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    Home > Active Ingredient News > Immunology News > A war without smoke, the immune system of small plants.

    A war without smoke, the immune system of small plants.

    • Last Update: 2020-07-22
    • Source: Internet
    • Author: User
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    I believe that for many young people, including the author, they have never paid more attention to their immunity.in the past, attention to immunity may only be the patent of parents and even grandparents.however, this year, a sudden outbreak of new coronavirus has made the concept of "improving one's own immunity" more deeply rooted in the hearts of young people.although the new coronavirus has been effectively controlled in China, the new round of outbreak in foreign countries has brought us a new test for the phased victory of anti epidemic.as the name of the virus shows, this is a new type of virus that has never been encountered by human beings, and there is still no specific drug.for those unfortunately infected with the virus, they can only rely on their own immune system to resist.the immune system is the gift of nature to human beings, and it is the basic guarantee for every individual to survive.we live in a dangerous environment, and we are surrounded by hundreds of millions of pathogens every moment! The immune system is the indefatigable "national defense forces" in our body. They fight all the time on the battlefield to resist the invasion of "foreign enemies".Where is the quiet time? It's just that the immune system is carrying weight for us! The immune system is an indefatigable "defense force". For plants, they are facing more challenges from pathogens than we are human beings! Different from the fact that we can move freely and actively seek advantages and avoid disadvantages, once plants take root and sprout in a place, they will basically live there for a lifetime.moreover, they do not have a circulating immune system, let alone vaccines, the ultimate weapon against pathogens.then, how do plants resist "alien invasion" when facing various pathogens? Today, let's learn about the immune system of plants.although there is no circulatory immune system, plants have "well-equipped" innate immune systems, which can sense and limit the growth of pathogens [1].in addition, since there are no mobile immune cells in plants, every cell of plants must have the ability to sense and resist pathogens. Br / > in the course of the evolution of plant pathogens, there have been hundreds of years of evolution of "receptors".immune receptors are the "arsenal" for plants and pathogens to fight each other. They can identify all pathogens and enable plants to make appropriate immune responses [2].plant immune receptors can be divided into two categories: PRRS (pattern recognition receptors) and NLR (nucleoside binding – leucine rich repeat) receptors.in general, PRRS are located on the cell membrane and belong to the receptor kinase family, including three typical domains: extracellular ligand binding domain, transmembrane domain and intracellular kinase domain [1].PRRS located on the cell surface can monitor the presence or absence of pathogen related molecules in the extracellular environment and determine whether the cells initiate the immune response. the extracellular domain of PRRS can specifically recognize pathogen conserved PAMP (pathogen associated molecular pattern), such as bacterial flagellin and fungal chitin, and activate intracellular kinase domain through transmembrane domain, thus activating downstream immune signal. this is the first layer of plant immune system, which is called PTI (PAMP triggered immunity) [3]. PTI can initiate a series of cytological and physiological reactions to make plants resist pathogen infection, such as calcium influx, ion efflux, actin remodeling, plasmodesmata and stomatal closure, callose deposition, production of ROS, no, phosphatidylic acid, plant antitoxin and excitant, and expression of disease resistance genes [3]. PTI is sufficient to immunize plants against most pathogens. however, stubborn pathogens will never be easily "captured" and they have an elite "special forces" that can sneak into the enemy's rear and kill the enemy invisibly. plant PRRS and PTI [3] in order to break through the first layer of immune system blockade, pathogenic organisms will secrete a class of small molecules called effectors into plant cells. effector can interfere with PTI by inhibiting the translation of PRRS, inhibiting the activity of PRRS and their complexes, affecting MAPK and its downstream signal transmission, affecting vesicle transport and callose deposition. in this way, the pathogen can be infected successfully. however, the plant cells will not be "slaughtered by others". in the face of this situation, plants will activate the second layer of immune system. NLR receptors located in cells can directly or indirectly recognize effectors and make plants make a second layer of immune response, which is called ETI (effector triggered immunity). compared with PTI, ETI has a stronger response and is generally accompanied by programmed cell death. this intense cell death process, known as HR, plays an important role in plant resistance to vegetative pathogens in vivo. the downstream immune response activated by ETI was similar to that of PTI, but its intensity was higher and its duration was longer [4]. ETI and PTI induce similar immune responses [5] the interaction of PRRS and NLR can make plants resist the infection of most pathogens. however, pathogenic organisms will never surrender easily. They will continue to invent "new weapons" to break through the existing immune system and successfully infect plant cells. similarly, plants will also evolve new immune receptors to cope with the constant attack of pathogens. this is an "arms race" lasting for millions of years. Both pathogens and plants must become stronger and stronger to survive in this cruel and fierce competition. this is a war without gunpowder! We have developed stronger resistance to pathogens in the global crop breeding process. according to this genetic behavior, flor proposed the famous "gene to gene hypothesis": for any host disease resistance gene, the pathogen species has a corresponding avirulent gene [6]. it was not until the 20th century that scientists gradually realized that many plant disease resistance traits were encoded by NLR immune receptors. interestingly, in the face of various effectors, NLR receptors have almost the same protein structure [7]. how does this "stereotyped" NLR receptor protein recognize thousands of different pathogens? How do they mediate the immune response of plant cells? For more information, please listen to the next section! References: [1] zipfel, C. (2014) zipfel, C. (2014), plant pattern recognition receptors. Trends in immunology, 35 (7), 345-351. [2] toruno, T.Y., stergiopoulos, I., & amp; coaker, G. (2016). Plant pattern effectors: cellular probes interacting with plant defenses in spatial and temporal manipulators. Annual review of Phytopathology, 54 (1), 419-441 [41 (9), 419-441. [3] 3] 3] 3] 3] VEGETATO, T.Y., y, stergiopoulos, I., & amp; coaker, G. (2016), plant-pattern effectors: cellular effectors: cellular proteins: interacting with plant defenses in spatial and temporal and temporary manipulators, annual review of Phytopathology, 54 (1), 419-441, 419-44yu, X., Feng, B., He, P., & Shan, L. (2017). From Chaos to Harmony: Responses and Signaling upon Microbial Pattern Recognition. Annual Review of Phytopathology, 55(1), 109-137.【4】Cui, H., Tsuda, K., & Parker, J. E. (2015). Effector-triggered immunity: from pathogen perception to robust defense. Annual review of plant biology, 66, 487-511.【5】Lolle, S., Stevens, D., & Coaker, G. (2020). Plant NLR-triggered immunity: from receptor activation to downstream signaling. Current Opinion in Immunology, 62, 99-105.【6】Flor, H. H. (1971). Current status of the gene-for-gene concept. Annual review of phytopathology, 9(1), 275-296.【7】Monteiro, F., & Nishimura, M. T. (2018). Structural, functional, and genetic diversity of plant NLR proteins: an evolved resource for rational engineering of plant immunity. Annual review of Phytopathology, 56, 243-267
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