Plants cannot move to escape environmental challenges. Biotic stresses result from a battery of potential pathogens: fungi, bacteria, nematodes and insects intercept the photosynthate produced by plants, and viruses use replication machinery at the host's expense. Plants, in turn, have evolved sophisticated mechanisms to perceive such attacks, and to translate that perception into an adaptive response. Here, we review the current knowledge of recognition-dependent disease resistance in plants. We include a few crucial concepts to compare and contrast plant innate immunity with that more commonly associated with animals. There are appreciable differences, but also surprising parallels.

Plant pathogens and integrated defence responses to infection.

It has been suggested that effective defense against biotrophic pathogens is largely due to programmed cell death in the host, and to associated activation of defense responses regulated by the salicylic acid-dependent pathway. In contrast, necrotrophic pathogens benefit from host cell death, so they are not limited by cell death and salicylic acid-dependent defenses, but rather by a different set of defense responses activated by jasmonic acid and ethylene signaling. This review summarizes results from Arabidopsis-pathogen systems regarding the contributions of various defense responses to resistance to several biotrophic and necrotrophic pathogens. While the model above seems generally correct, there are exceptions and additional complexities.

Contrasting Mechanisms of Defense Against Biotrophic and Necrotrophic Pathogens

MUCKE aims to mine a large volume of images, to structure them conceptually and to use this conceptual structuring in order to improve large-scale image retrieval. The last decade witnessed important progress concerning low-level image representations. However, there are a number problems which need to be solved in order to unleash the full potential of image mining in applications. The central problem with low-level representations is the mismatch between them and the human interpretation of image content. This problem can be instantiated, for instance, by the incapability of existing descriptors to capture spatial relationships between the concepts represented or by their incapability to convey an explanation of why two images are similar in a content-based image retrieval framework. We start by assessing existing local descriptors for image classification and by proposing to use co-occurrence matrices to better capture spatial relationships in images. The main focus in MUCKE is on cleaning large scale Web image corpora and on proposing image representations which are closer to the human interpretation of images. Consequently, we introduce methods which tackle these two problems and compare results to state of the art methods. Note: some aspects of this deliverable are withheld at this time as they are pending review. Please contact the authors for a preview.

http://ieeexplore.ieee.org/iel2/4524/12820/00592460.pdf

Image Processing

Jasmonate and related signalling compounds have a crucial role in both host immunity and development in plants, but the molecular details of the signalling mechanism are poorly understood. Here we identify members of the jasmonate ZIM-domain (JAZ) protein family as key regulators of jasmonate signalling. JAZ1 protein acts to repress transcription of jasmonate-responsive genes. Jasmonate treatment causes JAZ1 degradation and this degradation is dependent on activities of the SCF(COI1) ubiquitin ligase and the 26S proteasome. Furthermore, the jasmonoyl-isoleucine (JA-Ile) conjugate, but not other jasmonate-derivatives such as jasmonate, 12-oxo-phytodienoic acid, or methyl-jasmonate, promotes physical interaction between COI1 and JAZ1 proteins in the absence of other plant proteins. Our results suggest a model in which jasmonate ligands promote the binding of the SCF(COI1) ubiquitin ligase to and subsequent degradation of the JAZ1 repressor protein, and implicate the SCF(COI1)-JAZ1 protein complex as a site of perception of the plant hormone JA-Ile.

JAZ repressor proteins are targets of the SCF COI1 complex during jasmonate signalling

Jasmonates are essential phytohormones for plant development and survival. However, the molecular details of their signalling pathway remain largely unknown. The identification more than a decade ago of COI1 as an F-box protein suggested the existence of a repressor of jasmonate responses that is targeted by the SCF(COI1) complex for proteasome degradation in response to jasmonate. Here we report the identification of JASMONATE-INSENSITIVE 3 (JAI3) and a family of related proteins named JAZ (jasmonate ZIM-domain), in Arabidopsis thaliana. Our results demonstrate that JAI3 and other JAZs are direct targets of the SCF(COI1) E3 ubiquitin ligase and jasmonate treatment induces their proteasome degradation. Moreover, JAI3 negatively regulates the key transcriptional activator of jasmonate responses, MYC2. The JAZ family therefore represents the molecular link between the two previously known steps in the jasmonate pathway. Furthermore, we demonstrate the existence of a regulatory feed-back loop involving MYC2 and JAZ proteins, which provides a mechanistic explanation for the pulsed response to jasmonate and the subsequent desensitization of the cell.

