scholarly journals Elicitor and Receptor Molecules: Orchestrators of Plant Defense and Immunity

2020 ◽  
Vol 21 (3) ◽  
pp. 963 ◽  
Author(s):  
Nurul Azmina Abdul Malik ◽  
Ilakiya Sharanee Kumar ◽  
Kalaivani Nadarajah

Pathogen-associated molecular patterns (PAMPs), microbe-associated molecular patterns (MAMPs), herbivore-associated molecular patterns (HAMPs), and damage-associated molecular patterns (DAMPs) are molecules produced by microorganisms and insects in the event of infection, microbial priming, and insect predation. These molecules are then recognized by receptor molecules on or within the plant, which activates the defense signaling pathways, resulting in plant’s ability to overcome pathogenic invasion, induce systemic resistance, and protect against insect predation and damage. These small molecular motifs are conserved in all organisms. Fungi, bacteria, and insects have their own specific molecular patterns that induce defenses in plants. Most of the molecular patterns are either present as part of the pathogen’s structure or exudates (in bacteria and fungi), or insect saliva and honeydew. Since biotic stresses such as pathogens and insects can impair crop yield and production, understanding the interaction between these organisms and the host via the elicitor–receptor interaction is essential to equip us with the knowledge necessary to design durable resistance in plants. In addition, it is also important to look into the role played by beneficial microbes and synthetic elicitors in activating plants’ defense and protection against disease and predation. This review addresses receptors, elicitors, and the receptor–elicitor interactions where these components in fungi, bacteria, and insects will be elaborated, giving special emphasis to the molecules, responses, and mechanisms at play, variations between organisms where applicable, and applications and prospects.

2021 ◽  
Author(s):  
Brahim Oubaha ◽  
Abdellah Ezzanad ◽  
Hernando José Bolívar-Anillo

Potato (Solanum tuberosum) as a food source and culinary ingredient varies is the fourth most produced noncereal crop in the world. Among multiple biotic stresses, late blight caused by Phytophthora infestans is the most destructive disease. Control of this pathogen is usually by the synthetic fungicides which have been fueled by the public concern about toxicity and environmental impact and development of pathogens resistance. Biological control agents (BCAs) seems the potentially alternative to these pesticides, biological disease control is now recognized and constitute an important tool in integrated pest management. BCAs strains should be able to protect the host plant from pathogens and fulfill the requirement for strong colonization. Bacteria such as Bacillus, Pseudomonas and Streptomyces and fungi such as Trichoderma and Penicillium were the most reported as a BCA against P. infestans using different direct antagonistic mode on the pathogen (via e.g. parasitism, antibiosis, or competition) or via exerting their biocontrol activity indirectly by induction in the plant of an induced systemic resistance to the pathogen. In this study, we present an overview and discussion of the use of beneficial microbes (bacteria and fungi) as novel BCAs for biocontrol of P. infestans.


Author(s):  
Christopher Stephens ◽  
Kim E Hammond-Kosack ◽  
Kostya Kanyuka

Abstract With the requirement to breed more productive crop plants in order to feed a growing global population, compounded by increasingly widespread resistance to pesticides exhibited by pathogens, plant immunity is becoming an increasingly important area of research. Of the genes that contribute to disease resistance, the wall-associated receptor-like kinases (WAKs) are increasingly shown to play a major role, in addition to their contribution to plant growth and development or tolerance to abiotic stresses. Being transmembrane proteins, WAKs form a central pillar of a plant cell’s ability to monitor and interact with the extracellular environment. Found in both dicots and monocots, WAKs have been implicated in defence against pathogens with diverse lifestyles and contribute to plant immunity in a variety of ways. Whilst some act as cell surface-localized immune receptors recognizing either pathogen- or plant-derived invasion molecules (e.g. effectors or damage-associated molecular patterns, respectively), others promote innate immunity through cell wall modification and strengthening, thus limiting pathogen intrusion. The ability of some WAKs to provide both durable resistance against pathogens and other agronomic benefits makes this gene family important targets in the development of future crop ideotypes and important to a greater understanding of the complexity and robustness of plant immunity.


