A plant may be rooted in place, but it is never lonely. There are bacteria in, on and near it, munching away on their host, on each other, on compounds in the soil. Amoebae dine on bacteria, nematodes feast on roots, insects devour fruit — with consequences for the chemistry of the soil, the taste of a leaf or the productivity of a crop.
From 30 June to 2 July, more than 200 researchers gathered in Washington DC for the first meeting of the Phytobiomes Initiative, an ambitious proposal to catalogue and characterize a plant’s most intimate associates and their impact on agriculture. By the end of the year, attendees hope to carve out a project that will apply this knowledge in ways that will appeal to funders in industry and government.
“We want to get more money,” says plant pathologist Linda Kinkel at the University of Minnesota in St Paul. “But beyond that, let’s just all try to talk the same language and come up with some shared goals.”
Leach coined the term phytobiome in 2013,at a retreat about food security. She defines the phytobiome broadly, to encompass microbes, insects, nematodes and plants as well as the abiotic factors that influence all these.
Since then, she has visited companies, funding agencies and universities to call for a unifying phytobiomes initiative. She has teamed up with Kellye Eversole, a consultant based in Bethesda, Maryland, and the co-owner of a small family farm in Oklahoma, who has experience working on large agricultural genomics projects, including the US National Plant Genome Initiative. That initiative was launched in 1998 and continues to crank out databases and other tools for analysing plant genomes.
Leach hopes that the Phytobiomes Initiative will leave a similar legacy, but she is mindful that federal funding has tightened considerably since 1998. Still, she notes that the project can build on several emerging trends in agriculture. Industry has shown renewed interest in boosting plant growth by manipulating associated microbes (Nature 504, 199; 2013). Companies and farmers are also investing in ‘precision agriculture’, which uses high-tech monitors to track conditions in a field or even around individual plants, allowing farmers to water and fertilize in exactly the right places.
Eversole foresees a day when tractors will carry dipstick-like gauges that provide a snapshot of the microbial community in the soil. Data from the Phytobiomes Initiative would then help farmers to manipulate that community to their advantage, she says.
But first, the initiative needs to standardize protocols and metrics, the meeting’s attendees determined. Kinkel says that efforts are likely to focus initially on cataloguing microbes and insects and their interactions with different crops and habitats. “We’re where plant biologists were 150 years ago,” she says. “We’re still trying to inventory things.”
Work has already begun along these lines: for example, a group at the International Rice Research Institute in Los Baños in the Philippines is fishing for microbial DNA in data discarded from an effort to sequence the rice genome. The goal is to determine which microbes prefer which strains of the crop.
Kinkel, meanwhile, has begun experimenting with manipulating carbon levels in the soil to alter the microbial population, with the aim of improving plant productivity. “If we can understand better who lives on and within plants, we have the potential to manage them to have healthier, more resilient plants,” she says.
Projects such as these would move faster under an organized, cohesive framework, says Sarah Lebeis, a microbiologist at the University of Tennessee in Knoxville who is studying how plants manipulate microbial communities by secreting antibiotics into the soil. “Right now we’re working as individuals,” she says. “Having an initiative will give us focus and hopefully we’ll progress further, faster, better.”
Like other plant-pathogenic oomycetes, downy mildew species of the genus Hyaloperonosporamanipulate their hosts by secreting effector proteins. Despite intense research efforts devoted to deciphering the virulence and avirulence activities of effectors in the H. arabidopsidis/Arabidopsis thaliana pathosystem, there is only a single study in this pathosystem on the variation of effectors and resistance genes in natural populations, and the evolution of these effectors in the context of pathogen evolution is studied even less. In this work, the identification of Arabidopsisthalianarecognised (ATR)1-homologs is reported in two sister species of H. arabidopsidis, H. thlaspeos-perfoliati, and H. crispula, which are specialized on the host plants Microthlaspi perfoliatum and Reseda lutea, respectively. ATR1-diversity within these sister species of H. arabidopsidis was evaluated, and the ATR1-homologs from different isolates of H. thlaspeos-perfoliati and H. crispulawere tested to see if they would be recognised by the previously characterised RPP1-WsB protein from A. thaliana. None of the effectors from the sister species was recognised, suggesting that due to the adaptation to altered or new targets after a host jump, features of variable effectors might vary to a degree that recognition of orthologous Avr-causing effectors is no longer effective and probably does not contribute to non-host immunity.
