RXLR效应分子抑制植物免疫机制研究进展

植物病原卵菌是一类农业生产上为害巨大的病原物,其分泌大量的RXLR效应分子进入寄主植物细胞并干扰植物免疫系统,以协助病原菌成功侵染。尽管有一小部分RXLR效应分子会被植物识别成为无毒蛋白,但大部分RXLR效应分子则会逃避识别和抑制植物免疫。随着高通量测序和蛋白互作技术的广泛应用,大量RXLR效应分子干扰植物免疫的分子机制已经被揭示。本文综述了RXLR效应分子操纵植物免疫系统的分子策略,探讨了RXLR效应分子与植物免疫互作的研究方向和应用前景。     

可变剪接在植物免疫中的研究进展

可变剪接是生物重要的转录后修饰过程,是转录组和蛋白组多样性的重要来源.可变剪接参与了植物众多生理过程,包括植物昼夜节律、生长发育等,在植物响应生物和非生物胁迫过程中尤为普遍.近年来,可变剪接被认为是植物抵御病原菌侵染的重要调控机制.本文综述了可变剪接在植物免疫各个层面的调控作用,包括调节重要免疫受体、R基因、激素信号路...     

Tn-seq identifies Ralstonia solanacearum genes required for tolerance of plant immunity induced by exogenous salicylic acid

Ralstonia solanacearum, the causal agent of the devastating bacterial wilt disease, is of particular interest to the scientific community. The repertoire of type III effectors plays an important role in the evasion of plant immunity, but tolerance to plant immunity is also crucial for the survival and virulence of R. solanacearum. Nevertheless, a systematic study of R. solanacearum tolerance to plant immunity is lacking. In this study, we used exogenous salicylic acid (SA) to improve the immunity of tomato plants, followed by transposon insertion sequencing (Tn-seq) analysis and the identification of R. solanacearum genes associated with tolerance to plant immunity. Target gene deletion revealed that the lipopolysaccharide (LPS) production genes RS_RS02830, RS_RS03460, and RS_RS03465 are essential for R. solanacearum tolerance to plant immunity, and their expression is induced by plant immunity, thereby expanding our knowledge of the pathogenic function of R. solanacearum LPS. SA treatment increased the relative abundance of transposon insertion mutants of four genes, including two genes with unknown function, RS_RS11975 and RS_RS07760. Further verification revealed that deletion of RS_RS11975 or RS_RS07760 resulted in reduced in vivo competitive indexes but increased tolerance to plant immunity induced by SA treatment, suggesting that these two genes contribute to the trade-off between tolerance to plant immunity and fitness cost. In conclusion, this work identified and validated R. solanacearum genes required for tolerance to plant immunity and provided essential information for a more complete view of the interaction between R. solanacearum and the host plant.     

CRISPR/Cas systems versus plant viruses: engineering plant immunity and beyond

Molecular engineering of plant immunity to confer resistance against plant viruses holds great promise for mitigating crop losses and improving plant productivity and yields, thereby enhancing food security. Several approaches have been employed to boost immunity in plants by interfering with the transmission or lifecycles of viruses. In this review, we discuss the successful application of clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein (Cas) (CRISPR/Cas) systems to engineer plant immunity, increase plant resistance to viruses, and develop viral diagnostic tools. Furthermore, we examine the use of plant viruses as delivery systems to engineer virus resistance in plants and provide insight into the limitations of current CRISPR/Cas approaches and the potential of newly discovered CRISPR/Cas systems to engineer better immunity and develop better diagnostics tools for plant viruses. Finally, we outline potential solutions to key challenges in the field to enable the practical use of these systems for crop protection and viral diagnostics.

CRISPR-Cas systems unlock the potential of understanding the molecular basis of plant virus interactions, engineering immunity against plant viruses, and developing sensitive and specific diagnostics.     

