Project description:A first line of defense against pathogen infections is the recognition of pathogen-associated molecular patterns (PAMPs), leading to PAMP-triggered immunity (PTI). MicroRNAs (miRNAs) are primarily known as central regulators of plant development, but a few have also been connected to immunity. We have found that several fungal pathogens lead to a reduction in miR396 levels, suggesting that miR396 are negative regulators of downstream defense responses. In agreement with such as scenario, constitutive attenuation of miR396 activity enhances resistance to infection by fungal pathogens, while increased miR396 activity reduces pathogen resistance. We conclude that constitutive reduction of miR396 levels confer a primed state for enhanced defense reactions
Project description:A LysM Receptor-like Kinase Mediates Chitin Perception and Fungal Resistance in Arabidopsis; Jinrong Wan,1 Xuecheng Zhang,1 David Neece,2 Katrina M. Ramonell,3 Steve Clough,2,4 Sung-yong Kim,1 Minviluz Stacey,1 and Gary Stacey1*; 1Division of Plant Sciences, National Center for Soybean Biotechnology, C.S. Bond Life Sciences Center, University of Missouri-Columbia, Columbia, MO 65211, USA; 2Department of Crop Sciences, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA; 3Department of Biological Sciences, University of Alabama, Tuscaloosa, AL 35487, USA; 4US Department of Agriculture, Soybean/Maize Germplasm, Pathology and Genetics Research, Urbana, IL 61801, USA; *To whom correspondence should be addressed. E-mail: staceyg@missouri.edu; Abstract: Chitin, a polymer of N-acetyl-D-glucosamine, is found in fungal cell walls, but not in plants. Plant cells are capable of perceiving chitin fragments (chitooligosaccharides) to trigger various defense responses. We identified a LysM receptor-like protein (AtLysM RLK1) that is required for the perception of chitooligosaccharides in Arabidopsis. Mutation of this gene blocked the induction of almost all chitooligosaccharide-responsive genes (CRGs) and led to more susceptibility to fungal pathogens, but not to a bacterial pathogen. In addition, exogenously applied chitooligosaccharides enhanced resistance against both fungal and bacterial pathogens in the wild-type plants, but not in the mutant. Together, our data strongly suggest AtLysM RLK1 is the chitin receptor or a key part of the receptor complex and chitin is a PAMP (pathogen-associated molecular pattern) in fungi recognized by the receptor leading to the induction of plant innate immunity against fungal pathogens. Since LysM RLKs were also recently shown to be critical for the perception of the rhizobial lipo-chitin Nod signals, our data suggest that LysM RLKs not just recognize friendly symbiotic rhizobia (via their lipo-chitin Nod signals), but also hostile fungal pathogens (via their cell wall chitin). These data suggest a possible evolutionary relationship between the perception mechanisms of Nod signals and chitin by plants. Experiment Overall Design: wild type Col-0 and chitin receptor mutants treated with or without chitooctaose
Project description:In plants, recognition of immunogenic molecular patterns, such as bacterial flagellin (flg22 epitope), leads to an enhanced state of immunity, designated pattern-triggered immunity (PTI). Following cognate ligand perception, pattern recognition receptors initiate sequential phosphorylation events to activate defense responses against invading pathogens. To gain further insight into PTI signaling, we conducted phosphoproteome analyses in Arabidopsis seedlings with immunogenic molecular patterns.
Project description:Plants recognize and respond to pathogens relying on pattern recognition receptors (PRRs) which usually are receptor like kinases (RLKs) or receptor like proteins (RLPs). Upon binding to conserved structures or molecules, the so-called pathogen-associated molecular patterns (PAMPs), in pathogens, PRRs form complex with coreceptors and activate pattern triggered immunity (PTI). Here, we show that two U-box type E3 ligases (PUBs), PUB2 and PUB4, play important roles in PTI responses and disease resistance in Arabidopsis.
