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The domestication of wheat in the Fertile Crescent 10,000 years ago led to a genetic bottleneck. Modern agriculture has further narrowed the genetic base by introducing extreme levels of uniformity on a vast spatial and temporal scale. This reduction in genetic complexity renders the crop vulnerable to new and emerging pests and pathogens. The wild relatives of wheat represent an important source of genetic variation for disease resistance. For nearly a century farmers, breeders, and cytogeneticists have sought to access this variation for crop improvement. Several barriers restricting interspecies hybridization and introgression have been overcome, providing the opportunity to tap an extensive reservoir of genetic diversity. Resistance has been introgressed into wheat from at least 52 species from 13 genera, demonstrating the remarkable plasticity of the wheat genome and the importance of such natural variation in wheat breeding. Two main problems hinder the effective deployment of introgressed resistance genes for crop improvement: (1) the simultaneous introduction of genetically linked deleterious traits and (2) the rapid breakdown of resistance when deployed individually. In this review, we discuss how recent advances in molecular genomics are providing new opportunities to overcome these problems.
Via The Sainsbury Lab
Root-knot nematodes are sedentary biotrophic endoparasites that maintain a complex interaction with their host plants. Nematode effector proteins are synthesized in the oesophageal glands of nematodes and secreted into plant tissue through a needle-like stylet. Effectors characterized to date have been shown to mediate processes essential for nematode pathogenesis. To gain an insight into their site of action and putative function, the subcellular localization of 13 previously isolated Meloidogyne incognita effectors was determined. Translational fusions were created between effectors and EGFP-GUS (enhanced green fluorescent protein-β-glucuronidase) reporter genes, which were transiently expressed in tobacco leaf cells. The majority of effectors localized to the cytoplasm, with one effector, 7H08, imported into the nuclei of plant cells. Deletion analysis revealed that the nuclear localization of 7H08 was mediated by two novel independent nuclear localization domains. As a result of the nuclear localization of the effector, 7H08 was tested for the ability to activate gene transcription. 7H08 was found to activate the expression of reporter genes in both yeast and plant systems. This is the first report of a plant-parasitic nematode effector with transcriptional activation activity.
In nature plants are colonised by beneficial and pathogenic microbes. While plants benefit from the interactions with beneficial microbes (mutualists), pathogenic microbes cause diseases and arrest plant growth. Both mutualistic and pathogenic microbes are initially confronted with a highly effective immune system, which they have to overcome in order to colonise their hosts. Hence, despite the different outcomes of mutualistic and pathogenic interactions, both microbial groups face the same hurdles to establish their accommodation in the plant. A plethora of recent studies indicated that mutualists and pathogens secrete effectors, mainly proteins but also small interfering RNAs, with the purpose not only to manipulate host immunity but also to modify host metabolism in order to create an environment suitable for microbial reproduction.
The session will highlight the current knowledge of how mutualistic and pathogenic microbes employ effectors to successfully establish their respective interactions with plants. The aim is to bring together a group of experts in plant microbe interactions to identify commonalities and discrepancies in the mode of action of mutualistic and pathogenic effectors. Improving our understanding of effector biology will enable us to uncover the molecular principles governing mutualism and disease outbreaks and to synergistically apply this knowledge to sustainably enhance stress adaptation in crops.
A virulent pathogen that starves olive trees poses a serious threat to EU olive production, experts have warned.
"Major consequences", such as reduced yields and costly control measures, would be the outcome if it spreads to other olive producing regions.
It is already affecting a vast area in southern Italy and, as it has numerous hosts and vectors, the bacterium is expected to spread further.
