Alteration of iron responsive gene expression in Arabidopsis glutaredoxin S17 loss of function plants with or without iron stress.
Identifieur interne : 000091 ( Main/Exploration ); précédent : 000090; suivant : 000092Alteration of iron responsive gene expression in Arabidopsis glutaredoxin S17 loss of function plants with or without iron stress.
Auteurs : Ninghui Cheng [États-Unis] ; Han Yu [États-Unis] ; Xiaolan Rao [États-Unis] ; Sunghun Park [États-Unis] ; Erin L. Connolly [États-Unis] ; Kendal D. Hirschi [États-Unis] ; Paul A. Nakata [États-Unis]Source :
- Plant signaling & behavior [ 1559-2324 ] ; 2020.
Abstract
Iron (Fe) is a mineral nutrient and a metal cofactor essential for plants. Iron limitation can have detrimental effects on plant growth and development, while excess iron inside plant cells leads to oxidative damage. As a result, plants have evolved complex regulatory networks to respond to fluctuations in cellular iron concentrations. The mechanisms that regulate these responses however, are not fully understood. Heterologous expression of an Arabidopsis thaliana monothiol glutaredoxin S17 (GRXS17) suppresses the over-accumulation of iron in the Saccharomyces cerevisiae Grx3/Grx4 mutant and disruption of GRXS17 causes plant sensitivity to exogenous oxidants and iron deficiency stress. GRXS17 may act as an important regulator in the plant's ability to respond to iron deficiency stress and maintain redox homeostasis. Here, we extend this investigation by analyzing iron-responsive gene expression of the Fer-like iron deficiency-induced transcription factor (FIT) network (FIT, IRT1, FRO1, and FRO2) and the bHLH transcription factor POPEYE (PYE) network (PYE, ZIF1, FRO3, NAS4, and BTS) in GRXS17 KO plants and wildtype controls grown under iron sufficiency and deficiency conditions. Our findings suggest that GRXS17 is required for tolerance to iron deficiency, and plays a negative regulatory role under conditions of iron sufficiency.
DOI: 10.1080/15592324.2020.1758455
PubMed: 32351167
Affiliations:
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Hirschi</name><affiliation wicri:level="2"><nlm:affiliation>USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine , Houston, TX, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine , Houston, TX</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Nakata, Paul A" sort="Nakata, Paul A" uniqKey="Nakata P" first="Paul A" last="Nakata">Paul A. Nakata</name><affiliation wicri:level="2"><nlm:affiliation>USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine , Houston, TX, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine , Houston, TX</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author></analytic><series><title level="j">Plant signaling & behavior</title><idno type="eISSN">1559-2324</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 (Fe) is a mineral nutrient and a metal cofactor essential for plants. Iron limitation can have detrimental effects on plant growth and development, while excess iron inside plant cells leads to oxidative damage. As a result, plants have evolved complex regulatory networks to respond to fluctuations in cellular iron concentrations. The mechanisms that regulate these responses however, are not fully understood. Heterologous expression of an <i>Arabidopsis thaliana</i> monothiol glutaredoxin S17 (GRXS17) suppresses the over-accumulation of iron in the <i>Saccharomyces cerevisiae</i> Grx3/Grx4 mutant and disruption of <i>GRXS17</i> causes plant sensitivity to exogenous oxidants and iron deficiency stress. GRXS17 may act as an important regulator in the plant's ability to respond to iron deficiency stress and maintain redox homeostasis. Here, we extend this investigation by analyzing iron-responsive gene expression of the Fer-like iron deficiency-induced transcription factor (FIT) network (<i>FIT, IRT1, FRO1</i>, and <i>FRO2</i>) and the bHLH transcription factor POPEYE (PYE) network (<i>PYE, ZIF1, FRO3, NAS4</i>, and <i>BTS</i>) in <i>GRXS17</i> KO plants and wildtype controls grown under iron sufficiency and deficiency conditions. Our findings suggest that GRXS17 is required for tolerance to iron deficiency, and plays a negative regulatory role under conditions of iron sufficiency.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32351167</PMID><DateRevised><Year>2020</Year><Month>07</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1559-2324</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>6</Issue><PubDate><Year>2020</Year><Month>06</Month><Day>02</Day></PubDate></JournalIssue><Title>Plant signaling & behavior</Title><ISOAbbreviation>Plant Signal Behav</ISOAbbreviation></Journal><ArticleTitle>Alteration of iron responsive gene expression in Arabidopsis glutaredoxin <i>S17</i> loss of function plants with or without iron stress.