Project description:Understanding the gene regulation of plant pathogens is crucial for pest control and thus global food security. An integrated understanding of bacterial gene regulation in the host is dependent on multi-omic datasets, but these are largely lacking. Here, we simultaneously characterized the transcriptome and proteome of a bacterial pathogen in plants. We found a number of bacterial processes affected by plant immunity at the transcriptome and proteome levels. For instance, the salicylic acid-mediated plant immunity suppressed the accumulation of proteins comprising the tip component of bacterial type III secretion system. Interestingly, there were instances of concordant and discordant regulation of bacterial mRNAs and proteins. Gene co-expression analysis uncovered previously unknown gene regulatory modules underlying virulence. This study provides molecular insights into the multiple layers of gene regulation that contribute to bacterial growth in planta and elucidate the role of plant immunity in affecting pathogen responses.
Project description:Gene regulation of bacterial pathogens in the host is not comprehensively understood due to the difficulty in analyzing genome-wide mRNA and protein expression of bacteria during infection. Here, we jointly analyzed transcriptome and proteome of a foliar bacterial pathogen in plants. Bacterial transcriptome changes can explain to a large extent their proteome changes in resistant and susceptible plants. However, a part of bacterial type III secretion system was suppressed by plant immunity preferentially at the protein level. Also, gene co-expression analysis uncovered previously unknown gene regulatory modules underlying bacterial virulence. Collectively, integrated in planta bacterial omics provides molecular insights into multiple layers of bacterial gene regulation that contributes to virulence and roles of plant immunity in controlling it.
Project description:Agrobacterium tumefaciens is a special plant pathogen causing crown gall disease. This pathogen is well known for the technology Agrobacterium-mediated transformation. As a pathogen, Agrobacterium triggers plant immunity, and this affects transformation. But the signaling components and pathways in plant immunity to Agrobacterium remain elusive. We demonstrate two Arabidopsis MAPKKs MKK4/MKK5 and their downstream MAPKs MPK3/MPK6 play a major role in both Agrobacterium-triggered immunity and Agrobacterium-mediated transformation. Agrobacteria induce MPK3/MPK6 activity and plant defense responsive genes expression in a very early stage. This process is dependent on MKK4/MKK5 function. Loss of function of MKK4 and MKK5 or their downstream MPK3 and MPK6 abolishes plant immunity to agrobacteria, and increases the transformation frequency, while activation of MKK4 and MKK5 enhances the plant immunity and represses the transformation. Global transcriptome indicates agrobacteria induce various plant defense pathways, including ROS production, ethylene and SA-mediated defense responses, and MKK4/MKK5 is essential for these pathways induction. Activation of MKK4 and MKK5 promotes ROS production and cell death in agrobacteria infection process. Ethylene and SA act bypass of MKK4/MKK5 signaling to regulate transformation. Based on these results, we propose MKK4/5-MPK3/6 cascade is an essential signaling pathway to regulate Agrobacterium-mediated transformation by modulating Agrobacterium-triggered plant immunity.
Project description:Plants have evolved sophisticated mechanisms to regulate gene expression to activate immune responses against pathogen infections. However, how the translation system contributes to plant immunity is largely unknown. The evolutionarily conserved thiolation modification of tRNA ensures efficient decoding during translation. Here we show that tRNA thiolation is required for plant immunity in Arabidopsis. The Arabidopsis cgb mutant is hyper-susceptible to the pathogen Pseudomonas syringae. CGB encodes ROL5, a homolog of yeast NCS6 required for tRNA thiolation. ROL5 physically interacts with CTU2, a homolog of yeast NCS2. Mutations in either ROL5 or CTU2 result in loss of tRNA thiolation. Further analyses reveal that tRNA thiolation is required for both transcriptional reprogramming and translational reprogramming during immune responses. The translation efficiency of immune-related proteins reduces when tRNA thiolation is absent. Our study not only uncovers a new biological function of tRNA thiolation but also reveals a new mechanism for plant immunity.
