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A longer amino-terminal fragment interacts with the tomato Fen kinase, which mediates Prf resistance in the absence of Pto. The carboxyl terminus of AvrPtoB shares structural homology with eukaryotic E3 ubiquitin ligases and ubiquitinates Fen, but not Pto.

Martin discussed the means by which Pto resists the AvrPtoB E3 ligase activity and hypothesized that Pto actively inhibits ubiquitination by phosphorylation of the ligase or passively resists it due to a lack of key lysine residues.

He identified wild tomato accessions in which AvrPtoB-triggered resistance occurs independently of Pto, and thus Fen also appears resistant to AvrPtoB-mediated degradation in these plants, possibly due to the substitution of key lysine residues.

AvrPtoB thus has multiple functions and, as it can suppress both PAMP-triggered immunity and effector-triggered immunity, it provides clues to trace how plant-microbe coevolution has shaped the virulence strategy of a pathogen.

Regine Kahmann Max-Planck-Institute for Terrestrial Microbiology, Marburg, Germany presented a genomic approach to identifying effectors of the smut fungus Ustilago maydis.

Genome sequencing of U. Comparison of the genomes of U. The deletion of one poorly conserved pathogenicity cluster resulted in loss of pathogenesis in U.

The deletion mutants of U. This study emphasizes the power of comparative genomics combined with mutant analysis for the identification of effectors responsible for different stages of the infection process.

The oomycetes include some serious plant pathogens, such as Phytophthora infestans , the cause of potato blight. In these pathogens, as in bacteria, genome sequencing is a powerful tool for identifying the effector inventory.

Jim Beynon Warwick University, UK reported the genome sequencing of the oomycete Hyaloperonospora parasitica , and predicted the presence of about so-called RxLR effectors named after a shared RxLR amino acid motif.

Jean Greenberg University of Chicago, USA formulated an interesting question: why do pathogens encode so many effectors, for example, the effectors in P.

She proposed that pathogens require different sets of effectors in different infection phases, such as epiphytic growth and growth inside the plant.

He found that this effect is long lasting, and is conserved in different A. Jane Glazebrook University of Minnesota, Minneapolis-St Paul, USA described work with Fumi Katagiri on the use of DNA miniarrays to study the gene-expression profiles of pathogen-responsive genes in a large number of known defense and signaling mutants of Arabidopsis upon challenge with P.

Systems-biology principles were applied to the data to determine positive and negative interactions among components of plant immunity.

Mutations in the gene encoding this protein enhanced disease susceptibility and reduced PAMP-induced accumulation of SA.

We were reminded by Jonathan Jones Sainsbury Laboratory, Norwich, UK that many plant pathogens produce plant hormones, such as auxin or gibberellic acid.

He reported that auxin promotes pathogen propagation and compromises PAMP-induced expression of PR-1 , a well known marker gene for the SA pathway of defense responses.

Jones tested whether the auxin effect occurs through JA signaling antagonizing responses to SA, and found that virulence of the disarmed P.

Jones concluded that plant hormone pathways influence each other strongly, and thus the modulation of a single hormone pathway can greatly affect plant defenses.

Plant resistance R proteins monitor the actions of isolate-specific pathogen effectors, and can trigger programmed cell death, a defense reaction known as the hypersensitive response HR.

One prominent class of R proteins comprises the so-called nucleotide-binding site leucine-rich repeat NB-LRR proteins, which carry either a coiled coil CC domain or a Toll-interleukin receptor TIR -like domain at their amino termini.

He described the coexpression in N. Substitution of the conserved aspartate D residue in this motif caused autoactivation of four NB-LRR proteins tested, whereas replacement of the histidine H conferred either autoactivation or loss of function.

The generalization of this updated model will require further studies, however. Kirsten Bomblies Max-Planck-Institute for Developmental Biology, Tübingen, Germany described temperature-sensitive hybrid necrosis that occurs in crosses of normally healthy A.

R genes have been proposed to be costly for plant growth, and the risk of necrosis could cause constraints on their evolution.

Bomblies also referred to the Est-1 accession, in which an allele of ACD6 a positive regulator of defense causes HR-like lesions.

Thus, the risk of necrosis caused by auto-activation of cell-death inducers in plant immunity might in some situations present a barrier to gene flow.

Although the plant HR has been seen as the ultimate restriction of pathogen propagation ever since HH Flor first described gene-for-gene resistance in the s, little is known about how HR cell death is initiated and regulated.

LSD1 for lesion simulating disease resistance 1 is a plant-specific zinc finger protein that regulates the oxidative stress response that accompanies the HR.

Dangl described how a gradient of SA determines a cell for death. Mutation of AtMC1 suppresses runaway cell death in lsd1 and enhances the basal level of defense.

Consistent with this, AtMC1 appears to be stabilized in lsd1 mutants, and constitutive overexpression of AtMC1 induces cell death.