The JAZ family of repressors is the missing link in jasmonate signalling

Plant disease resistance (R) genes control the recognition of specific pathogens and activate subsequent defense responses. We show that the Arabidopsis thaliana locus RESISTANCE TO POWDERY MILDEW8 (RPW8) contains two naturally polymorphic, dominant R genes, RPW8.1 and RPW8.2, which individually control resistance to a broad range of powdery mildew pathogens. Although the predicted RPW8.1 and RPW8.2 proteins are different from the previously characterized R proteins, they induce localized, salicylic acid-dependent defenses similar to those induced by R genes that control specific resistance. Apparently, broad-spectrum resistance mediated by RPW8 uses the same mechanisms as specific resistance.

https://science.sciencemag.org/content/sci/291/5501/118.full.pdf

Broad-spectrum mildew resistance in Arabidopsis thaliana mediated by RPW8.

Jasmonates (JAs) regulate Arabidopsis thaliana wound and defence responses, pollen development, and stress-related growth inhibition. Significantly, each of these responses requires COI1, an F-box protein. Other F-box proteins interact with SKP1 and cullin proteins to form SCF complexes that selectively recruit regulatory proteins targeted for ubiquitination. To determine whether COI1 also functions in an SCF complex, we have characterized Arabidopsis proteins that bind to COI1. An Arabidopsis cDNA expression library was screened in yeast for clones that produce proteins which can bind to COI1. We recovered two SKP1 homologues and a histone deacetylase. The Arabidopsis F-box protein TIR1 interacted with SKP1 proteins, but not with the histone deacetylase. Mutant COI1 proteins revealed that the F-box is required for interaction with SKP1s, but that sequences in leucine-rich repeat domains are required for interaction with the histone deacetylase. Epitope-tagged COI1 was introduced into Arabidopsis plants and cell cultures. Co-immunoprecipitation experiments confirmed the interaction in planta of COI1 with SKP1-like proteins and histone deacetylase, and also indicated that COI1 interacted with cullin. These results suggest that COI1 forms an SCFCOI1 complex in vivo. COI1 is therefore expected to form a functional E3-type ubiquitin ligase in plants and to regulate expression of jasmonate responsive genes, possibly by targeted ubiquitination of a histone deacetylase.

/pdf/coi1-links-jasmonate-signalling-and-fertility-to-the-scf-ykt4qxkq6l.pdf

COI1 links jasmonate signalling and fertility to the SCF ubiquitin-ligase complex in Arabidopsis.

Jasmonate (JA) activates plant defense, promotes pollen maturation, and suppresses plant growth. An emerging theme in JA biology is its involvement in light responses; here, we examine the interdependence of the JA- and light-signaling pathways in Arabidopsis thaliana. We demonstrate that mutants deficient in JA biosynthesis and signaling are deficient in a subset of high irradiance responses in far-red (FR) light. These mutants display exaggerated shade responses to low, but not high, R/FR ratio light, suggesting a role for JA in phytochrome A (phyA) signaling. Additionally, we demonstrate that the FR light–induced expression of transcription factor genes is dependent on CORONATINE INSENSITIVE1 (COI1), a central component of JA signaling, and is suppressed by JA. phyA mutants had reduced JA-regulated growth inhibition and VSP expression and increased content of cis-(+)-12-oxophytodienoic acid, an intermediate in JA biosynthesis. Significantly, COI1-mediated degradation of JASMONATE ZIM DOMAIN1-b-glucuronidase (JAZ1-GUS) in response to mechanical wounding and JA treatment required phyA, and ectopic expression of JAZ1-GUS resulted in exaggerated shade responses. Together, these results indicate that JA and phyA signaling are integrated through degradation of the JAZ1 protein, and both are required for plant responses to light and stress.

