RESUMEN
The multi-pass transmembrane protein ACCELERATED CELL DEATH 6 (ACD6) is an immune regulator in Arabidopsis thaliana with an unclear biochemical mode of action. We have identified two loci, MODULATOR OF HYPERACTIVE ACD6 1 (MHA1) and its paralog MHA1-LIKE (MHA1L), that code for â¼7 kDa proteins, which differentially interact with specific ACD6 variants. MHA1L enhances the accumulation of an ACD6 complex, thereby increasing the activity of the ACD6 standard allele for regulating plant growth and defenses. The intracellular ankyrin repeats of ACD6 are structurally similar to those found in mammalian ion channels. Several lines of evidence link increased ACD6 activity to enhanced calcium influx, with MHA1L as a direct regulator of ACD6, indicating that peptide-regulated ion channels are not restricted to animals.
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Proteínas de Arabidopsis , Arabidopsis , Ancirinas/metabolismo , Arabidopsis/genética , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Muerte Celular , Canales Iónicos/genética , Canales Iónicos/metabolismo , Inmunidad de la Planta/genéticaRESUMEN
Plant immunity depends on the secretion of antimicrobial proteins, which occurs through yet-largely unknown mechanisms. The trans-Golgi network (TGN), a hub for intracellular and extracellular trafficking pathways, and the cytoskeleton, which is required for antimicrobial protein secretion, are emerging as pathogen targets to dampen plant immunity. In this work, we demonstrate that tgnap1-2, a loss-of-function mutant of Arabidopsis TGNap1, a TGN-associated and microtubule (MT)-binding protein, is susceptible to Pseudomonas syringae (Pst DC3000). Pst DC3000 infected tgnap1-2 is capable of mobilizing defense pathways, accumulating salicylic acid (SA), and expressing antimicrobial proteins. The susceptibility of tgnap1-2 is due to a failure to efficiently transport antimicrobial proteins to the apoplast in a partially MT-dependent pathway but independent from SA and is additive to the pathogen-antagonizing MIN7, a TGN-associated ARF-GEF protein. Therefore, our data demonstrate that plant immunity relies on TGNap1 for secretion of antimicrobial proteins, and that TGNap1 is a key immunity element that functionally links secretion and cytoskeleton in SA-independent pathogen responses.
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Antiinfecciosos , Proteínas de Arabidopsis , Arabidopsis , Proteínas Portadoras/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Arabidopsis/metabolismo , Antiinfecciosos/metabolismo , Ácido Salicílico/metabolismo , Microtúbulos/metabolismo , Pseudomonas syringae/fisiología , Enfermedades de las Plantas , Regulación de la Expresión Génica de las PlantasRESUMEN
Many animal- and plant-pathogenic bacteria use a type III secretion system to deliver effector proteins into host cells1,2. Elucidation of how these effector proteins function in host cells is critical for understanding infectious diseases in animals and plants3-5. The widely conserved AvrE-family effectors, including DspE in Erwinia amylovora and AvrE in Pseudomonas syringae, have a central role in the pathogenesis of diverse phytopathogenic bacteria6. These conserved effectors are involved in the induction of 'water soaking' and host cell death that are conducive to bacterial multiplication in infected tissues. However, the exact biochemical functions of AvrE-family effectors have been recalcitrant to mechanistic understanding for three decades. Here we show that AvrE-family effectors fold into a ß-barrel structure that resembles bacterial porins. Expression of AvrE and DspE in Xenopus oocytes results in inward and outward currents, permeability to water and osmolarity-dependent oocyte swelling and bursting. Liposome reconstitution confirmed that the DspE channel alone is sufficient to allow the passage of small molecules such as fluorescein dye. Targeted screening of chemical blockers based on the predicted pore size (15-20 Å) of the DspE channel identified polyamidoamine dendrimers as inhibitors of the DspE/AvrE channels. Notably, polyamidoamines broadly inhibit AvrE and DspE virulence activities in Xenopus oocytes and during E. amylovora and P. syringae infections. Thus, we have unravelled the biochemical function of a centrally important family of bacterial effectors with broad conceptual and practical implications in the study of bacterial pathogenesis.