</ArticleTitle><Pagination><MedlinePgn>1758455</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/15592324.2020.1758455</ELocationID><Abstract><AbstractText>Iron (Fe) is a mineral nutrient and a metal cofactor essential for plants. Iron limitation can have detrimental effects on plant growth and development, while excess iron inside plant cells leads to oxidative damage. As a result, plants have evolved complex regulatory networks to respond to fluctuations in cellular iron concentrations. The mechanisms that regulate these responses however, are not fully understood. Heterologous expression of an <i>Arabidopsis thaliana</i> monothiol glutaredoxin S17 (GRXS17) suppresses the over-accumulation of iron in the <i>Saccharomyces cerevisiae</i> Grx3/Grx4 mutant and disruption of <i>GRXS17</i> causes plant sensitivity to exogenous oxidants and iron deficiency stress. GRXS17 may act as an important regulator in the plant's ability to respond to iron deficiency stress and maintain redox homeostasis. Here, we extend this investigation by analyzing iron-responsive gene expression of the Fer-like iron deficiency-induced transcription factor (FIT) network (<i>FIT, IRT1, FRO1</i>, and <i>FRO2</i>) and the bHLH transcription factor POPEYE (PYE) network (<i>PYE, ZIF1, FRO3, NAS4</i>, and <i>BTS</i>) in <i>GRXS17</i> KO plants and wildtype controls grown under iron sufficiency and deficiency conditions. Our findings suggest that GRXS17 is required for tolerance to iron deficiency, and plays a negative regulatory role under conditions of iron sufficiency.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Ninghui</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine , Houston, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Han</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine , Houston, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rao</LastName><ForeName>Xiaolan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>BioDiscovery Institute and Department of Biological Sciences, College of Sciences, University of North Texas , Denton, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Sunghun</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Horticulture and Natural Resources, Kansas State University , Manhattan, KS, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Connolly</LastName><ForeName>Erin L</ForeName><Initials>EL</Initials><Identifier Source="ORCID">0000-0002-8032-8182</Identifier><AffiliationInfo><Affiliation>Department of Plant Science, Penn State University, State College , PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hirschi</LastName><ForeName>Kendal D</ForeName><Initials>KD</Initials><AffiliationInfo><Affiliation>USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine , Houston, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakata</LastName><ForeName>Paul A</ForeName><Initials>PA</Initials><Identifier Source="ORCID">0000-0002-6331-9700</Identifier><AffiliationInfo><Affiliation>USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine , Houston, TX, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>04</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Plant Signal Behav</MedlineTA><NlmUniqueID>101291431</NlmUniqueID><ISSNLinking>1559-2316</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">glutaredoxin</Keyword><Keyword MajorTopicYN="Y">iron acquisition</Keyword><Keyword MajorTopicYN="Y">iron homeostasis</Keyword><Keyword MajorTopicYN="Y">redox</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>5</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>5</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>5</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32351167</ArticleId><ArticleId IdType="doi">10.1080/15592324.2020.1758455</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Kansas</li><li>Pennsylvanie</li><li>Texas</li></region></list><tree><country name="États-Unis"><region name="Texas"><name sortKey="Cheng, Ninghui" sort="Cheng, Ninghui" uniqKey="Cheng N" first="Ninghui" last="Cheng">Ninghui Cheng</name></region><name sortKey="Connolly, Erin L" sort="Connolly, Erin L" uniqKey="Connolly E" first="Erin L" last="Connolly">Erin L. Connolly</name><name sortKey="Hirschi, Kendal D" sort="Hirschi, Kendal D" uniqKey="Hirschi K" first="Kendal D" last="Hirschi">Kendal D. Hirschi</name><name sortKey="Nakata, Paul A" sort="Nakata, Paul A" uniqKey="Nakata P" first="Paul A" last="Nakata">Paul A. Nakata</name><name sortKey="Park, Sunghun" sort="Park, Sunghun" uniqKey="Park S" first="Sunghun" last="Park">Sunghun Park</name><name sortKey="Rao, Xiaolan" sort="Rao, Xiaolan" uniqKey="Rao X" first="Xiaolan" last="Rao">Xiaolan Rao</name><name sortKey="Yu, Han" sort="Yu, Han" uniqKey="Yu H" first="Han" last="Yu">Han Yu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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