Project description:Plant pathogens can cause serious diseases that impact global agriculture1. Understanding how the plant immune system naturally restricts pathogen infection holds a key to sustainable disease control in modern agricultural practices. However, despite extensive studies into the molecular and genetic basis of plant defense against pathogens since the 1950s2,3, one of the most fundamental questions in plant pathology remains unanswered: how resistant plants halt pathogen growth during immune activation. In the case of bacterial infections, a major bottleneck is an inability to determine the global bacterial transcriptome and metabolic responses in planta. Here, we developed an innovative pipeline that allows for in planta high-resolution bacterial transcriptome analysis with RNA-Seq, using the model plant Arabidopsis thaliana and the foliar bacterial pathogen Pseudomonas syringae. We examined a total of 27 combinations of plant immunity and bacterial virulence mutants to gain an unprecedented insight into the bacterial transcriptomic responses during plant immunity. We were able to identify specific bacterial transcriptomic signatures that are linked to bacterial inhibition during two major forms of plant immunity: pattern-triggered immunity and effector-triggered immunity. Among them, regulation of a P. syringae sigma factor gene, involved in iron regulation and an unknown process(es), was found to play a causative role in bacterial restriction during plant immunity. This study unlocked the enigmatic mechanisms of bacterial growth inhibition during plant immunity; results have broad basic and practical implications for future study of plant diseases.
Project description:Plant pathogens can cause serious diseases that impact global agriculture1. Understanding how the plant immune system naturally restricts pathogen infection holds a key to sustainable disease control in modern agricultural practices. However, despite extensive studies into the molecular and genetic basis of plant defense against pathogens since the 1950s2,3, one of the most fundamental questions in plant pathology remains unanswered: how resistant plants halt pathogen growth during immune activation. In the case of bacterial infections, a major bottleneck is an inability to determine the global bacterial transcriptome and metabolic responses in planta. Here, we developed an innovative pipeline that allows for in planta high-resolution bacterial transcriptome analysis with RNA-Seq, using the model plant Arabidopsis thaliana and the foliar bacterial pathogen Pseudomonas syringae. We examined a total of 27 combinations of plant immunity and bacterial virulence mutants to gain an unprecedented insight into the bacterial transcriptomic responses during plant immunity. We were able to identify specific bacterial transcriptomic signatures that are linked to bacterial inhibition during two major forms of plant immunity: pattern-triggered immunity and effector-triggered immunity. Among them, regulation of a P. syringae sigma factor gene, involved in iron regulation and an unknown process(es), was found to play a causative role in bacterial restriction during plant immunity. This study unlocked the enigmatic mechanisms of bacterial growth inhibition during plant immunity; results have broad basic and practical implications for future study of plant diseases.
Project description:Bivalent chromatin modification containing opposing H3K4me3 and H3K27me3 marks controls various biological processes by fine-tuning gene expression in animals and plants, however how this bivalent modification regulates pathogenicity of fungal pathogen remains exclusive. Here, we provided a genome-wide landscape of H3K4me3 and H3K27me3 of wheat head blight fungus Fusarium graminearum (Fg), leading to the identification of infection-induced bivalent chromatin-marked genes (BCGs). Among those, BCG1, which encodes a novel xylanase with a G/Q rich motif, is required for the full virulence of Fg pathogenicity through degradation of host cell wall. However, the G/Q rich motif is recognized by pattern-recognition receptors and triggers plant innate immunity. Further data illustrates that Fg employs H3K4me3 modification to induce BCG1 expression rapidly during the early infection, and then switches to bivalent H3K4me3-H3K27me3 chromatin state that renders rapid epigenetic silencing of BCG1 for escaping from host immune monitor, therefore leading to the successful invasion. Collectively, our study highlights the molecular mechanism of how fungal pathogen employs bivalent epigenetic modification to facilitate the successful infection by escaping of host immunity, which provides conceptual insights into plant-microbe interaction.
Project description:Bivalent chromatin modification containing opposing H3K4me3 and H3K27me3 marks controls various biological processes by fine-tuning gene expression in animals and plants, however how this bivalent modification regulates pathogenicity of fungal pathogen remains exclusive. Here, we provided a genome-wide landscape of H3K4me3 and H3K27me3 of wheat head blight fungus Fusarium graminearum (Fg), leading to the identification of infection-induced bivalent chromatin-marked genes (BCGs). Among those, BCG1, which encodes a novel xylanase with a G/Q rich motif, is required for the full virulence of Fg pathogenicity through degradation of host cell wall. However, the G/Q rich motif is recognized by pattern-recognition receptors and triggers plant innate immunity. Further data illustrates that Fg employs H3K4me3 modification to induce BCG1 expression rapidly during the early infection, and then switches to bivalent H3K4me3-H3K27me3 chromatin state that renders rapid epigenetic silencing of BCG1 for escaping from host immune monitor, therefore leading to the successful invasion. Collectively, our study highlights the molecular mechanism of how fungal pathogen employs bivalent epigenetic modification to facilitate the successful infection by escaping of host immunity, which provides conceptual insights into plant-microbe interaction.