APOPTOSIS ◽  
2021 ◽  
Vol 26 (3-4) ◽  
pp. 152-162
Author(s):  
Atsushi Murao ◽  
Monowar Aziz ◽  
Haichao Wang ◽  
Max Brenner ◽  
Ping Wang

AbstractDamage-associated molecular patterns (DAMPs) are endogenous molecules which foment inflammation and are associated with disorders in sepsis and cancer. Thus, therapeutically targeting DAMPs has potential to provide novel and effective treatments. When establishing anti-DAMP strategies, it is important not only to focus on the DAMPs as inflammatory mediators but also to take into account the underlying mechanisms of their release from cells and tissues. DAMPs can be released passively by membrane rupture due to necrosis/necroptosis, although the mechanisms of release appear to differ between the DAMPs. Other types of cell death, such as apoptosis, pyroptosis, ferroptosis and NETosis, can also contribute to DAMP release. In addition, some DAMPs can be exported actively from live cells by exocytosis of secretory lysosomes or exosomes, ectosomes, and activation of cell membrane channel pores. Here we review the shared and DAMP-specific mechanisms reported in the literature for high mobility group box 1, ATP, extracellular cold-inducible RNA-binding protein, histones, heat shock proteins, extracellular RNAs and cell-free DNA.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Kiran Todkar ◽  
Lilia Chikhi ◽  
Véronique Desjardins ◽  
Firas El-Mortada ◽  
Geneviève Pépin ◽  
...  

AbstractMost cells constitutively secrete mitochondrial DNA and proteins in extracellular vesicles (EVs). While EVs are small vesicles that transfer material between cells, Mitochondria-Derived Vesicles (MDVs) carry material specifically between mitochondria and other organelles. Mitochondrial content can enhance inflammation under pro-inflammatory conditions, though its role in the absence of inflammation remains elusive. Here, we demonstrate that cells actively prevent the packaging of pro-inflammatory, oxidized mitochondrial proteins that would act as damage-associated molecular patterns (DAMPs) into EVs. Importantly, we find that the distinction between material to be included into EVs and damaged mitochondrial content to be excluded is dependent on selective targeting to one of two distinct MDV pathways. We show that Optic Atrophy 1 (OPA1) and sorting nexin 9 (Snx9)-dependent MDVs are required to target mitochondrial proteins to EVs, while the Parkinson’s disease-related protein Parkin blocks this process by directing damaged mitochondrial content to lysosomes. Our results provide insight into the interplay between mitochondrial quality control mechanisms and mitochondria-driven immune responses.


Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2566
Author(s):  
María Julia Lamberti ◽  
Annunziata Nigro ◽  
Vincenzo Casolaro ◽  
Natalia Belén Rumie Vittar ◽  
Jessica Dal Col

Immunogenic cell death (ICD) in cancer is a functionally unique regulated form of stress-mediated cell death that activates both the innate and adaptive immune response against tumor cells. ICD makes dying cancer cells immunogenic by improving both antigenicity and adjuvanticity. The latter relies on the spatiotemporally coordinated release or exposure of danger signals (DAMPs) that drive robust antigen-presenting cell activation. The expression of DAMPs is often constitutive in tumor cells, but it is the initiating stressor, called ICD-inducer, which finally triggers the intracellular response that determines the kinetics and intensity of their release. However, the contribution of cell-autonomous features, such as the epigenetic background, to the development of ICD has not been addressed in sufficient depth. In this context, it has been revealed that several microRNAs (miRNAs), besides acting as tumor promoters or suppressors, can control the ICD-associated exposure of some DAMPs and their basal expression in cancer. Here, we provide a general overview of the dysregulation of cancer-associated miRNAs whose targets are DAMPs, through which new molecular mediators that underlie the immunogenicity of ICD were identified. The current status of miRNA-targeted therapeutics combined with ICD inducers is discussed. A solid comprehension of these processes will provide a framework to evaluate miRNA targets for cancer immunotherapy.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1615
Author(s):  
Zhongwei Zhang ◽  
Yosuke Kurashima