Chloroplast stromules are induced during plant immune responses
Pro-PCD signals such as SA and H2O2 induce stromules
Stromules form dynamic connections with nucleus during immune responses
Constitutively induced stromules enhance PCD during plant immune responses
Inter-organellar communication is vital for successful innate immune responses that confer defense against pathogens. However, little is known about how chloroplasts, which are a major production site of pro-defense molecules, communicate and coordinate with other organelles during defense. Here we show that chloroplasts send out dynamic tubular extensions called stromules during innate immunity or exogenous application of the pro-defense signals, hydrogen peroxide (H2O2) and salicylic acid. Interestingly, numerous stromules surround nuclei during defense response, and these connections correlate with an accumulation of chloroplast-localized NRIP1 defense protein and H2O2 in the nucleus. Furthermore, silencing and knockout of chloroplast unusual positioning 1 (CHUP1) that encodes a chloroplast outer envelope protein constitutively induces stromules in the absence of pathogen infection and enhances programmed cell death. These results support a model in which stromules aid in the amplification and/or transport of pro-defense signals into the nucleus and other subcellular compartments during immunity.
Magnaporthe oryzae (Mo) is the causative pathogen of the damaging disease rice blast. The effector gene AvrPib, which confers avirulence to host carrying resistance gene Pib, was isolated via map-based cloning. The gene encodes a 75-residue protein, which includes a signal peptide. Phenotyping and genotyping of 60 isolates from each of five geographically distinct Mo populations revealed that the frequency of virulent isolates, as well as the sequence diversity within the AvrPib gene increased from a low level in the far northeastern region of China to a much higher one in the southern region, indicating a process of host-driven selection. Resequencing of the AvrPiballele harbored by a set of 108 diverse isolates revealed that there were four pathoways, transposable element (TE) insertion (frequency 81.7%), segmental deletion (11.1%), complete absence (6.7%), and point mutation (0.6%), leading to loss of the avirulence function. The lack of any TE insertion in a sample of non-rice infecting Moisolates suggested that it occurred after the host specialization of Mo. Both the deletions and the functional point mutation were confined to the signal peptide. The reconstruction of 16 alleles confirmed seven functional nucleotide polymorphisms for the AvrPiballeles, which generated three distinct expression profiles.
The HM1 gene in maize controls both race-specific resistance to the fungus Cochliobolus carbonum race 1 and expression of the NADPH (reduced form of nicotinamide adenine dinucleotide phosphate)-dependent HC toxin reductase (HCTR), which inactivates HC toxin, a cyclic tetrapeptide produced by the fungus to permit infection. Several HM1 alleles were generated and cloned by transposon-induced mutagenesis. The sequence of wild-type HM1 shares homology with dihydroflavonol-4-reductase genes from maize, petunia, and snap-dragon. Sequence homology is greatest in the beta alpha beta-dinucleotide binding fold that is conserved among NADPH- and NADH (reduced form of nicotinamide adenine dinucleotide)-dependent reductases and dehydrogenases. This indicates that HM1 encodes HCTR.
The avirulence gene avrBs3 from Xanthomonas campestris pv. vesicatoria was cloned and found to be localized on a self-transmissable plasmid. Genetic analysis of an avrBs3 insertion mutation revealed that avrBs3 constitutes a single locus, specifying the resistant phenotype on pepper plants. Southern blot experiments showed that no DNA sequences homologous to avrBs3 were present in other races of X. c. pv. vesicatoria, which are unable to induce a hypersensitive reaction on ECW-30R. However, the DNA of several different pathovars of X. campestris hybridized to the avrBs3 probe. A deletion analysis defined a region of 3.6–3.7 kb essential for avrBs3 activity. The nucleotide sequence of this region was determined. A 3561 nucleotide open reading frame (ORF1), encoding a 125000 dalton protein, was found in the 3.7 kb region that was sufficient for avrBs3activity. A second long ORF (2351 nucleotides) was identified on the other strand. A remarkable feature of both ORFs is the presence of 17 direct repeats of 102 bp which share 91%–100% homology with each other.