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Proteínas Bacterianas , Células Vegetales , Enfermedades de las Plantas , Porinas , Agua , Animales , Proteínas Bacterianas/química , Proteínas Bacterianas/metabolismo , Muerte Celular , Fluoresceína/metabolismo , Liposomas/metabolismo , Oocitos/metabolismo , Oocitos/microbiología , Células Vegetales/metabolismo , Células Vegetales/microbiología , Enfermedades de las Plantas/microbiología , Porinas/química , Porinas/metabolismo , Pliegue de Proteína , Soluciones/metabolismo , Agua/metabolismo , Xenopus laevis , Concentración OsmolarRESUMEN
Many animal and plant pathogenic bacteria utilize a type III secretion system to deliver effector proteins into the host cell 1,2 . Elucidation of how these effector proteins function in the host cell is critical for understanding infectious diseases in animals and plants 3-5 . The widely conserved AvrE/DspE-family effectors play a central role in the pathogenesis of diverse phytopathogenic bacteria 6 . These conserved effectors are involved in the induction of "water-soaking" and host cell death that are conducive to bacterial multiplication in infected tissues. However, the exact biochemical functions of AvrE/DspE-family effectors have been recalcitrant to mechanistic understanding for three decades. Here we show that AvrE/DspE-family effectors fold into a ß-barrel structure that resembles bacterial porins. Expression of AvrE and DspE in Xenopus oocytes results in (i) inward and outward currents, (ii) permeability to water and (iii) osmolarity-dependent oocyte swelling and bursting. Liposome reconstitution confirmed that the DspE channel alone is sufficient to allow the passage of small molecules such as fluorescein dye. Targeted screening of chemical blockers based on the predicted pore size (15-20 Å) of the DspE channel identified polyamidoamine (PAMAM) dendrimers as inhibitors of the DspE/AvrE channels. Remarkably, PAMAMs broadly inhibit AvrE/DspE virulence activities in Xenopus oocytes and during Erwinia amylovora and Pseudomonas syringae infections. Thus, we have unraveled the enigmatic function of a centrally important family of bacterial effectors with significant conceptual and practical implications in the study of bacterial pathogenesis.
RESUMEN
Bacterial type III effector proteins injected into the host cell play a critical role in mediating bacterial interactions with plant and animal hosts. Notably, some bacterial effectors are reported to target sequence-unrelated host proteins with unknown functional relationships. The Pseudomonas syringae effector HopM1 is such an example; it interacts with and/or degrades several HopM1-interacting (MIN) Arabidopsis proteins, including HopM1-interacting protein 2 (MIN2/RAD23), HopM1-interacting protein 7 (MIN7/BIG5), HopM1-interacting protein 10 (MIN10/14-3-3ĸ), and HopM1-interacting protein 13 (MIN13/BIG2). In this study, we purified the MIN7 complex formed in planta and found that it contains MIN7, MIN10, MIN13, as well as a tetratricopeptide repeat protein named HLB1. Mutational analysis showed that, like MIN7, HLB1 is required for pathogen-associated molecular pattern (PAMP)-, effector-, and benzothiadiazole (BTH)-triggered immunity. HLB1 is recruited to the trans-Golgi network (TGN)/early endosome (EE) in a MIN7-dependent manner. Both min7 and hlb1 mutant leaves contained elevated water content in the leaf apoplast and artificial water infiltration into the leaf apoplast was sufficient to phenocopy immune-suppressing phenotype of HopM1. These results suggest that multiple HopM1-targeted MIN proteins form a protein complex with a dual role in modulating water level and immunity in the apoplast, which provides an explanation for the dual phenotypes of HopM1 during bacterial pathogenesis.
