PhytophthoraV1, Main, Exploration, bibRecord, 000D43

Two cytoplasmic effectors of Phytophthora sojae regulate plant cell death via interactions with plant catalases.

Identifieur interne : 000D43 ( Main/Exploration ); précédent : 000D42; suivant : 000D44

Two cytoplasmic effectors of Phytophthora sojae regulate plant cell death via interactions with plant catalases.

Auteurs : Meixiang Zhang ; Qi Li ; Tingli Liu ; Li Liu ; Danyu Shen ; Ye Zhu ; Peihan Liu ; Jian-Min Zhou ; Daolong Dou [République populaire de Chine]

Source :

Plant physiology [ 1532-2548 ] ; 2015.

RBID : pubmed:25424308

Descripteurs français

KwdFr :
- Catalase (métabolisme), Catalase (physiologie), Maladies des plantes (parasitologie), Mort cellulaire (physiologie), Phytophthora (métabolisme), Phytophthora (physiologie), Protéines végétales (physiologie), Régulation de l'expression des gènes végétaux (physiologie), Soja (métabolisme), Soja (physiologie), Tabac (métabolisme), Tabac (physiologie).
MESH :
- métabolisme : Catalase, Phytophthora, Soja, Tabac.
- parasitologie : Maladies des plantes.
- physiologie : Catalase, Mort cellulaire, Phytophthora, Protéines végétales, Régulation de l'expression des gènes végétaux, Soja, Tabac.

English descriptors

KwdEn :
- Catalase (metabolism), Catalase (physiology), Cell Death (physiology), Gene Expression Regulation, Plant (physiology), Phytophthora (metabolism), Phytophthora (physiology), Plant Diseases (parasitology), Plant Proteins (physiology), Soybeans (metabolism), Soybeans (physiology), Tobacco (metabolism), Tobacco (physiology).
MESH :
- chemical , metabolism : Catalase.
- chemical , physiology : Catalase, Plant Proteins.
- metabolism : Phytophthora, Soybeans, Tobacco.
- parasitology : Plant Diseases.
- physiology : Cell Death, Gene Expression Regulation, Plant, Phytophthora, Soybeans, Tobacco.

Abstract

Plant pathogenic oomycetes, such as Phytophthora sojae, secrete an arsenal of host cytoplasmic effectors to promote infection. We have shown previously that P. sojae PsCRN63 (for crinkling- and necrosis-inducing proteins) induces programmed cell death (PCD) while PsCRN115 blocks PCD in planta; however, they are jointly required for full pathogenesis. Here, we find that PsCRN63 alone or PsCRN63 and PsCRN115 together might suppress the immune responses of Nicotiana benthamiana and demonstrate that these two cytoplasmic effectors interact with catalases from N. benthamiana and soybean (Glycine max). Transient expression of PsCRN63 increases hydrogen peroxide (H(2)O(2)) accumulation, whereas PsCRN115 suppresses this process. Transient overexpression of NbCAT1 (for N. benthamiana CATALASE1) or GmCAT1 specifically alleviates PsCRN63-induced PCD. Suppression of the PsCRN63-induced PCD by PsCRN115 is compromised when catalases are silenced in N. benthamiana. Interestingly, the NbCAT1 is recruited into the plant nucleus in the presence of PsCRN63 or PsCRN115; NbCAT1 and GmCAT1 are destabilized when PsCRN63 is coexpressed, and PsCRN115 inhibits the processes. Thus, PsCRN63/115 manipulates plant PCD through interfering with catalases and perturbing H(2)O(2) homeostasis. Furthermore, silencing of catalase genes enhances susceptibility to Phytophthora capsici, indicating that catalases are essential for plant resistance. Taken together, we suggest that P. sojae secretes these two effectors to regulate plant PCD and H(2)O(2) homeostasis through direct interaction with catalases and, therefore, overcome host immune responses.

DOI: 10.1104/pp.114.252437
PubMed: 25424308
PubMed Central: PMC4281015

Affiliations:

République populaire de Chine

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000F34
to stream Main, to step Curation: 000F34