Plant innate immunity depends on recognition of pathogen effectors and triggering of host defenses. Major classes of innate immune receptors, the nucleotide binding-leucine rich repeat receptors (NLRs) and leucine rich repeat (LRR) receptors are encoded by large families of resistance (R)-genes. NLR and LRRs are activated by recognition of specific pathogen effectors and once activated they trigger the hypersensitive cell-death response. While multiple NLRs and LRRs protect plants from diverse pathogens their inherent cell death activity and the large number of encoding R-genes in plant genomes require strict regulation.
Plant microRNAs (miRNAs) and small interfering RNAs (siRNAs) guide sequence-specific silencing of genes, repetitive DNA and viruses through Watson-Crick base pairing and play essential regulatory roles in development, genome function and host defines. We discovered novel miRNA families whose members silence R-gene encodingNLRs and LRRs including those that confer resistance to the major pathogens of Solanaceae crops. Many of these novel miRNAs belong to a structurally and functionally unique class of 22-nt miRNAs and amplify silencing by triggering the production of secondary trans-acting siRNAs (tasiRNAs) from cleaved transcripts. The lab further showed that miRNA overexpression leads to attenuated R-gene mediated pathogen resistance. We propose that the R-gene miRNAs and tasiRNAs form a regulatory silencing network to fine tune pathogen defense responses and facilitate expansion and evolution of new NLRs.
The Oomycota include many economically significant microbial pathogens of crop species. Understanding the mechanisms by which oomycetes infect plants and identifying methods to provide durable resistance are major research goals. Over the last few years, many elicitors that trigger plant immunity have been identified, as well as host genes that mediate susceptibility to oomycete pathogens. The mechanisms behind these processes have subsequently been investigated and many new discoveries made, marking a period of exciting research in the oomycete pathology field. This review provides an introduction to our current knowledge of the pathogenic mechanisms used by oomycetes, including elicitors and effectors, plus an overview of the major principles of host resistance: the established R gene hypothesis and the more recently defined susceptibility (S) gene model. Future directions for development of oomycete-resistant plants are discussed, along with ways that recent discoveries in the field of oomycete-plant interactions are generating novel means of studying how pathogen and symbiont colonizations overlap.
More than 40 million home gardens will be going in this spring and nearly all will have a tomato plant of some variety -- heirloom or hybrid.
Tomatoes are by far the most popular edible plant home gardeners grow. There are thousands of varieties out there and more appear every season.
Park Seed has just released a new tomato seed series called “Heirloom Marriages” that crosses favorites such as Brandywine with other open-pollinated varieties such as Big Dwarf. The elusive goal is to get the heirloom flavor and texture in a plant that is a heavy producer, ripens quickly and is disease-resistant.
For many tomato growers, keeping plants healthy until harvest is the most frustrating of tasks. Tomatoes can be attacked from the roots up to the top of the stem: wilting, rotting, stunting, damping off. The fruit can turn black, yellow, mottled, mushy or never appear at all.
The list of symptoms is long and the possible causes are depressingly complex: insects, parasites, fungi, viruses, bacteria, nutrition, weather, too much water, too little water, nematodes. It goes on and on.
Fortunately there is a new tool that is as essential in the garden as a trowel: Tomato MD, an inexpensive interactive phone app (Android/Apple-iOs) that allows fast identification of a plant’s problem: root, leaf, stem or fruit. The app is set up to take you through the most difficult part of dealing with a sick plant: what’s wrong and what is causing it. There is an index of diseases, insects, mites; an extensive photo gallery of the most common diseases; a list of diseases listed by their characteristics. Control solutions and other possible hosts for the problem are suggested when applicable.
The $3 app comes from the publishing arm of the American Phytopathological Society, a 100-year-old nonprofit that focuses on plant health management.
Most of the society's 300+ publications have been designed for professional farmers and growers but this app has the home gardener in mind. But if you want to definitively know the cause, there is a list of labs where you can send your sick plant, along with instructions on how to package the plant for shipment.