The dire warning was made in a report by the European Food Safety Authority http://www.efsa.europa.eu/en/efsajournal/pub/3989.htm
Perception of pathogen associated molecular patterns (PAMPs) by cell surface localized pattern recognition receptors (PPRs), activates plant basal defense responses in a process known as PAMP/PRR–triggered immunity (PTI). In turn, pathogens deploy effector proteins that interfere with different steps in PTI signaling. However, our knowledge of PTI suppression by filamentous plant pathogens, i.e. fungi and oomycetes, remains fragmentary. Previous work revealed that BAK1/SERK3, a regulatory receptor of several PRRs, contributes to basal immunity against the Irish potato famine pathogen Phytophthora infestans. Moreover BAK1/SERK3 is required for the cell death induced by P. infestans elicitin INF1, a protein with characteristics of PAMPs. The P. infestans host-translocated RXLR-WY effector AVR3a is known to supress INF1-mediated defense by binding the E3 ligase CMPG1. In contrast, AVR3aKI-Y147del, a deletion mutant of the C-terminal tyrosine of AVR3a, fails to bind CMPG1 and suppress INF1 cell death. Here we studied the extent to which AVR3a and its variants perturb additional BAK1/SERK3 dependent PTI responses using the plant PRR FLAGELLIN SENSING 2 (FLS2). We found that all tested variants of AVR3a, including AVR3aKI-Y147del, suppress early defense responses triggered by the bacterial flagellin-derived peptide flg22 and reduce internalization of activated FLS2 from the plasma membrane without disturbing its nonactivated localization. Consistent with this effect of AVR3a on FLS2 endocytosis, we discovered that AVR3a associates with the Dynamin-Related Protein DRP2, a plant GTPase implicated in receptor-mediated endocytosis. Interestingly, DRP2 is required for ligand-induced FLS2 internalization but does not affect internalization of the growth receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1). Furthermore, overexpression of DRP2 suppressed accumulation of reactive oxygen species triggered by PAMP treatment. We conclude that AVR3a associates with a key cellular trafficking and membrane-remodeling complex involved in immune receptor-mediated endocytosis and signaling. AVR3a is a multifunctional effector that can suppress BAK1/SERK3 mediated immunity through at least two different pathways.
Plants and microbes are in a continuous arms race to maintain their predominance within their particular niche. Understanding the complexity of these plant–microbe interactions is of utmost importance as it can provide new insights into the mechanisms mediating disease processes and in turn inspire new plant breeding strategies. The International Society for Molecular Plant–Microbe Interactions (IS-MPMI) invited scientists from around the world to share their findings during the XVI International Congress on Molecular Plant–Microbe Interactions, which was held on the beautiful island of Rhodes in Greece. The congress was organized by the Agricultural University of Athens, the Hellenic Phytopathology Society, and the Hellenic Society of Phytiatry and provided over 1100 participants from 55 countries with the opportunity to present and discuss their current and future research. A great number of talks and posters were presented, however our aim within this report is to provide a snapshot of the discipline by focusing on just some of the exciting research and discussions which took place. The key topics discussed were virulence factors, epigenetic regulation, hormones, symbiosis factors, toxins, signaling pathways, microbe recognition, immunity, and pathogen diagnostics. Effector biology was also a recurrent theme in many plenary and concurrent sessions, indicating the importance of a topic that was also highlighted recently by a Virtual Special Issue in New Phytologist (see Kuhn & Panstruga, 2014). In addition to this, throughout the meeting next generation sequencing (NGS) techniques were described and shown to be shedding new light on long-standing issues in microbial ecology.
A pathogen may cause infected plants to promote the performance of its transmitting vector, which accelerates the spread of the pathogen. This positive effect of a pathogen on its vector via their shared host plant is termed indirect mutualism. For example, terpene biosynthesis is suppressed in begomovirus-infected plants, leading to reduced plant resistance and enhanced performance of the whiteflies (Bemisia tabaci) that transmit these viruses. Although begomovirus-whitefly mutualism has been known, the underlying mechanism is still elusive. Here, we identified βC1 of Tomato yellow leaf curl China virus, a monopartite begomovirus, as the viral genetic factor that suppresses plant terpene biosynthesis. βC1 directly interacts with the basic helix-loop-helix transcription factor MYC2 to compromise the activation of MYC2-regulated terpene synthase genes, thereby reducing whitefly resistance. MYC2 associates with the bipartite begomoviral protein BV1, suggesting that MYC2 is an evolutionarily conserved target of begomoviruses for the suppression of terpene-based resistance and the promotion of vector performance. Our findings describe how this viral pathogen regulates host plant metabolism to establish mutualism with its insect vector.
Symposium aim - We aim to organize a cutting edge meeting focused on the application of cell biology approaches to understand the mechanisms that diverse microbes use to manipulate plant cells to benefit their life styles. The meeting will bring together researchers working on a broad spectrum of microbes across different taxa (bacteria, fungi, oomycetes) that form a variety of different interactions (pathogenic, symbiotic) with plant organs/tissues (leaves, roots). With the explosion in microbial/host genome sequences and the identification of genes/proteins involved in these interactions, the focus of the field is moving rapidly towards using cell and molecular biology techniques and new imaging technologies to understand the molecular dialogue between plants and their microbial pathogens/symbionts. The need for a conference on this topic, the first of its type, is evidenced by the growing prominence of cell biology in the literature. Students and scientists in this field face many challenges in the application and interpretation of cell biology data and would greatly benefit from a specialized conference on this topic. The symposium will bring together a broad representation of researchers focussing on different cell biology aspects and will allow researchers across the different disciplines to present and exchange their recent advances in this important topic of plant biology.
