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Inositol-requiring enzyme 1 (IRE1) plays for AvrRpt2-triggered immunity and RIN4 cleavage in Arabidopsis under endoplasmic reticulum (ER) stress.

Identifieur interne : 000127 ( Main/Exploration ); précédent : 000126; suivant : 000128

Inositol-requiring enzyme 1 (IRE1) plays for AvrRpt2-triggered immunity and RIN4 cleavage in Arabidopsis under endoplasmic reticulum (ER) stress.

Auteurs : Rupak Chakraborty [Corée du Sud] ; Shahab Uddin [Corée du Sud] ; Donah Mary Macoy [Corée du Sud] ; Si On Park [Corée du Sud] ; Duong Thu Van Anh [Corée du Sud] ; Gyeong Ryul Ryu [Corée du Sud] ; Young Hun Kim [Corée du Sud] ; Jong-Yeol Lee [Corée du Sud] ; Joon-Yung Cha [Corée du Sud] ; Woe-Yeon Kim [Corée du Sud] ; Sang Yeol Lee [Corée du Sud] ; Min Gab Kim [Corée du Sud]

Source :

RBID : pubmed:32927152

Abstract

Many stresses induce the accumulation of unfolded and misfolded proteins in the endoplasmic reticulum, a phenomenon known as ER stress. In response to ER stress, cells initiate a protective response, known as unfolded protein response (UPR), to maintain cellular homeostasis. The UPR sensor, inositol-requiring enzyme 1 (IRE1), catalyzes the cytoplasmic splicing of bZIP transcription factor-encoding mRNAs to activate the UPR signaling pathway. Recently, we reported that pretreatment of Arabidopsis thaliana plants with tunicamycin, an ER stress inducer, increased their susceptibility to bacterial pathogens; on the other hand, IRE1 deficient mutants were susceptible to Pseudomonas syringae pv. maculicola (Psm) and failed to induce salicylic acid (SA)-mediated systemic acquired resistance. However, the functional relationship of IRE1 with the pathogen and TM treatment remains unknown. In the present study, we showed that bacterial pathogen-associated molecular patterns (PAMPs) induced IRE1 expression; however, PAMP-triggered immunity (PTI) response such as callose deposition, PR1 protein accumulation, or Pst DC3000 hrcC growth was not altered in ire1 mutants. We observed that IRE1 enhanced plant immunity against the bacterial pathogen P. syringae pv. tomato DC3000 (Pst DC3000) under ER stress. Moreover, TM-pretreated ire1 mutants were more susceptible to the avirulent strain Pst DC3000 (AvrRpt2) and showed greater cell death than wild-type plants during effector-triggered immunity (ETI). Additionally, Pst DC3000 (AvrRpt2)-mediated RIN4 degradation was reduced in ire1 mutants under TM-induced ER stress. Collectively, our results reveal that IRE1 plays a pivotal role in the immune signaling pathway to activate plant immunity against virulent and avirulent bacterial strains under ER stress.

DOI: 10.1016/j.plaphy.2020.09.002
PubMed: 32927152


Affiliations:


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<div type="abstract" xml:lang="en">Many stresses induce the accumulation of unfolded and misfolded proteins in the endoplasmic reticulum, a phenomenon known as ER stress. In response to ER stress, cells initiate a protective response, known as unfolded protein response (UPR), to maintain cellular homeostasis. The UPR sensor, inositol-requiring enzyme 1 (IRE1), catalyzes the cytoplasmic splicing of bZIP transcription factor-encoding mRNAs to activate the UPR signaling pathway. Recently, we reported that pretreatment of Arabidopsis thaliana plants with tunicamycin, an ER stress inducer, increased their susceptibility to bacterial pathogens; on the other hand, IRE1 deficient mutants were susceptible to Pseudomonas syringae pv. maculicola (Psm) and failed to induce salicylic acid (SA)-mediated systemic acquired resistance. However, the functional relationship of IRE1 with the pathogen and TM treatment remains unknown. In the present study, we showed that bacterial pathogen-associated molecular patterns (PAMPs) induced IRE1 expression; however, PAMP-triggered immunity (PTI) response such as callose deposition, PR1 protein accumulation, or Pst DC3000 hrcC growth was not altered in ire1 mutants. We observed that IRE1 enhanced plant immunity against the bacterial pathogen P. syringae pv. tomato DC3000 (Pst DC3000) under ER stress. Moreover, TM-pretreated ire1 mutants were more susceptible to the avirulent strain Pst DC3000 (AvrRpt2) and showed greater cell death than wild-type plants during effector-triggered immunity (ETI). Additionally, Pst DC3000 (AvrRpt2)-mediated RIN4 degradation was reduced in ire1 mutants under TM-induced ER stress. Collectively, our results reveal that IRE1 plays a pivotal role in the immune signaling pathway to activate plant immunity against virulent and avirulent bacterial strains under ER stress.</div>
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<AbstractText>Many stresses induce the accumulation of unfolded and misfolded proteins in the endoplasmic reticulum, a phenomenon known as ER stress. In response to ER stress, cells initiate a protective response, known as unfolded protein response (UPR), to maintain cellular homeostasis. The UPR sensor, inositol-requiring enzyme 1 (IRE1), catalyzes the cytoplasmic splicing of bZIP transcription factor-encoding mRNAs to activate the UPR signaling pathway. Recently, we reported that pretreatment of Arabidopsis thaliana plants with tunicamycin, an ER stress inducer, increased their susceptibility to bacterial pathogens; on the other hand, IRE1 deficient mutants were susceptible to Pseudomonas syringae pv. maculicola (Psm) and failed to induce salicylic acid (SA)-mediated systemic acquired resistance. However, the functional relationship of IRE1 with the pathogen and TM treatment remains unknown. In the present study, we showed that bacterial pathogen-associated molecular patterns (PAMPs) induced IRE1 expression; however, PAMP-triggered immunity (PTI) response such as callose deposition, PR1 protein accumulation, or Pst DC3000 hrcC growth was not altered in ire1 mutants. We observed that IRE1 enhanced plant immunity against the bacterial pathogen P. syringae pv. tomato DC3000 (Pst DC3000) under ER stress. Moreover, TM-pretreated ire1 mutants were more susceptible to the avirulent strain Pst DC3000 (AvrRpt2) and showed greater cell death than wild-type plants during effector-triggered immunity (ETI). Additionally, Pst DC3000 (AvrRpt2)-mediated RIN4 degradation was reduced in ire1 mutants under TM-induced ER stress. Collectively, our results reveal that IRE1 plays a pivotal role in the immune signaling pathway to activate plant immunity against virulent and avirulent bacterial strains under ER stress.</AbstractText>
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<Affiliation>College of Pharmacy and Research Institute of Pharmaceutical Science, PMBBRC, Gyeongsang National University, Jinju, 660-701, Republic of Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Kim</LastName>
<ForeName>Young Hun</ForeName>
<Initials>YH</Initials>
<AffiliationInfo>
<Affiliation>College of Pharmacy and Research Institute of Pharmaceutical Science, PMBBRC, Gyeongsang National University, Jinju, 660-701, Republic of Korea.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Lee</LastName>
<ForeName>Jong-Yeol</ForeName>
<Initials>JY</Initials>
<AffiliationInfo>
<Affiliation>National Institute of Agricultural Sciences, Rural Development Administration, Jeonju, Republic of Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Cha</LastName>
<ForeName>Joon-Yung</ForeName>
<Initials>JY</Initials>
<AffiliationInfo>