One of the world's most important staple crops, the sweet potato, is a naturally transgenic plant that was genetically modified thousands of years ago by a soil bacterium. This surprising discovery may influence the public view of GM crops.
Strains of bacteria from the genus Agrobacterium have a well-characterized and widely utilized capacity to introduce DNA into plant cells1. The transferred DNA (T-DNA) is specified by short left and right border sequences, and is delivered from the bacterium into plant cells by a mechanism that evolved from bacterial conjugation2. Essentially, the bacteria have sex with the plant. The bacteria-derived genes perturb plant hormonal balances causing tumour-like galls, and also modify plant metabolism to support bacterial growth, by forcing the plant to produce sugar–amino acid conjugates called opines that can only be used as nutrients by agrobacteria. Previously, using less-refined methods, some evidence was found for Agrobacterium-derived sequences inherited in the germ lines of Nicotiana glauca and Linaria vulgaris species, so heritable genetic modification of plants without human intervention is not new3,4. But these plants are not important food crops. Now, Kyndt et al.5 report in Proceedings of the National Academy of Sciences USA that during or prior to domestication, Agrobacterium-derived T-DNA became incorporated into the genome of one of the world's staple crops, the hexaploid sweet potato (Ipomoea batatas).
Priming of defence genes for amplified response to secondary stress can be induced by application of the plant hormone salicylic acid or its synthetic analogue acibenzolar S‐methyl. In this study, we show that treatment with acibenzolar S‐methyl or pathogen infection of distal leaves induce chromatin modifications on defence gene promoters that are normally found on active genes, although the genes remain inactive. This is associated with an amplified gene response on challenge exposure to stress. Mutant analyses reveal a tight correlation between histone modification patterns and gene priming. The data suggest a histone memory for information storage in the plant stress response.
Hyphal fusion is a ubiquitous phenomenon in filamentous fungi. Although morphological aspects of hyphal fusion during vegetative growth are well described, molecular mechanisms associated with self-signaling and the cellular machinery required for hyphal fusion are just beginning to be revealed. Genetic analyses suggest that signal transduction pathways are conserved between mating cell fusion in Saccharomyces cerevisiaeand vegetative hyphal fusion in filamentous fungi. However, the mechanism of self-signaling and the role of vegetative hyphal fusion in the biology of filamentous fungi require further study. Understanding hyphal fusion in model genetic systems, such as Neurospora crassa, provides a paradigm for self-signaling mechanisms in eukaryotic microbes and might also provide a model for somatic cell fusion events in other eukaryotic species.
Hyphal fusion (anastomosis) occurs at crucial stages during the life cycle of filamentous fungi and serves many important functions. During the vegetative phase, fusion initially occurs between spore germlings, and later on in the interior of the mature vegetative colony. Figure 1 shows the interconnected mycelial network of a fungal colony that results from multiple fusion events. It is widely assumed that vegetative hyphal fusion is important for intra-hyphal communication, translocation of water and nutrients, and general homeostasis within a colony 1 and 2. However, these predicted roles still need to be analyzed experimentally.
Plants are the source of most of our food, whether directly or as feed for the animals we eat. Our dinner table is a trophic level we share with the microbes that also feed on the primary photosynthetic producers. Microbes that enter into close interactions with plants need to evade or suppress detection and host immunity to access nutrients. They do this by deploying molecular tools – effectors – which target host processes. The mode of action of effector proteins in these events is varied and complex. Recent data from diverse systems indicate that RNA-interacting proteins and RNA itself are delivered by eukaryotic microbes, such as fungi and oomycetes, to host plants and contribute to the establishment of successful interactions. This is evidence that pathogenic microbes can interfere with the host software. We are beginning to see that pathogenic microbes are capable of hacking into the plants' immunity programs.
