担当区分：筆頭著者   掲載種別：研究論文（学術雑誌）   出版者・発行元：Wiley  

Summary

Plant immune responses comprise two phases, pattern‐triggered immunity (PTI) and effector‐triggered immunity (ETI). Sensing of the pathogen effector by a nucleotide‐binding leucine‐rich repeat receptor (NLR) induces robust and sustained immune responses, resulting in hypersensitive response (HR) cell death. During HR, the reactive oxygen species (ROS) burst is achieved through Nicotiana benthamiana NbRBOHB. However, the detailed regulatory mechanisms of the ROS burst during HR are unclear.

Here, we show that calcium‐dependent protein kinases (CDPKs) contribute to the ROS burst associated with ongoing cell death using luminol‐based ROS assay together with immunodetection of the phosphorylated NbRBOHB in N. benthamiana . We found that NbCDPK4 and NbCDPK5 directly phosphorylate NbRBOHB Ser‐123 and provoke ROS bursts.

The phosphorylation of the Ser‐123 was strongly increased during AVRblb2‐ETI and INF1‐triggered PTI–ETI responses. On the contrary, the Ser‐123 was not phosphorylated during flg22‐triggered PTI. Moreover, the transient expression of NRC4 ^D478V , an autoactive helper NLR, indicated that phosphorylation of Ser‐123 was induced in a manner dependent on the N‐terminal conserved motif required for Ca ²⁺ channel activity of the NRC4.

These findings demonstrate a pivotal role for NbCDPKs in activating RBOH and sustained robust ROS bursts during plant immune cell death.

DOI： 10.1111/nph.71129

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その他リンク： https://nph.onlinelibrary.wiley.com/doi/full-xml/10.1111/nph.71129

担当区分：筆頭著者   出版者・発行元：Springer US  

DOI： 10.1007/978-1-0716-5138-4_7

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掲載種別：研究論文（学術雑誌）   出版者・発行元：Oxford University Press (OUP)  

Abstract

CALCIUM-DEPENDENT PROTEIN KINASE (CDPK) stimulates reactive oxygen species (ROS)-dependent signaling by activating RESPIRATORY BURST OXIDASE HOMOLOG (RBOH). The lysigenous aerenchyma is a gas space created by cortical cell death that facilitates oxygen diffusion from the shoot to the root tips. Previously, we showed that RBOHH is indispensable for the induction of aerenchyma formation in rice (Oryza sativa) roots under low-oxygen conditions. Here, we showed that CDPK5 and CDPK13 localize to the plasma membrane where RBOHH functions. Mutation analysis of the serine at residues 92 and 107 of RBOHH revealed that these residues are required for CDPK5- and CDPK13-mediated activation of ROS production. The requirement of Ca2+ for CDPK5 and CDPK13 function was confirmed using in vitro kinase assays. CRISPR/Cas9-based mutagenesis of CDPK5 and/or CDPK13 revealed that the double knockout almost completely suppressed inducible aerenchyma formation, whereas the effects were limited in the single knockout of either CDPK5 or CDPK13. Interestingly, the double knockout almost suppressed the induction of adventitious root formation, which is widely conserved in vascular plants, under low-oxygen conditions. Our results suggest that CDPKs are essential for the acclimation of rice to low-oxygen conditions and also for many other plant species conserving CDPK-targeted phosphorylation sites in RBOH homologs.

DOI： 10.1093/plphys/kiae293

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その他リンク： https://academic.oup.com/plphys/article-pdf/197/1/kiae293/58545955/kiae293.pdf

担当区分：筆頭著者   掲載種別：研究論文（学術雑誌）   出版者・発行元：Oxford University Press (OUP)  

Abstract

Reactive oxygen species (ROS) are rapidly generated during plant immune responses by respiratory burst oxidase homolog (RBOH), which is a plasma membrane-localized NADPH oxidase. Although regulatory mechanisms of RBOH activity have been well documented, the ROS-mediated downstream signaling is unclear. We here demonstrated that ROS sensor proteins play a central role in ROS signaling via oxidative post-translational modification of cysteine residues, sulfenylation. To detect protein sulfenylation, we used dimedone, which specifically and irreversibly binds to sulfenylated proteins. The sulfenylated proteins were labeled by dimedone in Nicotiana benthamiana leaves, and the conjugates were detected by immunoblot analyses. In addition, a reductant dissociated H2O2-induced conjugates, suggesting that cysteine persulfide and/or polysulfides are involved in sulfenylation. These sulfenylated proteins were continuously increased during both pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) in a RBOH-dependent manner. Pharmacological inhibition of ROS sensor proteins by dimedone perturbated cell death, ROS accumulation induced by INF1 and MEK2DD, and defense against fungal pathogens. On the other hand, Rpi-blb2-mediated ETI responses were enhanced by dimedone. These results suggest that the sulfenylation of cysteine and its derivatives in various ROS sensor proteins are important events downstream of the RBOH-dependent ROS burst to regulate plant immune responses.

DOI： 10.1093/jxb/erae111

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その他リンク： https://academic.oup.com/jxb/article-pdf/75/15/4641/58777007/erae111.pdf

掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/j.pmpp.2023.102000

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出版者・発行元：Scientific Societies  

The 12th iteration of the Japan-US Seminar in Plant Pathology was held in Ithaca, New York at Cornell University in the fall of 2022. Presentations covered a range of topics under the theme “Remodeling of the Plant-Microbe Environment During Disease, Defense, and Mutualism,” and the meeting included a panel discussion of best practices in science communication. This report presents highlights of the meeting, from the perspective of early career participants of the seminar.

[Formula: see text] Copyright © 2023 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

DOI： 10.1094/mpmi-04-23-0041-mr

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