RESUMEN
Although many studies have shown that microbes can ectopically stimulate or suppress plant immune responses, the fundamental question of whether the entire preexisting microbiota is indeed required for proper development of plant immune response remains unanswered. Using a recently developed peat-based gnotobiotic plant growth system, we found that Arabidopsis grown in the absence of a natural microbiota lacked age-dependent maturation of plant immune response and were defective in several aspects of pattern-triggered immunity. Axenic plants exhibited hypersusceptibility to infection by the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and the fungal pathogen Botrytis cinerea. Microbiota-mediated immunocompetence was suppressed by rich nutrient conditions, indicating a tripartite interaction between the host, microbiota and abiotic environment. A synthetic microbiota composed of 48 culturable bacterial strains from the leaf endosphere of healthy Arabidopsis plants was able to substantially restore immunocompetence similar to plants inoculated with a soil-derived community. In contrast, a 52-member dysbiotic synthetic leaf microbiota overstimulated the immune transcriptome. Together, these results provide evidence for a causal role of a eubiotic microbiota in gating proper immunocompetence and age-dependent immunity in plants.
Asunto(s)
Arabidopsis , Microbiota , Estado de Salud , Inmunocompetencia , Reconocimiento de Inmunidad Innata , SueloRESUMEN
Over the past three decades, researchers have isolated plant mutants that display constitutively activated defense responses in the absence of pathogen infection. These mutants are called autoimmune mutants and are typically dwarf and/or bearing chlorotic/necrotic lesions. From a genetic screen for Arabidopsis genes involved in maintaining a normal leaf microbiota, we identified TIP GROWTH DEFECTIVE 1 (TIP1), which encodes a S-acyltransferase, as a key player in guarding leaves against abnormal microbiota level and composition under high humidity conditions. The tip1 mutant has several characteristic phenotypes of classical autoimmune mutants, including a dwarf stature, displaying lesions, and having a high basal level of defense gene expression. Gnotobiotic experiments revealed that the autoimmune phenotypes of the tip1 mutant are largely dependent on the presence of microbiota as axenic tip1 plants have markedly reduced autoimmune phenotypes. We found that the microbiota dependency of autoimmune phenotypes is shared by several "lesion mimic"-type autoimmune mutants in Arabidopsis. Interestingly, autoimmune phenotypes caused by mutations in NLR genes do not require the presence of microbiota and can even be partially alleviated by microbiota. Our results therefore suggest the existence of two classes of autoimmunity (microbiota-dependent vs. microbiota-independent) in plants. The observed interplay between autoimmunity and microbiota in the lesion mimic class of autoimmunity is reminiscent of the interactions between autoimmunity and dysbiosis in the animal kingdom.
RESUMEN
The aboveground parts of terrestrial plants are colonized by a variety of microbes that collectively constitute the phyllosphere microbiota. Decades of pioneering work using individual phyllosphere microbes, including commensals and pathogens, have provided foundational knowledge about how individual microbes adapt to the phyllosphere environment and their role in providing biological control against pathogens. Recent studies have revealed a more complete repertoire of phyllosphere microbiota across plant taxa and how plants respond to and regulate the level and composition of phyllosphere microbiota. Importantly, the development of several gnotobiotic systems is allowing causative and mechanistic studies to determine the contributions of microbiota to phyllosphere health and productivity. New insights into how the phyllosphere carries out key biological processes, including photosynthesis, biomass accumulation, reproduction, and defense against biotic and abiotic insults, in either the presence or absence of a normal microbiota could unleash novel plant- and microbiota-based technologies to improve agriculturally relevant traits of crop plants.