The root hemiparasite witchweed (Striga spp.) is a devastating agricultural pest that causes losses of up to $1 billion US annually in sub-Saharan Africa. Development of resistant crops is one of the cost-effective ways to address this problem. However, the molecular mechanisms underlying resistance are not well understood. To understand molecular events upon Striga spp. infection, we conducted genome-scale RNA sequencing expression analysis using Striga hermonthica-infected rice (Oryza sativa) roots. We found that transcripts grouped under the Gene Ontology term defense response were significantly enriched in up-regulated differentially expressed genes. In particular, we found that both jasmonic acid (JA) and salicylic acid (SA) pathways were induced, but the induction of the JA pathway preceded that of the SA pathway. Foliar application of JA resulted in higher resistance. The hebiba mutant plants, which lack the JA biosynthesis gene ALLENE OXIDE CYCLASE, exhibited severe S. hermonthica susceptibility. The resistant phenotype was recovered by application of JA. By contrast, the SA-deficient NahG rice plants were resistant against S. hermonthica, indicating that endogenous SA is not required for resistance. However, knocking down WRKY45, a regulator of the SA/benzothiadiazole pathway, resulted in enhanced susceptibility. Interestingly, NahG plants induced the JA pathway, which was down-regulated in WRKY45-knockdown plants, linking the resistant and susceptible phenotypes to the JA pathway. Consistently, the susceptibility phenotype in the WRKY45-knockdown plants was recovered by foliar JA application. These results point to a model in which WRKY45 modulates a cross talk in resistance against S. hermonthica by positively regulating both SA/benzothiadiazole and JA pathways.
Cell-to-cell and long-distance trafficking of RNA is a rapidly evolving frontier of integrative plant biology that broadly impacts studies on plant growth and development, spread of infectious agents and plant defense responses. The fundamental questions being pursued at the forefronts revolve around function, mechanism and evolution. In the present review, we will first use specific examples to illustrate the biological importance of cell-to-cell and long-distance trafficking of RNA. We then focus our discussion on research findings obtained using viroids that have advanced our understanding of the underlying mechanisms involved in RNA trafficking. We further use viroid examples to illustrate the great diversity of trafficking machinery evolved by plants, as well as the promise for new insights in the years ahead. Finally, we discuss the prospect of integrating findings from different experimental systems to achieve a systems-based understanding of RNA trafficking function, mechanism and evolution.
The avirulence gene AvrLm4-7 of Leptosphaeria maculans, the causal agent of stem canker of oilseed rape, confers a dual specificity of recognition by two resistance genes (Rlm4 and Rlm7) and is strongly involved in fungal fitness. In order to elucidate the biological function of AvrLm4-7 and understand the specificity of recognition by Rlm4 and Rlm7, the AvrLm4-7 protein was produced in Pichia pastoris and its crystal structure determined. It revealed the presence of four disulfide bridges but no close structural analogs could be identified. A short stretch of amino acids in the C-terminus of the protein, (R/N)(Y/F)(R/S)E(F/W), was well-conserved among AvrLm4-7 homologs. Loss of recognition of AvrLm4-7 by Rlm4 is due to mutation of a single glycine to an arginine residue located in a loop of the protein. Loss of recognition by Rlm7 is governed by more complex mutational patterns, including gene loss or drastic modifications of the protein structure. Three point mutations altered residues in the well-conserved C-terminal motif or close to the glycine involved in Rlm4-mediated recognition, resulted in a loss of Rlm7-mediated recognition. Transient expression in tobacco and particle bombardment experiments on oilseed rape leaves suggested that AvrLm4-7 interacts with its cognate R proteins inside the plant cell, and can be translocated into plant cells in the absence of the pathogen. Translocation of AvrLm4-7 into oilseed rape leaves likely requires the (R/N)(Y/F)(R/S)E(F/W) motif as well as a RAWG motif located in a nearby loop that together form a positively charged region.
Coevolutionary interactions are thought to have spurred the evolution of key innovations and driven the diversification of much of life on Earth. However, the genetic and evolutionary basis of the innovations that facilitate such interactions remains poorly understood. We examined the coevolutionary interactions between plants (Brassicales) and butterflies (Pieridae), and uncovered evidence for an escalating evolutionary arms-race. Although gradual changes in trait complexity appear to have been facilitated by allelic turnover, key innovations are associated with gene and genome duplications. Furthermore, we show that the origins of both chemical defenses and of molecular counter adaptations were associated with shifts in diversification rates during the arms-race. These findings provide an important connection between the origins of biodiversity, coevolution, and the role of gene and genome duplications as a substrate for novel traits.
