethe-University, Altenhöferallee 1, 60438 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sen</LastName><ForeName>Nesli Ece</ForeName><Initials>NE</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Faculty of Biosciences, Goethe-University, Altenhöferallee 1, 60438 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arsović</LastName><ForeName>Aleksandar</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krämer</LastName><ForeName>Stella</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hülse</LastName><ForeName>Robert</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khan</LastName><ForeName>Natasha Nadeem</ForeName><Initials>NN</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meierhofer</LastName><ForeName>David</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0002-0170-868X</Identifier><AffiliationInfo><Affiliation>Max Planck Institute for Molecular Genetics, Ihnestraße 63-73, 14195 Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gispert</LastName><ForeName>Suzana</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koepf</LastName><ForeName>Gabriele</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Auburger</LastName><ForeName>Georg</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Experimental Neurology, Medical School, Goethe University, 60590 Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>01GS08138</GrantID><Agency>German Federal Ministry of Education</Agency><Country></Country></Grant><Grant><GrantID>PTJ 0315584A</GrantID><Agency>GerontoMitoSys network</Agency><Country></Country></Grant><Grant><GrantID>DLR 01EW1012</GrantID><Agency>European Union</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>10</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Cells</MedlineTA><NlmUniqueID>101600052</NlmUniqueID><ISSNLinking>2073-4409</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">CPT1A</Keyword><Keyword MajorTopicYN="N">Cyp46a1</Keyword><Keyword MajorTopicYN="N">Hmox1</Keyword><Keyword MajorTopicYN="N">Ireb2</Keyword><Keyword MajorTopicYN="N">MMP14</Keyword><Keyword MajorTopicYN="N">PYGL</Keyword><Keyword MajorTopicYN="N">Pgrmc1</Keyword><Keyword MajorTopicYN="N">Slc11a2</Keyword><Keyword MajorTopicYN="N">Slc25a37</Keyword><Keyword MajorTopicYN="N">Tfrc</Keyword><Keyword MajorTopicYN="N">iron overload versus deprivation</Keyword><Keyword MajorTopicYN="N">neurodegeneration</Keyword><Keyword MajorTopicYN="N">nucleotide metabolism</Keyword><Keyword 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Aleksandar" uniqKey="Arsovi A" first="Aleksandar" last="Arsovi">Aleksandar Arsovi</name><name sortKey="Auburger, Georg" sort="Auburger, Georg" uniqKey="Auburger G" first="Georg" last="Auburger">Georg Auburger</name><name sortKey="Gispert, Suzana" sort="Gispert, Suzana" uniqKey="Gispert S" first="Suzana" last="Gispert">Suzana Gispert</name><name sortKey="Hulse, Robert" sort="Hulse, Robert" uniqKey="Hulse R" first="Robert" last="Hülse">Robert Hülse</name><name sortKey="Key, Jana" sort="Key, Jana" uniqKey="Key J" first="Jana" last="Key">Jana Key</name><name sortKey="Khan, Natasha Nadeem" sort="Khan, Natasha Nadeem" uniqKey="Khan N" first="Natasha Nadeem" last="Khan">Natasha Nadeem Khan</name><name sortKey="Koepf, Gabriele" sort="Koepf, Gabriele" uniqKey="Koepf G" first="Gabriele" last="Koepf">Gabriele Koepf</name><name sortKey="Kr Mer, Stella" sort="Kr Mer, Stella" uniqKey="Kr Mer S" first="Stella" last="Kr Mer">Stella Kr Mer</name><name sortKey="Meierhofer, David" sort="Meierhofer, David" uniqKey="Meierhofer D" first="David" last="Meierhofer">David Meierhofer</name><name sortKey="Sen, Nesli Ece" sort="Sen, Nesli Ece" uniqKey="Sen N" first="Nesli Ece" last="Sen">Nesli Ece Sen</name><name sortKey="Sen, Nesli Ece" sort="Sen, Nesli Ece" uniqKey="Sen N" first="Nesli Ece" last="Sen">Nesli Ece Sen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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