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Microbiota , Microbiota/fisiología , Plantas , Fenotipo , Hojas de la PlantaRESUMEN
To defend themselves in the face of biotic stresses, plants employ a sophisticated immune system that requires the coordination of other biological and metabolic pathways. Photorespiration, a byproduct pathway of oxygenic photosynthesis that spans multiple cellular compartments and links primary metabolisms, plays important roles in defense responses. Hydrogen peroxide, whose homeostasis is strongly impacted by photorespiration, is a crucial signaling molecule in plant immunity. Photorespiratory metabolites, interaction between photorespiration and defense hormone biosynthesis, and other mechanisms, are also implicated. An improved understanding of the relationship between plant immunity and photorespiration may provide a much-needed knowledge basis for crop engineering to maximize photosynthesis without negative tradeoffs in plant immunity, especially because the photorespiratory pathway has become a major target for genetic engineering with the goal to increase photosynthetic efficiency.
RESUMEN
Phytohormone signalling pathways have an important role in defence against pathogens mediated by cell-surface pattern recognition receptors and intracellular nucleotide-binding leucine-rich repeat class immune receptors1,2 (NLR). Pathogens have evolved counter-defence strategies to manipulate phytohormone signalling pathways to dampen immunity and promote virulence3. However, little is known about the surveillance of pathogen interference of phytohormone signalling by the plant innate immune system. The pepper (Capsicum chinense) NLR Tsw, which recognizes the effector nonstructural protein NSs encoded by tomato spotted wilt orthotospovirus (TSWV), contains an unusually large leucine-rich repeat (LRR) domain. Structural modelling predicts similarity between the LRR domain of Tsw and those of the jasmonic acid receptor COI1, the auxin receptor TIR1 and the strigolactone receptor partner MAX2. This suggested that NSs could directly target hormone receptor signalling to promote infection, and that Tsw has evolved a LRR resembling those of phytohormone receptors LRR to induce immunity. Here we show that NSs associates with COI1, TIR1 and MAX2 through a common repressor-TCP21-which interacts directly with these phytohormone receptors. NSs enhances the interaction of COI1, TIR1 or MAX2 with TCP21 and blocks the degradation of corresponding transcriptional repressors to disable phytohormone-mediated host immunity to the virus. Tsw also interacts directly with TCP21 and this interaction is enhanced by viral NSs. Downregulation of TCP21 compromised Tsw-mediated defence against TSWV. Together, our findings reveal that a pathogen effector targets TCP21 to inhibit phytohormone receptor function, promoting virulence, and a plant NLR protein has evolved to recognize this interference as a counter-virulence strategy, thereby activating immunity.
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Capsicum , Enfermedades de las Plantas , Reguladores del Crecimiento de las Plantas , Inmunidad de la Planta , Proteínas de Plantas , Receptores de Reconocimiento de Patrones , Leucina , Enfermedades de las Plantas/inmunología , Enfermedades de las Plantas/virología , Reguladores del Crecimiento de las Plantas/metabolismo , Inmunidad de la Planta/inmunología , Proteínas de Plantas/química , Proteínas de Plantas/inmunología , Proteínas de Plantas/metabolismo , Receptores de Reconocimiento de Patrones/química , Receptores de Reconocimiento de Patrones/inmunología , Receptores de Reconocimiento de Patrones/metabolismo , Reconocimiento de Inmunidad Innata , Capsicum/inmunología , Capsicum/metabolismo , Capsicum/virología , VirulenciaRESUMEN
Rice false smut caused by Ustilaginoidea virens is becoming one of the most recalcitrant rice diseases worldwide. However, the molecular mechanisms underlying rice immunity against U. virens remain unknown. Using genetic, biochemical and disease resistance assays, we demonstrated that the xb24 knockout lines generated in non-Xa21 rice background exhibit an enhanced susceptibility to the fungal pathogens U. virens and Magnaporthe oryzae. Consistently, flg22- and chitin-induced oxidative burst and expression of pathogenesis-related genes in the xb24 knockout lines were greatly attenuated. As a central mediator of energy signaling, SnRK1A interacts with and phosphorylates XB24 at Thr83 residue to promote ATPase activity. SnRK1A is activated by pathogen-associated molecular patterns and positively regulates plant immune responses and disease resistance. Furthermore, the virulence effector SCRE1 in U. virens targets host ATPase XB24. The interaction inhibits ATPase activity of XB24 by blocking ATP binding to XB24. Meanwhile, SCRE1 outcompetes SnRK1A for XB24 binding, and thereby suppresses SnRK1A-mediated phosphorylation and ATPase activity of XB24. Our results indicate that the conserved SnRK1A-XB24 module in multiple crop plants positively contributes to plant immunity and uncover an unidentified molecular strategy to promote infection in U. virens and a novel host target in fungal pathogenesis.