Background - Mutation of Arabidopsis DMR1, encoding homoserine kinase, leads to elevation in homoserine and foliar resistance to the biotrophic pathogens Hyaloperonospora arabidopsidis and Oidium neolycopersici through activation of an unidentified defence mechanism. This study investigates the effect of mutation of dmr1 on resistance to the ascomycete pathogens Fusarium graminearum and F. culmorum, which cause Fusarium Ear Blight (FEB) disease on small grain cereals.
KANSAS CITY, Missouri—Forester Kevin Lapointe remembers clearly the day he and his colleagues at the Kansas City Parks and Recreation Department did their first autopsy on a dead ash tree. Under its peeling bark, they found S-shaped burrows running across every inch of the outer layer of wood. Looking closer, they discovered the killer: a slender green beetle smaller than a penny.
The emerald ash borer, or EAB, a native of East Asia, has already devastated entire ash populations in northern cities such as Detroit, where it first appeared in 2002. Since then, the insect has swept into 22 states across the country. In the summer of 2012 it reached the Kansas City metropolitan area.
There are seven billion ash trees in North America, and within the next few decades, the beetle could kill most of them—a die-off ten times bigger than the one caused by Dutch elm disease.
In big cities, where ash species account for up to a quarter of trees in public spaces, planners must consider the environmental consequences of the massive die-off—liability hazards, an increase in stormwater runoff, and the simple problem of disposing of millions of dead trees. And officials don't have time to waste.
Eight years after the initial discovery of the beetles in an area, about 50 percent of the ash population will die—all at once. The rest die within another two to three years. In the Kansas City metropolitan area, where Lapointe works, 6.4 million ashes are on track to die as early as 2015—unless they receive insecticide treatment.
Chad Tinkel, who inherited an EAB problem when he became the city arborist of Fort Wayne, Indiana, didn't have the luxury of early identification or a big city budget for prevention. Of the 18,000 ash trees that once shaded Fort Wayne's sidewalks and parking lots, only about 1,300 remain alive. Tinkel now speaks about EAB to municipalities across the country.
"If you know that it's coming, be proactive," he says. "Get your plan in place. Get your budget set. Too few decision-makers realize that trees are infrastructure—just like a city bench, just like a streetlight—and they pay back more than they cost to put in."
There are more than 7,000 species of rust fungi, including some of agriculture’s most devastating plant diseases such as Wheat Stem Rust, Wheat Stripe Rust and Asian Soybean Rust which all cause significant yield and financial losses. Rust fungi pose a significant challenge for growers and a serious threat to food security.
The Norwich Rust Group (NRG) brings together seven scientific teams from these leading institutes that all study rust fungi. The close proximity of the three collaborating institutes on the Norwich Research Park allows the seven teams to work as a single force, with rapid access to each others complementary expertise and technologies, and allows for joint appointments across institutes. Together, the Norwich Rust Group works with 52 collaborators in 23 countries around the world in order to develop new technologies and approaches to combat rust fungi in an efficient and durable way.
• A forward-genetic screen identifies loci regulating Arabidopsis immune signaling
Plant perception of pathogen-associated molecular patterns (PAMPs) triggers a phosphorylation relay leading to PAMP-triggered immunity (PTI). Despite increasing knowledge of PTI signaling, how immune homeostasis is maintained remains largely unknown. Here we describe a forward-genetic screen to identify loci involved in PTI and characterize the Arabidopsis calcium-dependent protein kinase CPK28 as a negative regulator of immune signaling. Genetic analyses demonstrate that CPK28 attenuates PAMP-triggered immune responses and antibacterial immunity. CPK28 interacts with and phosphorylates the plasma-membrane-associated cytoplasmic kinase BIK1, an important convergent substrate of multiple pattern recognition receptor (PRR) complexes. We find that BIK1 is rate limiting in PTI signaling and that it is continuously turned over to maintain cellular homeostasis. We further show that CPK28 contributes to BIK1 turnover. Our results suggest a negative regulatory mechanism that continually buffers immune signaling by controlling the turnover of this key signaling kinase.
