RESUMEN
Plant pathogens destroy crops and cause severe yield losses, leading to an insufficient food supply to sustain the human population. Apart from relying on natural plant immune systems to combat biological agents or waiting for the appropriate evolutionary steps to occur over time, researchers are currently seeking new breakthrough methods to boost disease resistance in plants through genetic engineering. Here, we summarize the past two decades of research in disease resistance engineering against an assortment of pathogens through modifying the plant immune components (internal and external) with several biotechnological techniques. We also discuss potential strategies and provide perspectives on engineering plant immune systems for enhanced pathogen resistance and plant fitness.
Asunto(s)
Sistemas CRISPR-Cas , Resistencia a la Enfermedad , Humanos , Resistencia a la Enfermedad/genética , Ingeniería Genética/métodos , Productos Agrícolas/genética , Caminata , Edición Génica/métodos , Enfermedades de las Plantas/genética , Genoma de Planta , FitomejoramientoRESUMEN
During pathogenesis, effector proteins are secreted from the pathogen to the host plant to provide virulence activity for invasion of the host. However, once the host plant recognizes one of the delivered effectors, effector-triggered immunity activates a robust immune and hypersensitive response (HR). In planta, the effector AvrRps4 is processed into the N-terminus (AvrRps4N ) and the C-terminus (AvrRps4C ). AvrRps4C is sufficient to trigger HR in turnip and activate AtRRS1/AtRPS4-mediated immunity in Arabidopsis; on the other hand, AvrRps4N induces HR in lettuce. Furthermore, AvrRps4N -mediated HR requires a conserved arginine at position 112 (R112), which is also important for full-length AvrRps4 (AvrRps4F ) processing. Here, we show that effector processing and effector recognition in lettuce are uncoupled for the AvrRps4 family. In addition, we compared effector recognition by lettuce of AvrRps4 and its homologues, HopK1 and XopO. Interestingly, unlike for AvrRps4 and HopK1, mutation of the conserved R111 in XopO by itself was insufficient to abolish recognition. The combination of amino acid substitutions arginine 111 to leucine with glutamate 114 to lysine abolished the XopO-mediated HR, suggesting that AvrRps4 family members have distinct structural requirements for perception by lettuce. Together, our results provide an insight into the processing and recognition of AvrRps4 and its homologues.
Asunto(s)
Arabidopsis , Lactuca , Arginina/metabolismo , Lactuca/genética , Enfermedades de las Plantas , Inmunidad de la Planta , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , VirulenciaRESUMEN
Plant immunity is mediated in large part by specific interactions between a host resistance protein and a pathogen effector protein, named effector-triggered immunity (ETI). ETI needs to be tightly controlled both positively and negatively to enable normal plant growth because constitutively activated defense responses are detrimental to the host. In previous work, we reported that mutations in SUPPRESSOR OF rps4-RLD1 (SRFR1), identified in a suppressor screen, reactivated EDS1-dependent ETI to Pseudomonas syringae pv. tomato (Pto) DC3000. Besides, mutations in SRFR1 boosted defense responses to the generalist chewing insect Spodoptera exigua and the sugar beet cyst nematode Heterodera schachtii. Here, we show that mutations in SRFR1 enhance susceptibility to the fungal necrotrophs Fusarium oxysporum f. sp. lycopersici (FOL) and Botrytis cinerea in Arabidopsis. To translate knowledge obtained in AtSRFR1 research to crops, we generated SlSRFR1 alleles in tomato using a CRISPR/Cas9 system. Interestingly, slsrfr1 mutants increased expression of SA-pathway defense genes and enhanced resistance to Pto DC3000. In contrast, slsrfr1 mutants elevated susceptibility to FOL. Together, these data suggest that SRFR1 is functionally conserved in both Arabidopsis and tomato and functions antagonistically as a negative regulator to (hemi-) biotrophic pathogens and a positive regulator to necrotrophic pathogens.
Asunto(s)
Proteínas de Arabidopsis/metabolismo , Arabidopsis/inmunología , Arabidopsis/microbiología , Botrytis/fisiología , Resistencia a la Enfermedad/inmunología , Fusarium/fisiología , Inmunidad de la Planta , Alelos , Arabidopsis/genética , Proteínas de Arabidopsis/genética , Secuencia de Bases , Sistemas CRISPR-Cas/genética , Resistencia a la Enfermedad/genética , Edición Génica , Regulación de la Expresión Génica de las Plantas , Genes de Plantas , Vectores Genéticos/metabolismo , Solanum lycopersicum/genética , Mutación/genética , Inmunidad de la Planta/genética , Plásmidos/genéticaRESUMEN
Flavonoids are well known for the coloration of plant organs to protect UV and ROS and to attract pollinators as well. Flavonoids also play roles in many aspects of physiological processes including pathogen resistance. However, the molecular mechanism to explain how flavonoids play roles in pathogen resistance was not extensively studied. In this study, we investigated how naringenin, the first intermediate molecule of the flavonoid biosynthesis, functions as an activator of pathogen resistances. The transcript levels of two pathogenesis-related (PR) genes were increased by the treatment with naringenin in Arabidopsis. Interestingly, we found that naringenin triggers the monomerization and nuclear translocation of non-expressor of pathogenesis-related genes 1 (NPR1) that is a transcriptional coactivator of PR gene expression. Naringenin can induce the accumulation of salicylic acid (SA) that is required for the monomerization of NPR1. Furthermore, naringenin activates MPK6 and MPK3 in ROS-dependent, but SA-independent manners. By using a MEK inhibitor, we showed that the activation of a MAPK cascade by naringenin is also required for the monomerization of NPR1. These results suggest that the pathogen resistance by naringenin is mediated by the MAPK- and SA-dependent activation of NPR1 in Arabidopsis.