<Affiliation>Division of Applied Life Sciences (BK21+) and PMBBRC, Gyeongsang National University, Jinju, 52828, Republic of Korea.</Affiliation>
</AffiliationInfo>
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<LastName>Kim</LastName>
<ForeName>Woe-Yeon</ForeName>
<Initials>WY</Initials>
<AffiliationInfo>
<Affiliation>Division of Applied Life Sciences (BK21+) and PMBBRC, Gyeongsang National University, Jinju, 52828, Republic of Korea.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Lee</LastName>
<ForeName>Sang Yeol</ForeName>
<Initials>SY</Initials>
<AffiliationInfo>
<Affiliation>Division of Applied Life Sciences (BK21+) and PMBBRC, Gyeongsang National University, Jinju, 52828, Republic of Korea.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Kim</LastName>
<ForeName>Min Gab</ForeName>
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<AffiliationInfo>
<Affiliation>College of Pharmacy and Research Institute of Pharmaceutical Science, PMBBRC, Gyeongsang National University, Jinju, 660-701, Republic of Korea. Electronic address: mgk1284@gnu.ac.kr.</Affiliation>
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<Language>eng</Language>
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<PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic">
<Year>2020</Year>
<Month>09</Month>
<Day>05</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo>
<Country>France</Country>
<MedlineTA>Plant Physiol Biochem</MedlineTA>
<NlmUniqueID>9882449</NlmUniqueID>
<ISSNLinking>0981-9428</ISSNLinking>
</MedlineJournalInfo>
<CitationSubset>IM</CitationSubset>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Bacterial growth</Keyword>
<Keyword MajorTopicYN="N">ER stress</Keyword>
<Keyword MajorTopicYN="N">IRE1</Keyword>
<Keyword MajorTopicYN="N">RIN4</Keyword>
<Keyword MajorTopicYN="N">Tunicamycin</Keyword>
<Keyword MajorTopicYN="N">UPR</Keyword>
</KeywordList>
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<Year>2020</Year>
<Month>05</Month>
<Day>02</Day>
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<Year>2020</Year>
<Month>08</Month>
<Day>25</Day>
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<PubMedPubDate PubStatus="accepted">
<Year>2020</Year>
<Month>09</Month>
<Day>01</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed">
<Year>2020</Year>
<Month>9</Month>
<Day>15</Day>
<Hour>6</Hour>
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<PubMedPubDate PubStatus="medline">
<Year>2020</Year>
<Month>9</Month>
<Day>15</Day>
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<PubMedPubDate PubStatus="entrez">
<Year>2020</Year>
<Month>9</Month>
<Day>14</Day>
<Hour>20</Hour>
<Minute>13</Minute>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">32927152</ArticleId>
<ArticleId IdType="pii">S0981-9428(20)30450-2</ArticleId>
<ArticleId IdType="doi">10.1016/j.plaphy.2020.09.002</ArticleId>
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<affiliations>
<list>
<country>
<li>Corée du Sud</li>
</country>
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<tree>
<country name="Corée du Sud">
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<name sortKey="Chakraborty, Rupak" sort="Chakraborty, Rupak" uniqKey="Chakraborty R" first="Rupak" last="Chakraborty">Rupak Chakraborty</name>
</noRegion>
<name sortKey="Cha, Joon Yung" sort="Cha, Joon Yung" uniqKey="Cha J" first="Joon-Yung" last="Cha">Joon-Yung Cha</name>
<name sortKey="Kim, Min Gab" sort="Kim, Min Gab" uniqKey="Kim M" first="Min Gab" last="Kim">Min Gab Kim</name>
<name sortKey="Kim, Woe Yeon" sort="Kim, Woe Yeon" uniqKey="Kim W" first="Woe-Yeon" last="Kim">Woe-Yeon Kim</name>
<name sortKey="Kim, Young Hun" sort="Kim, Young Hun" uniqKey="Kim Y" first="Young Hun" last="Kim">Young Hun Kim</name>
<name sortKey="Lee, Jong Yeol" sort="Lee, Jong Yeol" uniqKey="Lee J" first="Jong-Yeol" last="Lee">Jong-Yeol Lee</name>
<name sortKey="Lee, Sang Yeol" sort="Lee, Sang Yeol" uniqKey="Lee S" first="Sang Yeol" last="Lee">Sang Yeol Lee</name>
<name sortKey="Macoy, Donah Mary" sort="Macoy, Donah Mary" uniqKey="Macoy D" first="Donah Mary" last="Macoy">Donah Mary Macoy</name>
<name sortKey="Park, Si On" sort="Park, Si On" uniqKey="Park S" first="Si On" last="Park">Si On Park</name>
<name sortKey="Ryu, Gyeong Ryul" sort="Ryu, Gyeong Ryul" uniqKey="Ryu G" first="Gyeong Ryul" last="Ryu">Gyeong Ryul Ryu</name>
<name sortKey="Uddin, Shahab" sort="Uddin, Shahab" uniqKey="Uddin S" first="Shahab" last="Uddin">Shahab Uddin</name>
<name sortKey="Van Anh, Duong Thu" sort="Van Anh, Duong Thu" uniqKey="Van Anh D" first="Duong Thu" last="Van Anh">Duong Thu Van Anh</name>
</country>
</tree>
</affiliations>
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