• A species-wide genetic analysis identifies incompatibility hot spots in the genome
Intraspecific genetic incompatibilities prevent the assembly of specific alleles into single genotypes and influence genome- and species-wide patterns of sequence variation. A common incompatibility in plants is hybrid necrosis, characterized by autoimmune responses due to epistatic interactions between natural genetic variants. By systematically testing thousands of F1 hybrids of Arabidopsis thaliana strains, we identified a small number of incompatibility hot spots in the genome, often in regions densely populated by nucleotide-binding domain and leucine-rich repeat (NLR) immune receptor genes. In several cases, these immune receptor loci interact with each other, suggestive of conflict within the immune system. A particularly dangerous locus is a highly variable cluster of NLR genes, DM2, which causes multiple independent incompatibilities with genes that encode a range of biochemical functions, including NLRs. Our findings suggest that deleterious interactions of immune receptors limit the combinations of favorable disease resistance alleles accessible to plant genomes.
14-3-3 proteins define a eukaryotic-specific protein family with a general role in signal transduction. Primarily, 14-3-3 proteins act as phospho-sensors, binding phosphorylated client proteins and modulating their functions. Since phosphorylation regulates a plethora of different physiological responses in plants, 14-3-3 proteins play roles in multiple signalling pathways, including those controlling metabolism, hormone signalling, cell division, and responses to abiotic and biotic stimuli. Increasing evidence supports a prominent role of 14-3-3 proteins in regulating plant immunity against pathogens at various levels. In this review, potential links between 14-3-3 function and the regulation of plant-pathogen interactions are discussed, with a special focus on the regulation of 14-3-3s in response to pathogen perception, interactions between 14-3-3s and defence-related proteins, and 14-3-3s as targets of pathogen effectors.
Via The Sainsbury Lab
The widely held hypothesis that Glomeromycota fungi alone formed the ancestral land plant–fungus symbiosis (Pirozynski & Dalpé, 1989; Selosse & Le Tacon, 1998; Wang & Qiu, 2006; Parniske, 2008) has recently been challenged by new lines of evidence from molecular, cytological, functional and palaeontological studies. First, liverworts of the earliest divergent clade, the Haplomitriopsida, form a mutualistic mycorrhiza-like relationship, whereby there is reciprocal exchange of plant carbon (C) for fungal nitrogen (N) and phosphorus (P), with members of the Mucoromycotina (Bidartondo et al., 2011; Field et al., 2014), a fungal lineage considered basal or sister to the Glomeromycota (James et al., 2006; Lin et al., 2014). Secondly, other basal plants, including complex and simple thalloid liverworts and hornworts, enter into associations with both Mucoromycotina and Glomeromycota fungi, sometimes simultaneously (Bidartondo et al., 2011; Desirò et al., 2013). Thirdly, dual partnerships involving fungi with affinities to Glomeromycota and Mucoromycotina have been reported in fossils of early vascular plants from the Devonian (Strullu-Derrien et al., 2014).
Via Ronny Kellner
This script informs about importance of late blight in potato, explains both types of resistance, and discusses factors infl uencing resistance expression. The state of research on pathogenicity of P. infestans as well as on resistance on foliage and tubers is reviewed. Epidemiological aspects in assessment of late blight resistance, its stability and the strategy of its use are comprehensively considered. Breeding for late blight resistance in past and present is analysed and reasons for mainly globally insufficient results are given on the background of about 45 years successful pre-breeding under long-day conditions at JKI Gross Luesewitz.