Plant cytokine or phytocytokine

Peptide hormones play an important role in plant growth and development. Some of them are secreted by stem cells and also regulate plant immunity through cell-cell communication and reprogramming the expression of immune related genes, such as CLAVATA3p (CLV3p) and phytosulfokine (PSK). These peptides play similar roles as cytokines in plant innate immunity. As explosive progress of plant omics, more and more such functional peptides will be discovered. I recommend that they should be named as plant cytokines or phytocytokines. This nomenclature will be convenient for study of plant secretory peptides and plant innate immunity.     

Recent advances in plant immunity: recognition, signaling, response, and evolution

Innate immune system is employed by plants to defend against phytopathogenic microbes through specific perception of non-self molecules and subsequent initiation of resistance responses. Current researches elucidate that plants mostly rely on cell surface-located pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat proteins (NB-LRRs) to recognize pathogen-associated molecular patterns (PAMPs) and effector proteins from microbial pathogens, initiating PAMP- and effector-triggered immunity (PTI and ETI), respectively. Some pathogenic bacterial effector proteins are usually secreted into plant cells and play a virulence function by suppressing plant PTI, implying an evolutionary process of plant immunity from PTI to ETI. In the past several years, a great progress has been achieved to reveal fascinating molecular mechanisms underlying the pathogenic recognition, resistance signaling transduction, and plant immunity evolution. Here, we summarized the latest breakthroughs about these topics, and offered an integral understanding of plant molecular immunity.     

Elicitation and suppression of microbe-associated molecular pattern-triggered immunity in plant-microbe interactions

Recent studies have uncovered fascinating molecular mechanisms underlying plant-microbe interactions that coevolved dynamically. As in animals, the primary plant innate immunity is immediately triggered by the detection of common pathogen- or microbe-associated molecular patterns (PAMPs/MAMPs). Different MAMPs are often perceived by distinct cell-surface pattern-recognition receptors (PRRs) and activate convergent intracellular signalling pathways in plant cells for broad-spectrum immunity. Successful pathogens, however, have evolved multiple virulence factors to suppress MAMP-triggered immunity. Specifically, diverse pathogenic bacteria have employed the type III secretion system to deliver a repertoire of virulence effector proteins to interfere with host immunity and promote pathogenesis. Plants challenged by pathogens have evolved the secondary plant innate immunity. In particular, some plants possess the specific intracellular disease resistance (R) proteins to effectively counteract virulence effectors of pathogens for effector-triggered immunity. This potent but cultivar-specific effector-triggered immunity occurs rapidly with localized programmed cell death/hypersensitive response to limit pathogen proliferation and disease development. Remarkably, bacteria have further acquired virulence effectors to block effector-triggered immunity. This review covers the latest findings in the dynamics of MAMP-triggered immunity and its interception by virulence factors of pathogenic bacteria.     

Autophagy controls plant basal immunity in a pathogenic lifestyle-dependent manner

Plant genomes harbor autophagy-related (ATG) genes that encode major components of the eukaryotic autophagic machinery. Autophagy in plants has been functionally linked to senescence, oxidative stress adaptation and the nutrient starvation response. In addition, plant autophagy has been assigned negative ('anti-death') and positive ('pro-death') regulatory functions in controlling cell death programs that establish sufficient immunity to microbial infection. The role of autophagy in plant disease and basal immunity to microbial infection has, however, not been studied in detail. We have employed a series of autophagy-deficient genotypes of the genetic model plant Arabidopsis thaliana in various infection systems. Genotypes lacking ATG5, ATG10 or ATG18a develop spreading necrosis and enhanced disease susceptibility upon infection with toxin-producing pathogens preferring a necrotrophic lifestyle. These findings suggest that autophagy positively controls the containment of host tissue integrity upon infections by host-destructive microbes. In contrast, autophagy-deficient genotypes exhibit markedly increased immunity to infections by biotrophic pathogens through altered homeostasis of the plant hormone salicylic acid, thus suggesting an additional negative regulatory role of autophagy in plant basal immunity. In sum, our findings suggest that the role of plant autophagy in immunity cannot be generalized, and depends critically on the lifestyle and infection strategy of invading microbes.     