It is well known that mast cells (MCs) initiate type I allergic reactions and inflammation in a quick response to the various stimulants, including—but not limited to—allergens, pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs). MCs highly express receptors of these ligands and proteases (e.g., tryptase, chymase) and cytokines (TNF), and other granular components (e.g., histamine and serotonin) and aggravate the allergic reaction and inflammation. On the other hand, accumulated evidence has revealed that MCs also possess immune-regulatory functions, suppressing chronic inflammation and allergic reactions on some occasions. IL-2 and IL-10 released from MCs inhibit excessive immune responses. Recently, it has been revealed that allergen immunotherapy modulates the function of MCs from their allergic function to their regulatory function to suppress allergic reactions. This evidence suggests the possibility that manipulation of MCs functions will result in a novel approach to the treatment of various MCs-mediated diseases.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Weng Sheng Kong ◽  
Naohiro Tsuyama ◽  
Hiroko Inoue ◽  
Yun Guo ◽  
Sho Mokuda ◽  
...  

AbstractBreastfeeding influences the immune system development in infants and may even affect various immunological responses later in life. Breast milk provides a rich source of early nutrition for infant growth and development. However, the presence of certain compounds in breast milk, related to an unhealthy lifestyle or the diet of lactating mothers, may negatively impact infants. Based on a cohort study of atopic dermatitis (AD), we find the presence of damage-associated molecular patterns (DAMPs) activity in the mother’s milk. By non-targeted metabolomic analysis, we identify the long-chain saturated fatty acids (LCSFA) as a biomarker DAMPs (+) breast milk samples. Similarly, a mouse model in which breastfed offspring are fed milk high in LCSFA show AD onset later in life. We prove that LCSFA are a type of damage-associated molecular patterns, which initiate a series of inflammatory events in the gut involving type 3 innate lymphoid cells (ILC3s). A remarkable increase in inflammatory ILC3s is observed in the gut, and the migration of these ILC3s to the skin may be potential triggers of AD. Gene expression analysis of ILC3s isolated from the gut reveal upregulation of genes that increase ILC3s and chemokines/chemokine receptors, which may play a role in ILC migration to the skin. Even in the absence of adaptive immunity, Rag1 knockout mice fed a high-LCSFA milk diet develop eczema, accompanied by increased gut ILC3s. We also present that gut microbiota of AD-prone PA milk-fed mice is different from non-AD OA/ND milk-fed mice. Here, we propose that early exposure to LCSFAs in infants may affect the balance of intestinal innate immunity, inducing a highly inflammatory environment with the proliferation of ILC3s and production of interleukin-17 and interleukin-22, these factors may be potential triggers or worsening factors of AD.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 930
Author(s):  
Rianne D. W. Vaes ◽  
Lizza E. L. Hendriks ◽  
Marc Vooijs ◽  
Dirk De Ruysscher

Radiation therapy (RT) can induce an immunogenic variant of regulated cell death that can initiate clinically relevant tumor-targeting immune responses. Immunogenic cell death (ICD) is accompanied by the exposure and release of damage-associated molecular patterns (DAMPs), chemokine release, and stimulation of type I interferon (IFN-I) responses. In recent years, intensive research has unraveled major mechanistic aspects of RT-induced ICD and has resulted in the identification of immunogenic factors that are released by irradiated tumor cells. However, so far, only a limited number of studies have searched for potential biomarkers that can be used to predict if irradiated tumor cells undergo ICD that can elicit an effective immunogenic anti-tumor response. In this article, we summarize the available literature on potential biomarkers of RT-induced ICD that have been evaluated in cancer patients. Additionally, we discuss the clinical relevance of these findings and important aspects that should be considered in future studies.


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