ROS accumulation and associated cell death mediates susceptibility to Alternaria brassicae in Arabidopsis accessions

Mandal, Sayanti; Rajarammohan, Sivasubramanian; Kaur, Jagreet

doi:10.1016/j.pmpp.2019.06.001

Cited by 23 publications

(12 citation statements)

References 29 publications

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“…Previous studies on the infection of A. brassicae have identified two critical time points viz. 2 and 4 days post inoculation wherein it represented the time points before and after the mycelia penetrates the host tissue ( Mandal et al, 2019 ). Therefore, we studied the expression of AbrNLP1 and AbrNLP2 at these time points.…”

Section: Resultsmentioning

confidence: 99%

Functional Characterization of the Nep1-Like Protein Effectors of the Necrotrophic Pathogen – Alternaria brassicae

et al. 2021

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Alternaria brassicae is an important necrotrophic pathogen that infects the Brassicaceae family. A. brassicae, like other necrotrophs, also secretes various proteinaceous effectors and metabolites that cause cell death to establish itself in the host. However, there has been no systematic study of A. brassicae effectors and their roles in pathogenesis. The availability of the genome sequence of A. brassicae in public domain has enabled the search for effectors and their functional characterization. Nep1-like proteins (NLPs) are a superfamily of proteins that induce necrosis and ethylene biosynthesis. They have been reported from a variety of microbes including bacteria, fungi, and oomycetes. In this study, we identified two NLPs from A. brassicae viz. AbrNLP1 and AbrNLP2 and functionally characterized them. Although both AbrNLPs were found to be secretory in nature, they localized differentially inside the plant. AbrNLP2 was found to induce necrosis in both host and non-host species, while AbrNLP1 could not induce necrosis in both species. Additionally, AbrNLP2 was shown to induce pathogen-associated molecular pattern (PAMP)-triggered immunity in both host and non-host species. Overall, our study indicates that AbrNLPs are functionally and spatially (subcellular location) distinct and may play different but important roles during the pathogenesis of A. brassicae.

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Section: Resultsmentioning

confidence: 99%

Functional Characterization of the Nep1-Like Protein Effectors of the Necrotrophic Pathogen – Alternaria brassicae

et al. 2021

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“…GO analysis showed that 466 and 830 downregulated DEGs in OsERF65OE plants were associated with catalytic activity under both mock treatment and R. solani inoculation (Figures 4e and S6d ), especially for the activities of peroxidase, oxidoreductase and antioxidant (Figure 4e ), which have been well documented to participate in ROS scavenging (Liu et al, 2021 ; Torres et al, 2006 ). Increasing evidence suggests that ROS accumulation can lead to cell death and is beneficial to the infection of necrotrophic pathogens (Li et al, 2019 ; Mandal et al, 2019 ). We therefore focused on peroxidase genes, which directly function in scavenging H 2 O 2 , one of the important components of ROS.…”

Section: Resultsmentioning

confidence: 99%

“…The prevalence of ShB has significantly increased over the past decades, threatening rice production, accounting for 10%–30% yield loss annually and a reduction in grain quality (Molla et al, 2020 ; Zhu et al, 2019 ). Although cell death or hypersensitivity reactions in the host are beneficial for improving host resistance to biotrophic infection by limiting or cutting off the nutrient supply, they promote susceptibility to necrotrophy (Li et al, 2019 ; Mandal et al, 2019 ). R. solani , as a typically necrotrophic fungus, generally absorbs nutrients from dead cells or tissues for their reproduction, and during infection the pathogen can secrete large amounts of cell wall‐degrading enzymes, toxins and effector proteins to promote cell death (Bhaskar Rao et al, 2020 ; Oliver & Solomon, 2010 ; Singh et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Knockout of transcription factor OsERF65 enhances ROS scavenging ability and confers resistance to rice sheath blight

Xie,

Cao,

et al. 2023

Molecular Plant Pathology

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Rice sheath blight (ShB) is a devastating disease that severely threatens rice production worldwide. Induction of cell death represents a key step during infection by the ShB pathogen Rhizoctonia solani. Nonetheless, the underlying mechanisms remain largely unclear. In the present study, we identified a rice transcription factor, OsERF65, that negatively regulates resistance to ShB by suppressing cell death. OsERF65 was significantly upregulated by R. solani infection in susceptible cultivar Lemont and was highly expressed in the leaf sheath. Overexpression of OsERF65 (OsERF65OE) decreased rice resistance, while the knockout mutant (oserf65) exhibited significantly increased resistance against ShB. The transcriptome assay revealed that OsERF65 repressed the expression of peroxidase genes after R. solani infection. The antioxidative enzyme activity was significantly increased in oserf65 plants but reduced in OsERF65OE plants. Consistently, hydrogen peroxide content was apparently reduced in oserf65 plants but accumulated in OsERF65OE plants. OsERF65 directly bound to the GCC box in the promoter regions of four peroxidase genes and suppressed their transcription, reducing the ability to scavenge reactive oxygen species (ROS). The oserf65 mutant exhibited a slight decrease in plant height but increased grain yield. Overall, our results revealed an undocumented role of OsERF65 that acts as a crucial regulator of rice resistance to R. solani and a potential target for improving both ShB resistance and rice yield.

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“… 32 Similarly, NLRP12 was demonstrated to be crucial in the regulation of interferon and cytokine production, as well as the maintenance of immune homeostasis. 33 Moreover, cell death mediated by NLR-inflammasome activation protects host cells from attack by pathogens, by impeding the nutrient supply to the pathogens, 34 and the activated bystander cells can also secrete antimicrobial agents that arrest pathogen expansion and disease aggravation. 35 However, the specific molecular basis of the causal relationship between NLRs and IBD remains enigmatic.…”

Section: Nlrs Family and Signaling Mechanisms In The Intestinal Epith...mentioning

confidence: 99%

NOD-like receptors mediate homeostatic intestinal epithelial barrier function: promising therapeutic targets for inflammatory bowel disease

Zhou,

Zhang,

Tan

et al. 2023

Therap Adv Gastroenterol

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Inflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease that involves host genetics, the microbiome, and inflammatory responses. The current consensus is that the disruption of the intestinal mucosal barrier is the core pathogenesis of IBD, including intestinal microbial factors, abnormal immune responses, and impaired intestinal mucosal barrier. Cumulative data show that nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs) are dominant mediators in maintaining the homeostasis of the intestinal mucosal barrier, which play critical roles in sensing the commensal microbiota, maintaining homeostasis, and regulating intestinal inflammation. Blocking NLRs inflammasome activation by botanicals may be a promising way to prevent IBD progression. In this review, we systematically introduce the multiple roles of NLRs in regulating intestinal mucosal barrier homeostasis and focus on summarizing the activities and potential mechanisms of natural products against IBD. Aiming to propose new directions on the pathogenesis and precise treatment of IBD

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ROS accumulation and associated cell death mediates susceptibility to Alternaria brassicae in Arabidopsis accessions

Cited by 23 publications

References 29 publications

Functional Characterization of the Nep1-Like Protein Effectors of the Necrotrophic Pathogen – Alternaria brassicae

Functional Characterization of the Nep1-Like Protein Effectors of the Necrotrophic Pathogen – Alternaria brassicae

Knockout of transcription factor OsERF65 enhances ROS scavenging ability and confers resistance to rice sheath blight

NOD-like receptors mediate homeostatic intestinal epithelial barrier function: promising therapeutic targets for inflammatory bowel disease

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