Tomato Atypical Receptor Kinase1 Is Involved in the Regulation of Preinvasion Defense.
Identifieur interne : 000016 ( Main/Exploration ); précédent : 000015; suivant : 000017Tomato Atypical Receptor Kinase1 Is Involved in the Regulation of Preinvasion Defense.
Auteurs : Andrew R. Guzman [États-Unis] ; Jung-Gun Kim [États-Unis] ; Kyle W. Taylor [États-Unis] ; Daniel Lanver [États-Unis] ; Mary Beth Mudgett [États-Unis]Source :
- Plant physiology [ 1532-2548 ] ; 2020.
Abstract
Tomato Atypical Receptor Kinase 1 (TARK1) is a pseudokinase required for postinvasion immunity. TARK1 was originally identified as a target of the Xanthomonas euvesicatoria effector protein Xanthomonas outer protein N (XopN), a suppressor of early defense signaling. How TARK1 participates in immune signal transduction is not well understood. To gain insight into TARK1's role in tomato (Solanum lycopersicum) immunity, we used a proteomics approach to isolate and identify TARK1-associated immune complexes formed during infection. We found that TARK1 interacts with proteins predicted to be associated with stomatal movement. TARK1 CRISPR mutants and overexpression (OE) lines did not display differences in light-induced stomatal opening or abscisic acid-induced stomatal closure; however, they did show altered stomatal movement responses to bacteria and biotic elicitors. Notably, we found that TARK1 CRISPR plants were resistant to Pseudomonas syringae pathovar tomato strain DC3000-induced stomatal reopening, and TARK1 OE plants were insensitive to Psyringae pathovar tomato strain DC3118 (coronatine deficit)-induced stomatal closure. We also found that TARK1 OE in leaves resulted in increased susceptibility to bacterial invasion. Collectively, our results indicate that TARK1 functions in stomatal movement only in response to biotic elicitors and support a model in which TARK1 regulates stomatal opening postelicitation.
DOI: 10.1104/pp.19.01400
PubMed: 32385090
PubMed Central: PMC7333691
Affiliations:
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Guzman</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biology, Stanford University, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Kim, Jung Gun" sort="Kim, Jung Gun" uniqKey="Kim J" first="Jung-Gun" last="Kim">Jung-Gun Kim</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biology, Stanford University, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Taylor, Kyle W" sort="Taylor, Kyle W" uniqKey="Taylor K" first="Kyle W" last="Taylor">Kyle W. 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Guzman</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biology, Stanford University, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Kim, Jung Gun" sort="Kim, Jung Gun" uniqKey="Kim J" first="Jung-Gun" last="Kim">Jung-Gun Kim</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biology, Stanford University, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Taylor, Kyle W" sort="Taylor, Kyle W" uniqKey="Taylor K" first="Kyle W" last="Taylor">Kyle W. Taylor</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biology, Stanford University, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Lanver, Daniel" sort="Lanver, Daniel" uniqKey="Lanver D" first="Daniel" last="Lanver">Daniel Lanver</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biology, Stanford University, Stanford</wicri:cityArea></affiliation></author><author><name sortKey="Mudgett, Mary Beth" sort="Mudgett, Mary Beth" uniqKey="Mudgett M" first="Mary Beth" last="Mudgett">Mary Beth Mudgett</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020 mudgett@stanford.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Department of Biology, Stanford University, Stanford</wicri:regionArea><wicri:noRegion>Stanford</wicri:noRegion></affiliation></author></analytic><series><title level="j">Plant physiology</title><idno type="eISSN">1532-2548</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">Tomato Atypical Receptor Kinase 1 (TARK1) is a pseudokinase required for postinvasion immunity. TARK1 was originally identified as a target of the <i>Xanthomonas euvesicatoria</i> effector protein <i>Xanthomonas</i> outer protein N (XopN), a suppressor of early defense signaling. How TARK1 participates in immune signal transduction is not well understood. To gain insight into TARK1's role in tomato (<i>Solanum lycopersicum</i>) immunity, we used a proteomics approach to isolate and identify TARK1-associated immune complexes formed