Le document en format XML

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<term>Gene Expression Regulation, Plant (physiology)</term>
<term>Phytophthora (metabolism)</term>
<term>Phytophthora (physiology)</term>
<term>Plant Diseases (parasitology)</term>
<term>Plant Proteins (physiology)</term>
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<term>Tobacco (metabolism)</term>
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<term>Catalase (physiologie)</term>
<term>Maladies des plantes (parasitologie)</term>
<term>Mort cellulaire (physiologie)</term>
<term>Phytophthora (métabolisme)</term>
<term>Phytophthora (physiologie)</term>
<term>Protéines végétales (physiologie)</term>
<term>Régulation de l'expression des gènes végétaux (physiologie)</term>
<term>Soja (métabolisme)</term>
<term>Soja (physiologie)</term>
<term>Tabac (métabolisme)</term>
<term>Tabac (physiologie)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Catalase</term>
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<term>Plant Proteins</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Phytophthora</term>
<term>Soybeans</term>
<term>Tobacco</term>
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<term>Tabac</term>
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<keywords scheme="MESH" qualifier="parasitologie" xml:lang="fr"><term>Maladies des plantes</term>
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<front><div type="abstract" xml:lang="en">Plant pathogenic oomycetes, such as Phytophthora sojae, secrete an arsenal of host cytoplasmic effectors to promote infection. We have shown previously that P. sojae PsCRN63 (for crinkling- and necrosis-inducing proteins) induces programmed cell death (PCD) while PsCRN115 blocks PCD in planta; however, they are jointly required for full pathogenesis. Here, we find that PsCRN63 alone or PsCRN63 and PsCRN115 together might suppress the immune responses of Nicotiana benthamiana and demonstrate that these two cytoplasmic effectors interact with catalases from N. benthamiana and soybean (Glycine max). Transient expression of PsCRN63 increases hydrogen peroxide (H(2)O(2)) accumulation, whereas PsCRN115 suppresses this process. Transient overexpression of NbCAT1 (for N. benthamiana CATALASE1) or GmCAT1 specifically alleviates PsCRN63-induced PCD. Suppression of the PsCRN63-induced PCD by PsCRN115 is compromised when catalases are silenced in N. benthamiana. Interestingly, the NbCAT1 is recruited into the plant nucleus in the presence of PsCRN63 or PsCRN115; NbCAT1 and GmCAT1 are destabilized when PsCRN63 is coexpressed, and PsCRN115 inhibits the processes. Thus, PsCRN63/115 manipulates plant PCD through interfering with catalases and perturbing H(2)O(2) homeostasis. Furthermore, silencing of catalase genes enhances susceptibility to Phytophthora capsici, indicating that catalases are essential for plant resistance. Taken together, we suggest that P. sojae secretes these two effectors to regulate plant PCD and H(2)O(2) homeostasis through direct interaction with catalases and, therefore, overcome host immune responses.</div>
</front>
</TEI>
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<DateCompleted><Year>2015</Year>
<Month>09</Month>
<Day>29</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>167</Volume>
<Issue>1</Issue>
<PubDate><Year>2015</Year>
<Month>Jan</Month>
</PubDate>
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<Title>Plant physiology</Title>
<ISOAbbreviation>Plant Physiol</ISOAbbreviation>
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<ArticleTitle>Two cytoplasmic effectors of Phytophthora sojae regulate plant cell death via interactions with plant catalases.</ArticleTitle>
<Pagination><MedlinePgn>164-75</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1104/pp.114.252437</ELocationID>
<Abstract><AbstractText>Plant pathogenic oomycetes, such as Phytophthora sojae, secrete an arsenal of host cytoplasmic effectors to promote infection. We have shown previously that P. sojae PsCRN63 (for crinkling- and necrosis-inducing proteins) induces programmed cell death (PCD) while PsCRN115 blocks PCD in planta; however, they are jointly required for full pathogenesis. Here, we find that PsCRN63 alone or PsCRN63 and PsCRN115 together might suppress the immune responses of Nicotiana benthamiana and demonstrate that these two cytoplasmic effectors interact with catalases from N. benthamiana and soybean (Glycine max). Transient expression of PsCRN63 increases hydrogen peroxide (H(2)O(2)) accumulation, whereas PsCRN115 suppresses this process. Transient overexpression of NbCAT1 (for N. benthamiana CATALASE1) or GmCAT1 specifically alleviates PsCRN63-induced PCD. Suppression of the PsCRN63-induced PCD by PsCRN115 is compromised when catalases are silenced in N. benthamiana. Interestingly, the NbCAT1 is recruited into the plant nucleus in the presence of PsCRN63 or PsCRN115; NbCAT1 and GmCAT1 are destabilized when PsCRN63 is coexpressed, and PsCRN115 inhibits the processes. Thus, PsCRN63/115 manipulates plant PCD through interfering with catalases and perturbing H(2)O(2) homeostasis. Furthermore, silencing of catalase genes enhances susceptibility to Phytophthora capsici, indicating that catalases are essential for plant resistance. Taken together, we suggest that P. sojae secretes these two effectors to regulate plant PCD and H(2)O(2) homeostasis through direct interaction with catalases and, therefore, overcome host immune responses.</AbstractText>
<CopyrightInformation>© 2015 American Society of Plant Biologists. All Rights Reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Meixiang</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China (M.Z., Q.L., T.L., L.L., D.S., Y.Z., P.L., D.D.); andCenter for Genome Biology and State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China (Q.L., J.-M.Z.).</Affiliation>
</AffiliationInfo>
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Two cytoplasmic effectors of Phytophthora sojae regulate plant cell death via interactions with plant catalases.

Two cytoplasmic effectors of Phytophthora sojae regulate plant cell death via interactions with plant catalases.

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