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Proteomics analysis reveals the defense priming effect of chitosan oligosaccharides in Arabidopsis-Pst DC3000 interaction.

Identifieur interne : 000078 ( Main/Exploration ); précédent : 000077; suivant : 000079

Proteomics analysis reveals the defense priming effect of chitosan oligosaccharides in Arabidopsis-Pst DC3000 interaction.

Auteurs : Xiaochen Jia [République populaire de Chine] ; Hongqiang Qin [République populaire de Chine] ; Santosh Kumar Bose [République populaire de Chine] ; Tongmei Liu [République populaire de Chine] ; Jinxia He [République populaire de Chine] ; Shangqiang Xie [République populaire de Chine] ; Mingliang Ye [République populaire de Chine] ; Heng Yin [République populaire de Chine]

Source :

RBID : pubmed:32120172

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English descriptors

Abstract

Chitosan oligosaccharides (COS) worked effectively in multiple plant-pathogen interactions as plant immunity regulator, however, due to the complexity of the COS-induced immune signaling network, the topic requires further investigation. In the present study, quantitative analysis of proteins was performed to investigate the underlying mechanism of COS induced resistance to Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) in Arabidopsis thaliana. 4303 proteins were successfully quantified, 186, 217 and 207 proteins were differently regulated in mock + Pst, COS, and COS + Pst treated plants, respectively, compared with mock plants. From detailed functional and hierarchical clustering analysis, a priming effect of COS on plant immune system by pre-regulated the key proteins related to signaling transduction, defense response, cell wall biosynthesis and modification, plant growth and development, gene transcription and translation, which confers enhanced resistance when Pst DC3000 infection in Arabidopsis. Moreover, RACK1B which has the potential to be the key kinase receptor for COS signals was found out by protein-protein interaction network analysis of COS responsive proteins. In conclusion, COS treatment enable plant to fine-tuning its defense mechanisms for a more rapid and stronger response to future pathogen attacks, which obviously enhances plants defensive capacity that makes COS worked effectively in multiple plant-pathogen interactions.

DOI: 10.1016/j.plaphy.2020.01.037
PubMed: 32120172


Affiliations:


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<div type="abstract" xml:lang="en">Chitosan oligosaccharides (COS) worked effectively in multiple plant-pathogen interactions as plant immunity regulator, however, due to the complexity of the COS-induced immune signaling network, the topic requires further investigation. In the present study, quantitative analysis of proteins was performed to investigate the underlying mechanism of COS induced resistance to Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) in Arabidopsis thaliana. 4303 proteins were successfully quantified, 186, 217 and 207 proteins were differently regulated in mock + Pst, COS, and COS + Pst treated plants, respectively, compared with mock plants. From detailed functional and hierarchical clustering analysis, a priming effect of COS on plant immune system by pre-regulated the key proteins related to signaling transduction, defense response, cell wall biosynthesis and modification, plant growth and development, gene transcription and translation, which confers enhanced resistance when Pst DC3000 infection in Arabidopsis. Moreover, RACK1B which has the potential to be the key kinase receptor for COS signals was found out by protein-protein interaction network analysis of COS responsive proteins. In conclusion, COS treatment enable plant to fine-tuning its defense mechanisms for a more rapid and stronger response to future pathogen attacks, which obviously enhances plants defensive capacity that makes COS worked effectively in multiple plant-pathogen interactions.</div>
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</MedlineJournalInfo>
<ChemicalList>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D029681">Arabidopsis Proteins</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>9012-76-4</RegistryNumber>
<NameOfSubstance UI="D048271">Chitosan</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList>
<MeshHeading>
<DescriptorName UI="D017360" MajorTopicYN="Y">Arabidopsis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D029681" MajorTopicYN="Y">Arabidopsis Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D048271" MajorTopicYN="Y">Chitosan</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D060467" MajorTopicYN="Y">Disease Resistance</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018506" MajorTopicYN="N">Gene Expression Regulation, Plant</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D040901" MajorTopicYN="N">Proteomics</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D044224" MajorTopicYN="N">Pseudomonas syringae</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Arabidopsis</Keyword>
<Keyword MajorTopicYN="N">Chitosan oligosaccharides</Keyword>
<Keyword MajorTopicYN="N">Defense priming</Keyword>
<Keyword MajorTopicYN="N">Plant defense</Keyword>
<Keyword MajorTopicYN="N">Proteomics</Keyword>
<Keyword MajorTopicYN="N">Pst DC3000</Keyword>
</KeywordList>
<CoiStatement>Declaration of competing interest The authors declare that the submitted work was not carried out in the presence of any personal, professional or financial relationships that could potentially be constructed as a conflict of interest. This paper is not being submitted to any other journal and all authors approve this submission.</CoiStatement>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="received">
<Year>2019</Year>
<Month>08</Month>
<Day>18</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised">
<Year>2020</Year>
<Month>01</Month>
<Day>29</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2020</Year>
<Month>01</Month>
<Day>30</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed">
<Year>2020</Year>
<Month>3</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2020</Year>
<Month>7</Month>
<Day>18</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2020</Year>
<Month>3</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">32120172</ArticleId>
<ArticleId IdType="pii">S0981-9428(20)30045-0</ArticleId>
<ArticleId IdType="doi">10.1016/j.plaphy.2020.01.037</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
</list>
<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Jia, Xiaochen" sort="Jia, Xiaochen" uniqKey="Jia X" first="Xiaochen" last="Jia">Xiaochen Jia</name>
</noRegion>
<name sortKey="Bose, Santosh Kumar" sort="Bose, Santosh Kumar" uniqKey="Bose S" first="Santosh Kumar" last="Bose">Santosh Kumar Bose</name>
<name sortKey="He, Jinxia" sort="He, Jinxia" uniqKey="He J" first="Jinxia" last="He">Jinxia He</name>
<name sortKey="Liu, Tongmei" sort="Liu, Tongmei" uniqKey="Liu T" first="Tongmei" last="Liu">Tongmei Liu</name>
<name sortKey="Qin, Hongqiang" sort="Qin, Hongqiang" uniqKey="Qin H" first="Hongqiang" last="Qin">Hongqiang Qin</name>
<name sortKey="Xie, Shangqiang" sort="Xie, Shangqiang" uniqKey="Xie S" first="Shangqiang" last="Xie">Shangqiang Xie</name>
<name sortKey="Ye, Mingliang" sort="Ye, Mingliang" uniqKey="Ye M" first="Mingliang" last="Ye">Mingliang Ye</name>
<name sortKey="Yin, Heng" sort="Yin, Heng" uniqKey="Yin H" first="Heng" last="Yin">Heng Yin</name>
</country>
</tree>
</affiliations>
</record>

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