during infection. We found that TARK1 interacts with proteins predicted to be associated with stomatal movement. TARK1 CRISPR mutants and overexpression (OE) lines did not display differences in light-induced stomatal opening or abscisic acid-induced stomatal closure; however, they did show altered stomatal movement responses to bacteria and biotic elicitors. Notably, we found that TARK1 CRISPR plants were resistant to <i>Pseudomonas syringae</i> pathovar tomato strain DC3000-induced stomatal reopening, and TARK1 OE plants were insensitive to <i>P</i><i>syringae</i> pathovar tomato strain DC3118 (coronatine deficit)-induced stomatal closure. We also found that TARK1 OE in leaves resulted in increased susceptibility to bacterial invasion. Collectively, our results indicate that TARK1 functions in stomatal movement only in response to biotic elicitors and support a model in which TARK1 regulates stomatal opening postelicitation.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32385090</PMID><DateRevised><Year>2020</Year><Month>08</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-2548</ISSN><JournalIssue CitedMedium="Internet"><Volume>183</Volume><Issue>3</Issue><PubDate><Year>2020</Year><Month>07</Month></PubDate></JournalIssue><Title>Plant physiology</Title><ISOAbbreviation>Plant Physiol</ISOAbbreviation></Journal><ArticleTitle>Tomato Atypical Receptor Kinase1 Is Involved in the Regulation of Preinvasion Defense.</ArticleTitle><Pagination><MedlinePgn>1306-1318</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1104/pp.19.01400</ELocationID><Abstract><AbstractText>Tomato Atypical Receptor Kinase 1 (TARK1) is a pseudokinase required for postinvasion immunity. TARK1 was originally identified as a target of the <i>Xanthomonas euvesicatoria</i> effector protein <i>Xanthomonas</i> outer protein N (XopN), a suppressor of early defense signaling. How TARK1 participates in immune signal transduction is not well understood. To gain insight into TARK1's role in tomato (<i>Solanum lycopersicum</i>) immunity, we used a proteomics approach to isolate and identify TARK1-associated immune complexes formed during infection. We found that TARK1 interacts with proteins predicted to be associated with stomatal movement. TARK1 CRISPR mutants and overexpression (OE) lines did not display differences in light-induced stomatal opening or abscisic acid-induced stomatal closure; however, they did show altered stomatal movement responses to bacteria and biotic elicitors. Notably, we found that TARK1 CRISPR plants were resistant to <i>Pseudomonas syringae</i> pathovar tomato strain DC3000-induced stomatal reopening, and TARK1 OE plants were insensitive to <i>P</i><i>syringae</i> pathovar tomato strain DC3118 (coronatine deficit)-induced stomatal closure. We also found that TARK1 OE in leaves resulted in increased susceptibility to bacterial invasion. Collectively, our results indicate that TARK1 functions in stomatal movement only in response to biotic elicitors and support a model in which TARK1 regulates stomatal opening postelicitation.</AbstractText><CopyrightInformation>© 2020 American Society of Plant Biologists. All Rights Reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Guzman</LastName><ForeName>Andrew R</ForeName><Initials>AR</Initials><Identifier Source="ORCID">0000-0002-1600-268X</Identifier><AffiliationInfo><Affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Jung-Gun</ForeName><Initials>JG</Initials><AffiliationInfo><Affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Taylor</LastName><ForeName>Kyle W</ForeName><Initials>KW</Initials><Identifier Source="ORCID">0000-0001-6794-5664</Identifier><AffiliationInfo><Affiliation>Department of Biology, Stanford University, Stanford, California 94305-5020.</Affiliation></AffiliationInfo></Author><Author 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Guzman</name></region><name sortKey="Kim, Jung Gun" sort="Kim, Jung Gun" uniqKey="Kim J" first="Jung-Gun" last="Kim">Jung-Gun Kim</name><name sortKey="Lanver, Daniel" sort="Lanver, Daniel" uniqKey="Lanver D" first="Daniel" last="Lanver">Daniel Lanver</name><name sortKey="Mudgett, Mary Beth" sort="Mudgett, Mary Beth" uniqKey="Mudgett M" first="Mary Beth" last="Mudgett">Mary Beth Mudgett</name><name sortKey="Taylor, Kyle W" sort="Taylor, Kyle W" uniqKey="Taylor K" first="Kyle W" last="Taylor">Kyle W. Taylor</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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