Jasmonate and Phytochrome A Signaling in Arabidopsis Wound and Shade Responses Are Integrated through JAZ1 Stability

The Arabidopsis disease resistance (R) genes RPW8.1 and RPW8.2 couple the recognition of powdery mildew pathogens of this plant with the subsequent induction of a localized necrosis, or hypersensitive response (HR). The HR restricts the spread of the infection and renders the plant resistant. One-third of Arabidopsis plants transformed with a genomic fragment containing RPW8.1 and RPW8.2 developed spontaneous HR-like lesions (SHL) in the absence of pathogens. We demonstrate that SHL occurs in transgenic lines that contain multiple copies of the transgene and express RPW8.1 and RPW8.2 at high levels. SHL is associated with salicylic acid (SA) accumulation, and at the site of the lesion, there is increased expression of RPW8.1, increased production of H2O2, and increased expression of pathogenesis-related genes. These lesions are physiologically similar to the pathogen-induced HR mediated by RPW8.1 and RPW8.2. Significantly, environmental conditions that suppress SHL suppress the transcription of RPW8.1 and RPW8.2 and also suppress resistance to powdery mildews, even in transgenic lines containing RPW8.1 and RPW8.2 that normally do not express SHL. Furthermore, treatment with SA increases the transcription of RPW8.1 and RPW8.2, induces SHL, and enhances resistance to powdery mildews. We conclude that HR requires the transcription of RPW8.1 and RPW8.2, which is regulated independently of the pathogen by SA-dependent feedback amplification.

/pdf/enhanced-transcription-of-the-arabidopsis-disease-resistance-c4rbnsn6wj.pdf

Enhanced Transcription of the Arabidopsis Disease Resistance Genes RPW8.1 and RPW8.2 via a Salicylic Acid–Dependent Amplification Circuit Is Required for Hypersensitive Cell Death

Genetic studies have identified a number of components of signal transduction pathways leading to plant disease resistance and the accompanying hypersensitive response (HR) following detection of pathogens by plant resistance (R) genes. In Arabidopsis, the majority of R proteins so far characterized belong to a plant superfamily that have a central nucleotide-binding site and C-terminal leucine-rich-repeats (NB-LRRs). Another much less prevalent class comprises RPW8.1 and RPW8.2, two related proteins that possess a putative N-terminal transmembrane domain and a coiled-coil motif, and confer broad-spectrum resistance to powdery mildew. Here we investigated whether RPW8.1 and RPW8.2 engage known pathway(s) for defence signalling. We show that RPW8.1 and RPW8.2 recruit, in addition to salicylic acid and EDS1, the other NB-LRR gene-signalling components PAD4, EDS5, NPR1 and SGT1b for activation of powdery mildew resistance and HR. In contrast, NDR1, RAR1 and PBS3 that are required for function of certain NB-LRR R genes, and COI1 and EIN2 that operate, respectively, in the jasmonic acid and ethylene signalling pathways, do not contribute to RPW8.1 and RPW8.2-mediated resistance. We further demonstrate that EDR1, a gene encoding a conserved MAPKK kinase, exerts negative regulation on HR cell death and powdery mildew resistance by limiting the transcriptional amplification of RPW8.1 and RPW8.2. Our results suggest that RPW8.1 and RPW8.2 stimulate a conserved basal defence pathway that is negatively regulated by EDR1.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-313X.2005.02356.x

Elaine Patrick

Papers

Broad-spectrum mildew resistance in Arabidopsis thaliana mediated by RPW8.

COI1 links jasmonate signalling and fertility to the SCF ubiquitin-ligase complex in Arabidopsis.

Jasmonate and Phytochrome A Signaling in Arabidopsis Wound and Shade Responses Are Integrated through JAZ1 Stability

Enhanced Transcription of the Arabidopsis Disease Resistance Genes RPW8.1 and RPW8.2 via a Salicylic Acid–Dependent Amplification Circuit Is Required for Hypersensitive Cell Death

The atypical resistance gene, RPW8, recruits components of basal defence for powdery mildew resistance in Arabidopsis