Formation of NPR1 Condensates Promotes Cell Survival during the Plant Immune Response.
Identifieur interne : 000162 ( Main/Exploration ); précédent : 000161; suivant : 000163Formation of NPR1 Condensates Promotes Cell Survival during the Plant Immune Response.
Auteurs : Raul Zavaliev [États-Unis] ; Rajinikanth Mohan [États-Unis] ; Tianyuan Chen [États-Unis] ; Xinnian Dong [États-Unis]Source :
- Cell [ 1097-4172 ] ; 2020.
Abstract
In plants, pathogen effector-triggered immunity (ETI) often leads to programmed cell death, which is restricted by NPR1, an activator of systemic acquired resistance. However, the biochemical activities of NPR1 enabling it to promote defense and restrict cell death remain unclear. Here we show that NPR1 promotes cell survival by targeting substrates for ubiquitination and degradation through formation of salicylic acid-induced NPR1 condensates (SINCs). SINCs are enriched with stress response proteins, including nucleotide-binding leucine-rich repeat immune receptors, oxidative and DNA damage response proteins, and protein quality control machineries. Transition of NPR1 into condensates is required for formation of the NPR1-Cullin 3 E3 ligase complex to ubiquitinate SINC-localized substrates, such as EDS1 and specific WRKY transcription factors, and promote cell survival during ETI. Our analysis of SINCs suggests that NPR1 is centrally integrated into the cell death or survival decisions in plant immunity by modulating multiple stress-responsive processes in this quasi-organelle.
DOI: 10.1016/j.cell.2020.07.016
PubMed: 32810437
PubMed Central: PMC7484032
Affiliations:
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Electronic address: xdong@duke.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Howard Hughes Medical Institute, Duke University, Durham, NC 27708, USA; Department of Biology, Duke University, Durham, NC 27708</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author></analytic><series><title level="j">Cell</title><idno type="eISSN">1097-4172</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">In plants, pathogen effector-triggered immunity (ETI) often leads to programmed cell death, which is restricted by NPR1, an activator of systemic acquired resistance. However, the biochemical activities of NPR1 enabling it to promote defense and restrict cell death remain unclear. Here we show that NPR1 promotes cell survival by targeting substrates for ubiquitination and degradation through formation of salicylic acid-induced NPR1 condensates (SINCs). SINCs are enriched with stress response proteins, including nucleotide-binding leucine-rich repeat immune receptors, oxidative and DNA damage response proteins, and protein quality control machineries. Transition of NPR1 into condensates is required for formation of the NPR1-Cullin 3 E3 ligase complex to ubiquitinate SINC-localized substrates, such as EDS1 and specific WRKY transcription factors, and promote cell survival during ETI. Our analysis of SINCs suggests that NPR1 is centrally integrated into the cell death or survival decisions in plant immunity by modulating multiple stress-responsive processes in this quasi-organelle.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">32810437</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-4172</ISSN><JournalIssue CitedMedium="Internet"><Volume>182</Volume><Issue>5</Issue><PubDate><Year>2020</Year><Month>Sep</Month><Day>03</Day></PubDate></JournalIssue><Title>Cell</Title><ISOAbbreviation>Cell</ISOAbbreviation></Journal><ArticleTitle>Formation of NPR1 Condensates Promotes Cell Survival during the Plant Immune Response.</ArticleTitle><Pagination><MedlinePgn>1093-1108.e18</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0092-8674(20)30881-3</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cell.2020.07.016</ELocationID><Abstract><AbstractText>In plants, pathogen effector-triggered immunity (ETI) often leads to programmed cell death, which is restricted by NPR1, an activator of systemic acquired resistance. However, the biochemical activities of NPR1 enabling it to promote defense and restrict cell death remain unclear. Here we show that NPR1 promotes cell survival by targeting substrates for ubiquitination and degradation through formation of salicylic acid-induced NPR1 condensates (SINCs). SINCs are enriched with stress response proteins, including nucleotide-binding leucine-rich repeat immune receptors, oxidative and DNA damage response proteins, and protein quality control machineries. Transition of NPR1 into condensates is required for formation of the NPR1-Cullin 3 E3 ligase complex to ubiquitinate SINC-localized substrates, such as EDS1 and specific WRKY transcription factors, and promote cell survival during ETI. Our analysis of SINCs suggests that NPR1 is centrally integrated into the cell death or survival decisions in plant immunity by modulating multiple stress-responsive processes in this quasi-organelle.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zavaliev</LastName><ForeName>Raul</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Howard Hughes Medical Institute, Duke University, Durham, NC 27708, USA; Department of Biology, Duke University, Durham, NC 27708, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mohan</LastName><ForeName>Rajinikanth</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Biology, Duke University, Durham, NC 27708, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Tianyuan</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Howard Hughes Medical Institute, Duke University, Durham, NC 27708, USA; Department of Biology, Duke University, Durham, NC 27708, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dong</LastName><ForeName>Xinnian</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Howard Hughes Medical Institute, Duke University, Durham, NC 27708, USA; Department of Biology, Duke University, Durham, NC 27708, USA. Electronic address: xdong@duke.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R35 GM118036</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>08</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cell</MedlineTA><NlmUniqueID>0413066</NlmUniqueID><ISSNLinking>0092-8674</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">NPR1</Keyword><Keyword MajorTopicYN="N">cell survival</Keyword><Keyword MajorTopicYN="N">cullin 3 RING E3 ligase</Keyword><Keyword MajorTopicYN="N">effector-triggered immunity</Keyword><Keyword MajorTopicYN="N">plant immunity</Keyword><Keyword MajorTopicYN="N">protein homeostasis</Keyword><Keyword MajorTopicYN="N">salicylic acid-induced NPR1 condensate (SINC)</Keyword><Keyword MajorTopicYN="N">systemic acquired resistance</Keyword><Keyword MajorTopicYN="N">ubiquitination</Keyword></KeywordList><CoiStatement>Declaration of Interests X.D. is a cofounder of Upstream Biotechnologies and a Scientific Advisory Board member of Inari Agriculture.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>09</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>04</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>07</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2021</Year><Month>09</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>8</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>8</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32810437</ArticleId><ArticleId IdType="pii">S0092-8674(20)30881-3</ArticleId><ArticleId IdType="doi">10.1016/j.cell.2020.07.016</ArticleId><ArticleId IdType="pmc">PMC7484032</ArticleId><ArticleId IdType="mid">NIHMS1613335</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Caroline du Nord</li></region></list><tree><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Zavaliev, Raul" sort="Zavaliev, Raul" uniqKey="Zavaliev R" first="Raul" last="Zavaliev">Raul Zavaliev</name></region><name sortKey="Chen, Tianyuan" sort="Chen, Tianyuan" uniqKey="Chen T" first="Tianyuan" last="Chen">Tianyuan Chen</name><name sortKey="Dong, Xinnian" sort="Dong, Xinnian" uniqKey="Dong X" first="Xinnian" last="Dong">Xinnian Dong</name><name sortKey="Mohan, Rajinikanth" sort="Mohan, Rajinikanth" uniqKey="Mohan R" first="Rajinikanth" last="Mohan">Rajinikanth Mohan</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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