Robert D. Hancock, Saskia Hogenhout, and Christine H. Foyer
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Simon A. Zebelo and Massimo E. Maffei
Joe Louis and Jyoti Shah
Toby J. A. Bruce
Akiko Sugio, Géraldine Dubreuil, David Giron, and Jean-Christophe Simon
Pankaj Barah and Atle M. Bones
Christine H. Foyer, Susan R. Verrall, and Robert D. Hancock
M. O. Harris, T. L. Friesen, S. S. Xu, M. S. Chen, D. Giron, and J. J. Stuart
Alexandra C. U. Furch, Aart J. E. van Bel, and Torsten Will
A. D. Coleman, R. H. M. Wouters, S. T. Mugford, and S. A. Hogenhout
Godshen R. Pallipparambil, Ronald J. Sayler, Jeffrey P. Shapiro, Jean M. G. Thomas, Timothy J. Kring, and Fiona L. Goggin
Chengjun Wu, Carlos A. Avila, and Fiona L. Goggin
Mariam Betsiashvili, Kevin R. Ahern, and Georg Jander
Ishita Ahuja, Nicole Marie van Dam, Per Winge, Marianne Trælnes, Aysel Heydarova, Jens Rohloff, Mette Langaas, and Atle Magnar Bones
Jian Yan, Alexander E. Lipka, Eric A. Schmelz, Edward S. Buckler, and Georg Jander
Ivan Hiltpold, Geoffrey Jaffuel, and Ted C. J. Turlings
James M. W. Ryalls, Ben D. Moore, Markus Riegler, Andrew N. Gherlenda, and Scott N. Johnson
Vesicular trafficking has emerged as an important means by which eukaryotes modulate responses to microbial pathogens, likely by contributing to the correct localization and levels of host components necessary for effective immunity. However, considering the complexity of membrane trafficking in plants, relatively few vesicular trafficking components with functions in plant immunity are known. Here we demonstrate that Arabidopsis thaliana Dynamin-Related Protein 2B (DRP2B), which has been previously implicated in constitutive clathrin-mediated endocytosis (CME), functions in responses to flg22 (the active peptide derivative of bacterial flagellin) and immunity against flagellated bacteria Pseudomonas syringae pv. tomato (Pto) DC3000. Consistent with a role of DRP2B in Pattern-Triggered Immunity (PTI), drp2b null mutant plants also showed increased susceptibility to Pto DC3000 hrcC−, which lacks a functional Type 3 Secretion System, thus is unable to deliver effectors into host cells to suppress PTI. Importantly, analysis of drp2b mutant plants revealed three distinct branches of the flg22-signaling network that differed in their requirement for RESPIRATORY BURST OXIDASE HOMOLOGUE D (RBOHD), the NADPH oxidase responsible for flg22-induced apoplastic reactive oxygen species production. Furthermore, in drp2b, normal MAPK signaling and increased immune responses via the RbohD/Ca2+-branch were not sufficient for promoting robust PR1 mRNA expression nor immunity against Pto DC3000 and PtoDC3000 hrcC−. Based on live-cell imaging studies, flg22-elicited internalization of the plant flagellin-receptor, FLAGELLIN SENSING 2 (FLS2), was found to be partially dependent on DRP2B, but not the closely related protein DRP2A, thus providing genetic evidence for a component, implicated in CME, in ligand-induced endocytosis of FLS2. Reduced trafficking of FLS2 in response to flg22 may contribute in part to the non-canonical combination of immune signaling defects observed in drp2b. In conclusion, this study adds DRP2B to the relatively short list of known vesicular trafficking proteins with roles in flg22-signaling and PTI in plants.
Despite causing considerable damage to host tissue during the onset of parasitism, nematodes establish remarkably persistent infections in both animals and plants. It is thought that an elaborate repertoire of effector proteins in nematode secretions suppresses damage-triggered immune responses of the host. However, the nature and mode of action of most immunomodulatory compounds in nematode secretions are not well understood. Here, we show that venom allergen-like proteins of plant-parasitic nematodes selectively suppress host immunity mediated by surface-localized immune receptors. Venom allergen-like proteins are uniquely conserved in secretions of all animal- and plant-parasitic nematodes studied to date, but their role during the onset of parasitism has thus far remained elusive. Knocking-down the expression of the venom allergen-like protein Gr-VAP1 severely hampered the infectivity of the potato cyst nematode Globodera rostochiensis. By contrast, heterologous expression of Gr-VAP1 and two other venom allergen-like proteins from the beet cyst nematode Heterodera schachtii in plants resulted in the loss of basal immunity to multiple unrelated pathogens. The modulation of basal immunity by ectopic venom allergen-like proteins in Arabidopsis thaliana involved extracellular protease-based host defenses and non-photochemical quenching in chloroplasts. Non-photochemical quenching regulates the initiation of the defense-related programmed cell death, the onset of which was commonly suppressed by venom allergen-like proteins from G. rostochiensis, H. schachtii, and the root-knot nematode Meloidogyne incognita. Surprisingly, these venom allergen-like proteins only affected the programmed cell death mediated by surface-localized immune receptors. Furthermore, the delivery of venom allergen-like proteins into host tissue coincides with the enzymatic breakdown of plant cell walls by migratory nematodes. We, therefore, conclude that parasitic nematodes most likely utilize venom allergen-like proteins to suppress the activation of defenses by immunogenic breakdown products in damaged host tissue.
