Abstract:SummaryPerception of pathogen-associated molecular patterns (PAMPs) by surface-localized pattern-recognition receptors activates RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD) through direct phosphorylation by BOTRYTIS-INDUCED KINASE 1 (BIK1) and induces the production of reactive oxygen species (ROS). ROS have direct antimicrobial properties but also serve as signaling molecules to activate additional defense responses such as stomatal closure. RBOHD activity must be tightly controlled to avoid the detrimental e… Show more
“…Thus, we used the constitutive cassava vein mosaic virus (CsVMV) promoter to express GFP:RBOHD in Col‐0 and ateca4‐1 plants. Similarly, a strong promoter, CaMV 35S, was used to overexpress mScarlet‐RBOHD and RBOHD in the study of ROS production in plant immunity and responses to salinity stress, respectively (Goto et al., 2020; Luo et al., 2021). In addition, many other proteins expressed by the CaMV 35S promoter showed normal trafficking (Marhavy et al., 2011; Nguyen et al., 2018; Park et al., 2016; Wolff et al., 2021).…”
SUMMARY
Various environmental stresses can induce production of reactive oxygen species (ROS) to turn on signaling for proper responses to those stresses. Plasma membrane (PM)‐localized respiratory burst oxidase homologs (RBOHs), in particular RBOHD, produce ROS via the post‐translational activation upon abiotic and biotic stresses. Although the mechanisms of RBOHD activation upon biotic stress have been elucidated in detail, it remains elusive how salinity stress activates RBOHD. Here, we present evidence that trafficking of PM‐localized RBOHD to endosomes and then its recycling back to the PM is critical for ROS accumulation upon salinity stress. ateca4 plants that were defective in recycling of proteins from endosomes to the PM and clc2‐1 and chc2‐1 plants that were defective in endocytosis showed a defect in salinity stress‐induced ROS production. In addition, ateca4 plants showed a defect in transient accumulation of GFP:RBOHD to the PM at the early stage of salinity stress. By contrast, ateca4 plants showed no defect in the increase in the ROS level and accumulation of RBOHD to the PM upon flg22 treatment as wild‐type plants. Based on these observations, we propose that factors involved in the trafficking machinery such as AtECA4 and clathrin are important players in salt stress‐induced, but not flg22‐induced, ROS accumulation.
“…Thus, we used the constitutive cassava vein mosaic virus (CsVMV) promoter to express GFP:RBOHD in Col‐0 and ateca4‐1 plants. Similarly, a strong promoter, CaMV 35S, was used to overexpress mScarlet‐RBOHD and RBOHD in the study of ROS production in plant immunity and responses to salinity stress, respectively (Goto et al., 2020; Luo et al., 2021). In addition, many other proteins expressed by the CaMV 35S promoter showed normal trafficking (Marhavy et al., 2011; Nguyen et al., 2018; Park et al., 2016; Wolff et al., 2021).…”
SUMMARY
Various environmental stresses can induce production of reactive oxygen species (ROS) to turn on signaling for proper responses to those stresses. Plasma membrane (PM)‐localized respiratory burst oxidase homologs (RBOHs), in particular RBOHD, produce ROS via the post‐translational activation upon abiotic and biotic stresses. Although the mechanisms of RBOHD activation upon biotic stress have been elucidated in detail, it remains elusive how salinity stress activates RBOHD. Here, we present evidence that trafficking of PM‐localized RBOHD to endosomes and then its recycling back to the PM is critical for ROS accumulation upon salinity stress. ateca4 plants that were defective in recycling of proteins from endosomes to the PM and clc2‐1 and chc2‐1 plants that were defective in endocytosis showed a defect in salinity stress‐induced ROS production. In addition, ateca4 plants showed a defect in transient accumulation of GFP:RBOHD to the PM at the early stage of salinity stress. By contrast, ateca4 plants showed no defect in the increase in the ROS level and accumulation of RBOHD to the PM upon flg22 treatment as wild‐type plants. Based on these observations, we propose that factors involved in the trafficking machinery such as AtECA4 and clathrin are important players in salt stress‐induced, but not flg22‐induced, ROS accumulation.
“…In an article published in this issue of New Phytologist , Goto et al . (2024; 1763–1779) report a new negative regulator of RBOHD activity that antagonizes BIK1 during PTI responses and may contribute to fine‐tuning the production of ROS in immunity.‘PB1CP emerges as a new RBOHD interactor that negatively regulates the active oxidase, contributing to fine‐tuning ROS production in immunity.’…”
Section: Figmentioning
confidence: 99%
“…However, our knowledge is limited when it comes to the mechanisms that deactivate the oxidase and make ROS production transient. In an article published in this issue of New Phytologist, Goto et al (2024;1763-1779 report a new negative regulator of RBOHD activity that antagonizes BIK1 during PTI responses and may contribute to finetuning the production of ROS in immunity.…”
“…Відомо, що у фотосинтезуючих тканинах найбільша концентрація внутрішньоклітинного пероксиду водню знаходиться у пероксисомах, а головним джерелом утворення Н 2 О 2 є фотодихання, що посилюється за біотичного стресу [7]. Регуляція рівня ендогенного пероксиду водню здійснюється антиоксидантними ферментами, зокрема каталазою та аскорбатпероксидазою з аскорбат-глутатіонового циклу [7][8][9]. Таким чином, пероксид водню як вторинний месенджер пов'язаний зі станом фотосинтезуючого апарату рослин.…”
Section: результати та обговоренняunclassified
“…Зокрема, супероксиддисмутаза пероксисом здатна регулювати накопичення пероксинітриту -результату взаємодії активного кисню з оксидом азоту ΝΟ [10]. Встановлено, що і оксид азоту, і пероксид водню впливають на метаболізм клітини через індуковані ними як вторинними месенджерами модифікації білків [7][8][9][10].…”
Aim. The aim of research was to analyze the activation of Triticum aestivum L. non-specific resistance by the effect of ferulic acid and NO on H2O2 content against fungal pathogen from environment in field trials. Methods. Content of endogenous H2O2 was measured in elicitor treated and infected wheat plants (cv. Oberig myronivskij and Svitanok myronivskij) during different ontogenesis phases. The extent of disease development, morphometric parameters and yield structure were analyzed. Results. The data obtained suggest that different levels of endogenous hydrogen peroxide were induced in wheat leaves by treatment. The growth and yield were stimulated. The infection damage decreased. Conclusions. The role of endogenous hydrogen peroxide is crucial for wheat defense during all vegetation period. The elicitor and donor NO induced effective defense responses and resistance in winter wheat against Erysiphe graminis.
Keywords: Triticum aestivum L., ferulic acid, NO, induced resistance, powdery mildew.
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