Project description:A LysM Receptor-like Kinase Mediates Chitin Perception and Fungal Resistance in Arabidopsis Jinrong Wan,1 Xuecheng Zhang,1 David Neece,2 Katrina M. Ramonell,3 Steve Clough,2,4 Sung-yong Kim,1 Minviluz Stacey,1 and Gary Stacey1* 1Division of Plant Sciences, National Center for Soybean Biotechnology, C.S. Bond Life Sciences Center, University of Missouri-Columbia, Columbia, MO 65211, USA 2Department of Crop Sciences, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA 3Department of Biological Sciences, University of Alabama, Tuscaloosa, AL 35487, USA 4US Department of Agriculture, Soybean/Maize Germplasm, Pathology and Genetics Research, Urbana, IL 61801, USA *To whom correspondence should be addressed. E-mail: staceyg@missouri.edu Abstract: Chitin, a polymer of N-acetyl-D-glucosamine, is found in fungal cell walls, but not in plants. Plant cells are capable of perceiving chitin fragments (chitooligosaccharides) to trigger various defense responses. We identified a LysM receptor-like protein (AtLysM RLK1) that is required for the perception of chitooligosaccharides in Arabidopsis. Mutation of this gene blocked the induction of almost all chitooligosaccharide-responsive genes (CRGs) and led to more susceptibility to fungal pathogens, but not to a bacterial pathogen. In addition, exogenously applied chitooligosaccharides enhanced resistance against both fungal and bacterial pathogens in the wild-type plants, but not in the mutant. Together, our data strongly suggest AtLysM RLK1 is the chitin receptor or a key part of the receptor complex and chitin is a PAMP (pathogen-associated molecular pattern) in fungi recognized by the receptor leading to the induction of plant innate immunity against fungal pathogens. Since LysM RLKs were also recently shown to be critical for the perception of the rhizobial lipo-chitin Nod signals, our data suggest that LysM RLKs not just recognize friendly symbiotic rhizobia (via their lipo-chitin Nod signals), but also hostile fungal pathogens (via their cell wall chitin). These data suggest a possible evolutionary relationship between the perception mechanisms of Nod signals and chitin by plants. Keywords: chitooctaose, chitin receptor mutant
Project description:Yield loss in crop plants due to biotic stresses is a major problem and pyramiding of R genes is often suggested for sustained and durable resistance against target pests. Information is available for single R gene interaction in rice and other crop plants, but not much data is available for multiple R gene interaction against multiple pathogens/pests. In this study we carried out transcriptional analysis of two rice lines introgressed with either R gene against bacterial blight and gall midge or, against bacterial blight and fungal blast. The gene expression changes were investigated through microarray and the expression pattern upon co-infection with multiple pathogens was analyzed to study the synergistic effect of R gene mediated defense responses as well as to explore the possibility of any antagonism between the R genes as defense pathway employed due to R gene mediated resistance variesaccording to the attacking pathogen/pest. Keywords: Expression profiling by array
Project description:Yield loss in crop plants due to biotic stresses is a major problem and pyramiding of R genes is often suggested for sustained and durable resistance against target pests. Information is available for single R gene interaction in rice and other crop plants, but not much data is available for multiple R gene interaction against multiple pathogens/pests. In this study we carried out transcriptional analysis of two rice lines introgressed with either R gene against bacterial blight and gall midge or, against bacterial blight and fungal blast. The gene expression changes were investigated through microarray and the expression pattern upon co-infection with multiple pathogens was analyzed to study the synergistic effect of R gene mediated defense responses as well as to explore the possibility of any antagonism between the R genes as defense pathway employed due to R gene mediated resistance varies as per the attacking pathogen/pest. Keywords: Expression profiling by array
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:We revealed that mycosubtilin, a lipopeptide from Bacillus subtilis, protects wheat against the hemibiotrophic fungal pathogen Zymoseptoria tritici. Foliar application of the biomolecule primes, during the early stages of infection, the expression of genes associated with sixteen functional groups, including responses to pathogens, abiotic and oxidative stresses, secondary metabolism, cell-wall structure and function, and primary metabolic pathways (carbohydrate, amino acid, protein, lipid, and energy metabolisms).