Understanding how plants balance between enabling microbial symbionts and fending off pathogens has direct implications both for basic plant biology and optimal use of crop plants in agriculture. The degree to which the processes associated with these two types of interactions overlap is poorly known. Recent studies revealed that symbiotic and pathogenic filamentous microbes require common plant genetic elements to establish colonization (Wang et al., 2012; Rey et al., 2013), supporting the long-held view that plants have evolved the ability to accommodate microbes (Parniske, 2000) and that pathogens have exploited these pathways. However, the extent to which plant genes implicated in fungal or bacterial symbioses are involved in interactions with biotrophic pathogens is unknown and research has been hampered by the lack of suitable common host experimental systems.
In this study, we took advantage of a newly established quantitative Phytophthora palmivora–Medicago truncatula system to assess the extent to which mutants perturbed in colonization by arbuscular mycorrhiza fungi (AM fungi) and/or bacterial root nodule symbiosis are affected in the early/biotrophic stages of oomycete pathogenesis (Supporting Information Table S1). We devised and implemented a high throughput seedling infection assay and applied it to 19 M. truncatula lines mutated in 14 genes (for details see Methods S1; for explanation of gene abbreviations see Table S1). We measured both the overall root length and disease development, then plotted them as a ratio (Figs 1a,c, S1; Table S2). Of the 14 genes tested, seven (nine alleles) showed an altered response to P. palmivora inoculation compared with the wild-type Jemalong A17. Mutants in RAM2 and NIP/LATD showed enhanced resistance whereas mutants in five genes, NFP, LYK3, ERN, EFD, and LIN, all of which are impaired in the interaction with nitrogen fixing rhizobia displayed enhanced susceptibility. Expression levels of two defence response genes in M. truncatula mutants with altered disease symptoms were not overall significantly different from levels observed during infection of wild-type A17 seedlings (Fig. S2). This suggests that observed differences in disease extent are not attributable to altered defence responses in these mutants. These findings reveal a significant overlap between processes that define symbiosis and disease in M. truncatula roots. However, the remaining M. truncatula mutants unaltered in P. palmivora disease development include the common symbiotic signalling pathway (CSSP) mutants dmi1, dmi2 and dmi3, suggesting that the CSSP is not a major modulator of susceptibility to P. palmivora in M. truncatula.
Necrosis and ethylene-inducing peptide 1 (Nep1)-like proteins (NLPs) are secreted by a wide range of plant-associated microorganisms. They are best known for their cytotoxicity in dicot plants that leads to the induction of rapid tissue necrosis and plant immune responses. The biotrophic downy mildew pathogen Hyaloperonospora arabidopsidis encodes 10 different noncytotoxic NLPs (HaNLPs) that do not cause necrosis. We discovered that these noncytotoxic NLPs, however, act as potent activators of the plant immune system in Arabidopsis thaliana. Ectopic expression of HaNLP3 in Arabidopsis triggered resistance to H. arabidopsidis, activated the expression of a large set of defense-related genes, and caused a reduction of plant growth that is typically associated with strongly enhanced immunity. N- and C-terminal deletions of HaNLP3, as well as amino acid substitutions, pinpointed to a small central region of the protein that is required to trigger immunity, indicating the protein acts as a microbe-associated molecular pattern (MAMP). This was confirmed in experiments with a synthetic peptide of 24 aa, derived from the central part of HaNLP3 and corresponding to a conserved region in type 1 NLPs that induces ethylene production, a well-known MAMP response. Strikingly, corresponding 24-aa peptides of fungal and bacterial type 1 NLPs were also able to trigger immunity in Arabidopsis. The widespread phylogenetic distribution of type 1 NLPs makes this protein family (to our knowledge) the first proteinaceous MAMP identified in three different kingdoms of life.
Happy holidays from the @KamounLab!