Plant immunity: Evolutionary insights from PBS1, Pto and RIN4

Two layers of plant immune systems are used by plants to defend against phytopathogens. The first layer is pathogen-associate molecular patterns (PAMPs)-triggered immunity (PTI), which is activated by plant cell-surface pattern recognition receptors (PRRs) upon perception of microbe general elicitors. The second layer is effector-triggered immunity (ETI), which is initiated by specific recognition of pathogen type III secreted effectors (T3SEs) with plant intracellular resistance (R) proteins. Current opinions agree that ETI was evolved from PTI, and the impetus for the evolution of plant immunity is pathogen T3SEs, which exhibit virulence functions through blocking PTI, but show avirulence functions for triggering ETI. A decoy model was put forward and explained that the avirulence targets of pathogen T3SEs were evolved as decoys to compete with the virulence targets for binding with pathogen T3SEs. However, little direct evidence for the evolutionary mode has been offered. Here we reviewed the recent progresses about Pto, PBS1 and RIN4 to present our viewpoints about the evolution of plant immunity.Key words: plant immunity, evolution, Pto, PBS1, RIN4     

Plant innate immunity: An updated insight into defense mechanism

Plants are invaded by an array of pathogens of which only a few succeed in causing disease. The attack by others is countered by a sophisticated immune system possessed by the plants. The plant immune system is broadly divided into two, viz. microbial-associated molecular-patterns-triggered immunity (MTI) and effector-triggered immunity (ETI). MTI confers basal resistance, while ETI confers durable resistance, often resulting in hypersensitive response. Plants also possess systemic acquired resistance (SAR), which provides long-term defense against a broad-spectrum of pathogens. Salicylic-acid-mediated systemic acquired immunity provokes the defense response throughout the plant system during pathogen infection at a particular site. Trans-generational immune priming allows the plant to heritably shield their progeny towards pathogens previously encountered. Plants circumvent the viral infection through RNA interference phenomena by utilizing small RNAs. This review summarizes the molecular mechanisms of plant immune system, and the latest breakthroughs reported in plant defense. We discuss the plant–pathogen interactions and integrated defense responses in the context of presenting an integral understanding in plant molecular immunity.     

Loss of susceptibility as a novel breeding strategy for durable and broad-spectrum resistance

Recent studies on plant immunity have suggested that a pathogen should suppress induced plant defense in order to infect a plant species, which otherwise would have been a nonhost to the pathogen. For this purpose, pathogens exploit effector molecules to interfere with different layers of plant defense responses. In this review, we summarize the latest findings on plant factors that are activated by pathogen effectors to suppress plant immunity. By looking from a different point of view into host and nonhost resistance, we propose a novel breeding strategy: disabling plant disease susceptibility genes (S-genes) to achieve durable and broad-spectrum resistance.     

Integrated systems view on networking by hormones in Arabidopsis immunity reveals multiple crosstalk for cytokinin

Phytohormones signal and combine to maintain the physiological equilibrium in the plant. Pathogens enhance host susceptibility by modulating the hormonal balance of the plant cell. Unlike other plant hormones, the detailed role of cytokinin in plant immunity remains to be fully elucidated. Here, extensive data mining, including of pathogenicity factors, host regulatory proteins, enzymes of hormone biosynthesis, and signaling components, established an integrated signaling network of 105 nodes and 163 edges. Dynamic modeling and system analysis identified multiple cytokinin-mediated regulatory interactions in plant disease networks. This includes specific synergism between cytokinin and salicylic acid pathways and previously undiscovered aspects of antagonism between cytokinin and auxin in plant immunity. Predicted interactions and hormonal effects on plant immunity are confirmed in subsequent experiments with Pseudomonas syringae pv tomato DC3000 and Arabidopsis thaliana. Our dynamic simulation is instrumental in predicting system effects of individual components in complex hormone disease networks and synergism or antagonism between pathways.     