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Oryza , Oryza/metabolismo , Adenosina Trifosfatasas/metabolismo , Fosforilación , Enfermedades de las Plantas/microbiología , Resistencia a la Enfermedad , Moléculas de Patrón Molecular Asociado a Patógenos/metabolismo , Quitina/metabolismo , Adenosina Trifosfato/metabolismoRESUMEN
Walking through a garden or a crop field, you may notice that plants damaged by pests (insects or pathogens) look smaller than the same kind of plants nearby that are not damaged. An obvious explanation would be that damaged plants may have lost substantial photosynthetic tissue due to insect and pathogen activities. As such, plants may have a reduced ability to capture light and perform photosynthesis, which fuels the growth of plants. While this is likely part of the reason why damaged plants look smaller, there is also another and perhaps more fascinating explanation that we would like to discuss here in this primer. It turns out that plants attacked by insects, pathogens and other biotic stressors may 'purposely' slow down their growth and that this response is often systemic, meaning that it occurs throughout the plant and beyond the tissue that is damaged by pests. Interestingly, some chemicals or plant genetic mutations that simulate insect or pathogen attacks without causing a loss of photosynthetic tissue can also slow plant growth, suggesting the physical loss of photosynthetic tissue per se is not always a prerequisite for slowing down plant growth. In contrast, there are conditions under which plants need to grow rapidly. For example, plants grow quickly when searching for light during germination or under a shaded canopy due to crowding from neighboring plants. Under these conditions, rapid plant growth is often accompanied by increased susceptibility to pests, presumably because growth is prioritized over defense. This inverse growth-defense relationship is commonly known as the 'growth-defense trade-off' and may be considered one of the most fundamental principles of 'plant economics' that allows plants to adjust growth and defense based on external conditions (Figure 1). As plants must both grow and defend in order to reproduce and survive in the natural world, growth-defense trade-offs have important ecological consequences. In agricultural settings, crops have often been bred to maximize growth-related traits, which could inadvertently result in the loss of useful genetic traits for biotic defenses. Thus, deciphering the molecular mechanisms underlying growth-defense trade-off phenomena could impact future crop breeding strategies aimed at designing superior crop plants with high yields as well as the ability to defend against biotic stressors. Here, we discuss some of the prevailing hypotheses about growth-defense trade-offs, our current understanding of the underlying mechanisms, and the ongoing efforts to optimize growth-defense trade-offs in crop plants.
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Fitomejoramiento , Desarrollo de la Planta , Animales , Productos Agrícolas/genética , Insectos , Desarrollo de la Planta/fisiologíaRESUMEN
Extreme weather conditions associated with climate change affect many aspects of plant and animal life, including the response to infectious diseases. Production of salicylic acid (SA), a central plant defence hormone1-3, is particularly vulnerable to suppression by short periods of hot weather above the normal plant growth temperature range via an unknown mechanism4-7. Here we show that suppression of SA production in Arabidopsis thaliana at 28 °C is independent of PHYTOCHROME B8,9 (phyB) and EARLY FLOWERING 310 (ELF3), which regulate thermo-responsive plant growth and development. Instead, we found that formation of GUANYLATE BINDING PROTEIN-LIKE 3 (GBPL3) defence-activated biomolecular condensates11 (GDACs) was reduced at the higher growth temperature. The altered GDAC formation in vivo is linked to impaired recruitment of GBPL3 and SA-associated Mediator subunits to the promoters of CBP60g and SARD1, which encode master immune transcription factors. Unlike many other SA signalling components, including the SA receptor and biosynthetic genes, optimized CBP60g expression was sufficient to broadly restore SA production, basal immunity and effector-triggered immunity at the elevated growth temperature without significant growth trade-offs. CBP60g family transcription factors are widely conserved in plants12. These results have implications for safeguarding the plant immune system as well as understanding the concept of the plant-pathogen-environment disease triangle and the emergence of new disease epidemics in a warming climate.