In his concluding remarks, Dangl noted that one reason for the successful growth of the field of plant-microbe interactions had been the sharing of resources and unpublished information between researchers, and he hoped that this would continue.

In this respect, this meeting was a prime example of the further nourishment of our plant immunity studies.

Correspondence to Silke Robatzek. Reprints and Permissions. Chen, J. Xu, G. Sullivan, S. Liu, Y. Information about the latest finalized video coding standard High Efficiency Video Coding HEVC is available from numerous sources, among them there are:.

Overview paper: Sullivan, G. IEEE Trans. The reference software implementation of HEVC is available at this website. Staff Present Staff Former Staff.

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Boris Stavrev. Hidden categories: Articles with short description All set index articles. Take part in our 30 minute study. This host-pathogen incompatibility is typically accompanied by visit web page hypersensitive response HR. Views Read Edit View history. Vladislav Varna. Nikola Mutavchiev. Chen, J.

Overview paper: Sullivan, G. IEEE Trans. The reference software implementation of HEVC is available at this website. Staff Present Staff Former Staff.

Courses Student projects. Thorsten Laude. Show selected publications only. In these pathogens, as in bacteria, genome sequencing is a powerful tool for identifying the effector inventory.

Jim Beynon Warwick University, UK reported the genome sequencing of the oomycete Hyaloperonospora parasitica , and predicted the presence of about so-called RxLR effectors named after a shared RxLR amino acid motif.

Jean Greenberg University of Chicago, USA formulated an interesting question: why do pathogens encode so many effectors, for example, the effectors in P.

She proposed that pathogens require different sets of effectors in different infection phases, such as epiphytic growth and growth inside the plant.

He found that this effect is long lasting, and is conserved in different A. Jane Glazebrook University of Minnesota, Minneapolis-St Paul, USA described work with Fumi Katagiri on the use of DNA miniarrays to study the gene-expression profiles of pathogen-responsive genes in a large number of known defense and signaling mutants of Arabidopsis upon challenge with P.

Systems-biology principles were applied to the data to determine positive and negative interactions among components of plant immunity.

Mutations in the gene encoding this protein enhanced disease susceptibility and reduced PAMP-induced accumulation of SA. We were reminded by Jonathan Jones Sainsbury Laboratory, Norwich, UK that many plant pathogens produce plant hormones, such as auxin or gibberellic acid.

He reported that auxin promotes pathogen propagation and compromises PAMP-induced expression of PR-1 , a well known marker gene for the SA pathway of defense responses.

Jones tested whether the auxin effect occurs through JA signaling antagonizing responses to SA, and found that virulence of the disarmed P.

Jones concluded that plant hormone pathways influence each other strongly, and thus the modulation of a single hormone pathway can greatly affect plant defenses.

Plant resistance R proteins monitor the actions of isolate-specific pathogen effectors, and can trigger programmed cell death, a defense reaction known as the hypersensitive response HR.

One prominent class of R proteins comprises the so-called nucleotide-binding site leucine-rich repeat NB-LRR proteins, which carry either a coiled coil CC domain or a Toll-interleukin receptor TIR -like domain at their amino termini.

He described the coexpression in N. Substitution of the conserved aspartate D residue in this motif caused autoactivation of four NB-LRR proteins tested, whereas replacement of the histidine H conferred either autoactivation or loss of function.

The generalization of this updated model will require further studies, however. Kirsten Bomblies Max-Planck-Institute for Developmental Biology, Tübingen, Germany described temperature-sensitive hybrid necrosis that occurs in crosses of normally healthy A.

R genes have been proposed to be costly for plant growth, and the risk of necrosis could cause constraints on their evolution.

Bomblies also referred to the Est-1 accession, in which an allele of ACD6 a positive regulator of defense causes HR-like lesions.

Thus, the risk of necrosis caused by auto-activation of cell-death inducers in plant immunity might in some situations present a barrier to gene flow.

Although the plant HR has been seen as the ultimate restriction of pathogen propagation ever since HH Flor first described gene-for-gene resistance in the s, little is known about how HR cell death is initiated and regulated.

LSD1 for lesion simulating disease resistance 1 is a plant-specific zinc finger protein that regulates the oxidative stress response that accompanies the HR.

Dangl described how a gradient of SA determines a cell for death. Mutation of AtMC1 suppresses runaway cell death in lsd1 and enhances the basal level of defense.

Consistent with this, AtMC1 appears to be stabilized in lsd1 mutants, and constitutive overexpression of AtMC1 induces cell death.

In his concluding remarks, Dangl noted that one reason for the successful growth of the field of plant-microbe interactions had been the sharing of resources and unpublished information between researchers, and he hoped that this would continue.

In this respect, this meeting was a prime example of the further nourishment of our plant immunity studies. Nikola Mutavchiev.

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