Effector-triggered immunity signaling: from gene-for-gene pathways to protein-protein interaction networks

In its simplicity and testability, Flor's gene-for-gene hypothesis has been a powerful driver in plant immunity research for decades. Once the molecular underpinnings of gene-for-gene resistance had come into sharper focus, there was a reassessment of Flor's hypothesis and a name change to effector-triggered immunity. As implied by the name change and exemplified by pioneering studies, plant immunity is increasingly described in terms of protein rather than genetic interactions. This progress leads to a reinterpretation of old concepts of pathogen recognition and resistance signaling and, of course, opens up new questions. Here, we provide a brief historical overview of resistance gene function and how a new focus on protein interactions can lead to a deeper understanding of the logic of plant innate immunity signaling.     

Autophagy controls plant basal immunity in a pathogenic lifestyle-dependent manner

Plant genomes harbor autophagy-related (ATG) genes that encode major components of the eukaryotic autophagic machinery. Autophagy in plants has been functionally linked to senescence, oxidative stress adaptation and the nutrient starvation response. In addition, plant autophagy has been assigned negative (‘anti-death’) and positive (‘pro-death’) regulatory functions in controlling cell death programs that establish sufficient immunity to microbial infection. The role of autophagy in plant disease and basal immunity to microbial infection has, however, not been studied in detail. We have employed a series of autophagy-deficient genotypes of the genetic model plant Arabidopsis thaliana in various infection systems. Genotypes lacking ATG5, ATG10 or ATG18a develop spreading necrosis and enhanced disease susceptibility upon infection with toxin-producing pathogens preferring a necrotrophic lifestyle. These findings suggest that autophagy positively controls the containment of host tissue integrity upon infections by host-destructive microbes. In contrast, autophagy-deficient genotypes exhibit markedly increased immunity to infections by biotrophic pathogens through altered homeostasis of the plant hormone salicylic acid, thus suggesting an additional negative regulatory role of autophagy in plant basal immunity. In sum, our findings suggest that the role of plant autophagy in immunity cannot be generalized, and depends critically on the lifestyle and infection strategy of invading microbes.     

New faces in plant innate immunity: heterotrimeric G proteins

Co-existence of species seems to inevitably result in origin of parasitism and hence development of molecular mechanisms of attack and defense. Certain similarities between plant and animal defense systems point to an ancient inheritance of the innate immunity. Heterotrimeric G proteins are structurally conserved signaling molecules connecting plasma membrane bound receptors to cytoplasmic effectors. They were found in most eukaryotic organisms. Their role in human pathophysiology and animal diseases was well established. In plants these proteins were also recently implicated in innate immunity. However, molecular mechanisms governed by G proteins and providing resistance against plant pathogens seem to be different from those in animal systems and largely remain elusive. In this review we attempted to sketch current ideas of plant defense system and to present a contemporary status of heterotrimeric G proteins in plant innate immunity.     

Plant immunity: a lesson from pathogenic bacterial effector proteins

Phytopathogenic bacteria inject an array of effector proteins into host cells to alter host physiology and assist the infection process. Some of these effectors can also trigger disease resistance as a result of recognition in the plant cell by cytoplasmic immune receptors. In addition to effector-triggered immunity, plants immunity can be triggered upon the detection of Pathogen/Microbe-Associated Molecular Patterns by surface-localized immune receptors. Recent progress indicates that many bacterial effector proteins use a variety of biochemical properties to directly attack key components of PAMP-triggered immunity and effector-triggered immunity, providing new insights into the molecular basis of plant innate immunity. Emerging evidence indicate that the evolution of disease resistance in plants is intimately linked to the mechanism by which bacterial effectors promote parasitism. This review focuses on how these studies have conceptually advanced our understanding of plant–pathogen interactions.