FiFi (Phytophthora) The Oomycete
Fifi the oomycete is a scary parasite,
Fifi the oomycete is a heterokont, they say,
There must have been some magic in those
Fifi the oomycete has a big genome, they say,
O, Fifi the oomycete
Fifi the oomycete found
There must have been some magic in those
For Fifi the oomycete
Oligogalacturonides (OGs) are oligomers of alpha-1,4-linked galacturonosyl residues released from plant cell walls upon partial degradation of homogalacturonan. OGs are able to elicit defense responses, including accumulation of reactive oxygen species and pathogenesis-related proteins, and protect plants against pathogen infections. Recent studies demonstrated that OGs are perceived by wall-associated kinases and share signaling components with microbe-associated molecular patterns. For this reason OGs are now considered true damage-associated molecular patterns that activate the plant innate immunity and may also be involved in the activation of responses to mechanical wounding. Furthermore, OGs appear to modulate developmental processes, likely through their ability to antagonize auxin responses. Here we review our current knowledge on the role and mode of action of this class of oligosaccharides in plant defense and development.
The biogenesis and functions of the extrahaustorial membrane (EHM), an intimate interface between plants and filamentous pathogens, are poorly understood. One long-standing puzzle is why several membrane proteins, such as some cell surface receptors, are missing from the EHM. We gained a significant insight into how the EHM is formed and made an important step in understanding why certain membrane proteins are missing from the EHM. We discovered that late endosomes targeted to the vacuoles are rerouted to the EHM. This process is dynamic because, upon activation, a cell surface immune receptor traffics to this compartment. We propose a model in which some cell surface receptors that undergo ligand induced endocytosis and traffic to late endosomes get sorted to the host pathogen interface, instead of taking the default route to the vacuole as in uninfected cells.
--- A number of plant pathogenic and symbiotic microbes produce specialized cellular structures that invade host cells where they remain enveloped by host-derived membranes. The mechanisms underlying the biogenesis and functions of host-microbe interfaces are poorly understood. Here, we show that plant late endocytic trafficking is diverted towards the extrahaustorial membrane; a host-pathogen interface that develops in plant cells invaded by Irish potato famine pathogen Phytophthora infestans. A late endosome and tonoplast marker protein Rab7 GTPase RabG3c, but not a tonoplast-localized sucrose transporter, is recruited to the extrahaustorial membrane suggesting specific rerouting of vacuole targeted late endosomes to a host pathogen interface. We revealed the dynamic nature of this process by showing that, upon activation, a cell surface immune receptor traffics towards the haustorial interface. Our work provides insight into the biogenesis of the extrahaustorial membrane and reveals dynamic processes that recruit membrane compartments and immune receptors to this host-pathogen interface.
THERE are concerns for the future of Tasmania’s poppy industry — source for half the world’s morphine and related pharmaceutical opiates — as a so-far unstoppable disease threatens the $400 million crop.
In the six weeks since a virulent strain of downy mildew began to be noticed in the state’s poppy crops, up to 10 per cent has been hit by the disease.
There have been some promising trials of new chemical treatments but existing fungicides have so far failed to abate the fungus, whose spores can travel hundreds of kilometres on the wind.
An urgent research effort was launched this week by growers, government and industry to try to identify and tackle the mildew, which stunts plant growth and can decimate entire paddocks. While growers and experts insist the industry will survive, The Weekend Australian has learned of fears that because of the increased cost of more frequent fungicide treatments, farmers may dump poppies.
Poppy Growers Tasmania president Glynn Williams said such an increased burden, at a time of a decline in prices paid to poppy growers, could force some to walk away from the crop.
“I’m now spraying my crops on a weekly basis and that’s time and diesel and a lot of money spent on chemicals,” Mr Williams said.
“Prices (paid to farmers for poppies) haven’t risen for two years … and we’ve had a 12.5 per cent decrease from one company.
“And if you then see a significant increase in the cost of growing the crop, that could be something you have to look at pretty hard. If they don’t start raising prices, farmers will stop growing poppies.”
The crop is the state’s third most valuable agricultural product and is worth about $90 million at the farm gate and $400m to Tasmania’s gross state product.
While downy mildew has been present in Tasmanian poppy crops for more than a decade, damaging leaves of the plant, the new strain stunts entire plant growth, preventing flowering.
One of two lead researchers trying to identify and tackle the disease, Jason Scott, told The Weekend Australian an early task was to use DNA testing to discover if the new strain evolved from the existing one or had been recently introduced.
Dr Scott said if it was the existing strain involved, the research would have to work out why it had developed resistance to existing chemical treatments.
A $320,000 research fund will pay for a visit from Austrian expert Hermann Voglmayr, who has mapped gene sequences of poppy mildew species.