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Aclimatación , Proteínas de Arabidopsis , Arabidopsis , Ambiente , Calentamiento Global , Inmunidad de la Planta , Temperatura , Arabidopsis/crecimiento & desarrollo , Arabidopsis/inmunología , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Proteínas de Unión a Calmodulina/genética , Regulación de la Expresión Génica de las Plantas , Calentamiento Global/estadística & datos numéricos , Interacciones Huésped-Patógeno , Fitocromo B , Enfermedades de las Plantas/genética , Inmunidad de la Planta/genética , Ácido Salicílico/metabolismo , Factores de TranscripciónRESUMEN
Stomata exert considerable effects on global carbon and water cycles by mediating gas exchange and water vapour1,2. Stomatal closure prevents water loss in response to dehydration and limits pathogen entry3,4. However, prolonged stomatal closure reduces photosynthesis and transpiration and creates aqueous apoplasts that promote colonization by pathogens. How plants dynamically regulate stomatal reopening in a changing climate is unclear. Here we show that the secreted peptides SMALL PHYTOCYTOKINES REGULATING DEFENSE AND WATER LOSS (SCREWs) and the cognate receptor kinase PLANT SCREW UNRESPONSIVE RECEPTOR (NUT) counter-regulate phytohormone abscisic acid (ABA)- and microbe-associated molecular pattern (MAMP)-induced stomatal closure. SCREWs sensed by NUT function as immunomodulatory phytocytokines and recruit SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) co-receptors to relay immune signalling. SCREWs trigger the NUT-dependent phosphorylation of ABA INSENSITIVE 1 (ABI1) and ABI2, which leads to an increase in the activity of ABI phosphatases towards OPEN STOMATA 1 (OST1)-a key kinase that mediates ABA- and MAMP-induced stomatal closure5,6-and a reduction in the activity of S-type anion channels. After induction by dehydration and pathogen infection, SCREW-NUT signalling promotes apoplastic water loss and disrupts microorganism-rich aqueous habitats to limit pathogen colonization. The SCREW-NUT system is widely distributed across land plants, which suggests that it has an important role in preventing uncontrolled stomatal closure caused by abiotic and biotic stresses to optimize plant fitness.
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Ácido Abscísico , Reguladores del Crecimiento de las Plantas , Inmunidad de la Planta , Estomas de Plantas , Plantas , Agua , Proteínas de Arabidopsis , Deshidratación , DesecaciónRESUMEN
Global crop production is greatly reduced by vascular diseases. These diseases include bacterial blight of rice and crucifer black rot caused by Xanthomonas oryzae pv. oryzae (Xoo) and Xanthomonas campestris pv. campestris (Xcc). The molecular mechanisms that activate vascular defense against such pathogens remains underexplored. Here, we show that an Arabidopsis MAPK phosphatase 1 (MKP1) mutant has increased host susceptibility to the adapted pathogen Xcc and is compromised in nonhost resistance to the rice pathogen Xoo. MKP1 regulates MAPK-mediated phosphorylation of the transcription factor MYB4 that negatively regulates vascular lignification through inhibiting lignin biosynthesis. Induction of lignin biosynthesis is, therefore, an important part of vascular-specific immunity. The role of MKP-MAPK-MYB signaling in lignin biosynthesis and vascular resistance to Xoo is conserved in rice, indicating that these factors form a tissue-specific defense regulatory network. Our study likely reveals a major vascular immune mechanism that underlies tissue-specific disease resistance against bacterial pathogens in plants.
