Regulatory role of receptor-like cytoplasmic kinases in early immune signaling events in plants.
Identifieur interne : 000062 ( Main/Exploration ); précédent : 000061; suivant : 000063Regulatory role of receptor-like cytoplasmic kinases in early immune signaling events in plants.
Auteurs : Lifan Sun [République populaire de Chine] ; Jie Zhang [République populaire de Chine]Source :
- FEMS microbiology reviews [ 1574-6976 ] ; 2020.
Abstract
Receptor-like cytoplasmic kinases (RLCKs) play crucial roles in regulating plant development and immunity. Conserved pathogen-associated molecular patterns (PAMPs) derived from microbes are recognized by plant pattern recognition receptors to activate PAMP-triggered immunity (PTI). Microbial effectors, whose initial function is to promote virulence, are recognized by plant intracellular nucleotide-binding domain and leucine-rich repeat receptors (NLRs) to initiate effector-triggered immunity (ETI). Both PTI and ETI trigger early immune signaling events including the production of reactive oxygen species, induction of calcium influx, and activation of mitogen-activated protein kinases. Research progress has revealed the important roles of RLCKs in the regulation of early PTI signaling. Accordingly, RLCKs are often targeted by microbial effectors that are evolved to evade PTI via diverse modulations. In some cases, modulation of RLCKs by microbial effectors triggers the activation of NLRs. This review covers the mechanisms by which RLCKs engage diverse substrates to regulate early PTI signaling and the regulatory roles of RLCKs in triggering NLR activation. Accumulating evidence suggests evolutionary links and close connections between PAMP- and effector-triggered early immune signaling that are mediated by RLCKs. As key immune regulators, RLCKs can be considered targets with broad prospects for the improvement of plant resistance via genetic engineering.
DOI: 10.1093/femsre/fuaa035
PubMed: 32717059
Affiliations:
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sortKey="Sun, Lifan" sort="Sun, Lifan" uniqKey="Sun L" first="Lifan" last="Sun">Lifan Sun</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101</wicri:regionArea><wicri:noRegion>100101</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Zhang, Jie" sort="Zhang, Jie" uniqKey="Zhang J" first="Jie" last="Zhang">Jie Zhang</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101</wicri:regionArea><wicri:noRegion>100101</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">FEMS microbiology reviews</title><idno type="eISSN">1574-6976</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">Receptor-like cytoplasmic kinases (RLCKs) play crucial roles in regulating plant development and immunity. Conserved pathogen-associated molecular patterns (PAMPs) derived from microbes are recognized by plant pattern recognition receptors to activate PAMP-triggered immunity (PTI). Microbial effectors, whose initial function is to promote virulence, are recognized by plant intracellular nucleotide-binding domain and leucine-rich repeat receptors (NLRs) to initiate effector-triggered immunity (ETI). Both PTI and ETI trigger early immune signaling events including the production of reactive oxygen species, induction of calcium influx, and activation of mitogen-activated protein kinases. Research progress has revealed the important roles of RLCKs in the regulation of early PTI signaling. Accordingly, RLCKs are often targeted by microbial effectors that are evolved to evade PTI via diverse modulations. In some cases, modulation of RLCKs by microbial effectors triggers the activation of NLRs. This review covers the mechanisms by which RLCKs engage diverse substrates to regulate early PTI signaling and the regulatory roles of RLCKs in triggering NLR activation. Accumulating evidence suggests evolutionary links and close connections between PAMP- and effector-triggered early immune signaling that are mediated by RLCKs. As key immune regulators, RLCKs can be considered targets with broad prospects for the improvement of plant resistance via genetic engineering.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">32717059</PMID><DateRevised><Year>2020</Year><Month>07</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1574-6976</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Jul</Month><Day>27</Day></PubDate></JournalIssue><Title>FEMS microbiology reviews</Title><ISOAbbreviation>FEMS Microbiol Rev</ISOAbbreviation></Journal><ArticleTitle>Regulatory role of receptor-like cytoplasmic kinases in early immune signaling events in plants.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">fuaa035</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1093/femsre/fuaa035</ELocationID><Abstract><AbstractText>Receptor-like cytoplasmic kinases (RLCKs) play crucial roles in regulating plant development and immunity. Conserved pathogen-associated molecular patterns (PAMPs) derived from microbes are recognized by plant pattern recognition receptors to activate PAMP-triggered immunity (PTI). Microbial effectors, whose initial function is to promote virulence, are recognized by plant intracellular nucleotide-binding domain and leucine-rich repeat receptors (NLRs) to initiate effector-triggered immunity (ETI). Both PTI and ETI trigger early immune signaling events including the production of reactive oxygen species, induction of calcium influx, and activation of mitogen-activated protein kinases. Research progress has revealed the important roles of RLCKs in the regulation of early PTI signaling. Accordingly, RLCKs are often targeted by microbial effectors that are evolved to evade PTI via diverse modulations. In some cases, modulation of RLCKs by microbial effectors triggers the activation of NLRs. This review covers the mechanisms by which RLCKs engage diverse substrates to regulate early PTI signaling and the regulatory roles of RLCKs in triggering NLR activation. Accumulating evidence suggests evolutionary links and close connections between PAMP- and effector-triggered early immune signaling that are mediated by RLCKs. As key immune regulators, RLCKs can be considered targets with broad prospects for the improvement of plant resistance via genetic engineering.</AbstractText><CopyrightInformation>© FEMS 2020.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Lifan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>07</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>FEMS Microbiol Rev</MedlineTA><NlmUniqueID>8902526</NlmUniqueID><ISSNLinking>0168-6445</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">NLR</Keyword><Keyword MajorTopicYN="N">PAMP-triggered immunity</Keyword><Keyword MajorTopicYN="N">PRR</Keyword><Keyword MajorTopicYN="N">effector-triggered immunity</Keyword><Keyword MajorTopicYN="N">phosphorylation</Keyword><Keyword MajorTopicYN="N">receptor-like cytoplasmic kinase</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>7</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>7</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>7</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32717059</ArticleId><ArticleId IdType="pii">5876876</ArticleId><ArticleId IdType="doi">10.1093/femsre/fuaa035</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Sun, Lifan" sort="Sun, Lifan" uniqKey="Sun L" first="Lifan" last="Sun">Lifan Sun</name></noRegion><name sortKey="Sun, Lifan" sort="Sun, Lifan" uniqKey="Sun L" first="Lifan" last="Sun">Lifan Sun</name><name sortKey="Zhang, Jie" sort="Zhang, Jie" uniqKey="Zhang J" first="Jie" last="Zhang">Jie Zhang</name><name sortKey="Zhang, Jie" sort="Zhang, Jie" uniqKey="Zhang J" first="Jie" last="Zhang">Jie Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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