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Proteínas de Arabidopsis , Arabidopsis , Oryza , Xanthomonas , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Lignina/metabolismo , Oryza/genética , Oryza/metabolismo , Fosforilación , Enfermedades de las Plantas/genética , Enfermedades de las Plantas/microbiología , Proteínas Tirosina Fosfatasas/metabolismo , Proteínas Represoras/metabolismo , Xanthomonas/metabolismoRESUMEN
SignificancePlants evolved in an environment colonized by a vast number of microbes, which collectively constitute the plant microbiota. The majority of microbiota taxa are nonpathogenic and may be beneficial to plants under certain ecological or environmental conditions. We conducted experiments to understand the features of long-term interactions of nonpathogenic microbiota members with plants. We found that a multiplication-death equilibrium explained the shared long-term static populations of nonpathogenic bacteria and that in planta bacterial transcriptomic signatures were characteristic of the stationary phase, a physiological state in which stress protection responses are induced. These results may have significant implications in understanding the bulk of "nonpathogenic" plant-microbiota interactions that occur in agricultural and natural ecosystems.
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Microbiota , Transcriptoma , Bacterias/genética , Microbiota/genética , Hojas de la Planta/microbiología , Plantas/microbiologíaRESUMEN
High atmospheric humidity levels profoundly impact host-pathogen interactions in plants by enabling the establishment of an aqueous living space that benefits pathogens. The effectors HopM1 and AvrE1 of the bacterial pathogen Pseudomonas syringae have been shown to induce an aqueous apoplast under such conditions. However, the mechanisms by which this happens remain unknown. Here, we show that HopM1 and AvrE1 work redundantly to establish an aqueous living space by inducing a major reprogramming of the Arabidopsis thaliana transcriptome landscape. These effectors induce a strong abscisic acid (ABA) signature, which promotes stomatal closure, resulting in reduced leaf transpiration and water-soaking lesions. Furthermore, these effectors preferentially increase ABA accumulation in guard cells, which control stomatal aperture. Notably, a guard-cell-specific ABA transporter, ABCG40, is necessary for HopM1 induction of water-soaking lesions. This study provides molecular insights into a chain of events of stomatal manipulation that create an ideal microenvironment to facilitate infection.
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Proteínas de Arabidopsis , Arabidopsis , Ácido Abscísico/farmacología , Arabidopsis/microbiología , Proteínas de Arabidopsis/genética , Estomas de Plantas/microbiología , Pseudomonas syringae , AguaRESUMEN
Application of nanopesticides may substantially increase surface attachment and internalization of engineered nanoparticles (ENPs) in food crops. This study investigated the role of stomata in the internalization of silver nanoparticles (Ag NPs) using abscisic acid (ABA)-responsive ecotypes (Ler and Col-7) and ABA-insensitive mutants (ost1-2 and scord7) of Arabidopsis thaliana in batch sorption experiments, in combination with microscopic visualization. Compared with those of the ABA-free control, stomatal apertures were significantly smaller for the Ler and Col-7 ecotypes (p Ë 0.05) but remained unchanged for the ost1-2 and scord7 mutants, after exposure to 10 µM ABA for 1 h. Generally Ag NP sorption to the leaves of the Ler and Col-7 ecotypes treated with 10 µM ABA was lower than that in the ABA-free control, mainly due to ABA-induced stomatal closure. The difference in Ag NP sorption with and without ABA was less pronounced for Col-7 than for Ler, suggesting different sorption behaviors between these two ecotypes. In contrast, there was no significant difference in foliar sorption of Ag NPs by the ost1-2 and scord7 mutants with and without ABA treatment. Ag NPs were widely attached to the Arabidopsis leaf surface, and found at cell membrane, cytoplasm, and plasmodesmata, as revealed by scanning electron microscopy and transmission electron microscopy, respectively. These results highlight the important role of stomata in the internationalization of ENPs in plants and may have broad implications in foliar application of nanopesticides and minimizing contamination of food crops by ENPs.