It has spread across the Pacific and already reached Oz – so what will myrtle rust mean for our native flora?
Most New Zealand gardeners will be familiar with the consequences of the arrival of a new kid in town. In the late 1970s, oriental fruit moth arrived and immediately begun stuffing up any ripening peaches in the North Island.
Painted apple moth was targeted through an aerial spraying programme and eradicated for a mere million dollars or so; the same with salt marsh mosquitoes. Varroa escaped into our beehives, tomato psyllid into our backyard and the fruit fly outbreak in inner city Auckland is currently threatening half of our export economy.
And that's just the pests. We rarely talk about diseases illegally arriving here. The last one to seriously affect gardeners were the two fungal diseases that kill box hedges which are now widespread in the north.
The bad news is, myrtle rust is about to break in via our back door; we know it's coming but we don't know when. Perhaps it's only a matter of some strong westerlies over the Tasman Sea or the hapless flight of a moth, aphid or butterfly from east Australia to New Zealand.
More often than not, this appears to be the direct route for organisms. Even wingless and flightless mites and spiders successfully and regularly make it from Australia to Aotearoa, pushed by fast-moving fronts.
Myrtle rust (Puccinia psidii) is a particularly vigorous traveller. It originated in South America, floated up to North America, and flew to Hawaii, China, Japan and South Africa, before reaching Australia in 2010 and New Caledonia in 2013. It's a particularly nasty rust disease of most, if not all, members of the myrtacea family; it behaves just like the rust on your roses and the rust species you'll find infesting poplar shelterbelts, especially in the cooler parts of our country.
The leaves display small, purple spots at first, which become lesions that grow and grow. Yellow pustules of spores are formed, which start to dominate the diagnostic pattern of myrtle rust. Those spores are microscopic in size and can easily float in the breeze or be splashed around in rain showers.
As soon as those spores land on a moist or wet leaf of a suitable host, infection is on the cards. A plant with many lesions not only produces billions of spores, it also quickly goes backwards in terms of health. Die-back of twigs and branches will spread, signalling the terminal decline of the host tree.
Seedlings are particularly susceptible to this rust disease; mortality can be enormous. If the carnage in eastern Australia is anything to go by, we'd better be prepared for this yellow peril. Their main myrtaceous plants are eucalypts – and there are quite a few of those in Oz! Our forestry industry frequently grows this genus too and there's no doubt that the rust would hammer our gum tree stands, especially in the North Island. (The cooler parts of the South Island may be marginal or even inhospitable for Puccinia psidii.)
But remember: pohutukawa, rata, manuka and kanuka are also in the myrtle family, so our native icons are likely to be just as much at risk. Imagine a wholesale decline of our Christmas tree (Metrosideros excelsa) and rata species; Project Crimson would have to start all over again!
The products of plant disease resistance genes are postulated to recognize invading pathogens and rapidly trigger host defense responses. Here we describe isolation of the resistance gene N of tobacco that mediates resistance to the viral pathogen tobacco mosaic virus (TMV). The N gene was isolated by transposon tagging using the maize Activator transposon. A genomic DNA fragment containing the N gene conferred TMV resistance to TMV susceptible tobacco. Sequence analysis of the N gene shows that it encodes a protein of 131.4 kDa with an amino-terminal domain similar to that of the cytoplasmic domain of the Drosophila Toll protein and the interleukin-1 receptor (IL-1R) in mammals, a nucleotide-binding site (NBS), and 4 imperfect leucine-rich repeats (LRR). The sequence similarity of N, Toll, and IL-1R suggests that N mediates rapid gene induction and TMV resistance through a Toll-IL-1-like pathway.
Leaves are among the most abundant organs on earth and are a defining feature of most terrestrial ecosystems. However, a leaf is also a potential meal for a hungry animal and the question therefore arises, why does so much foliage survive in nature? What mechanisms protect leaves so that, on a global scale, only a relatively small proportion of living leaf material is consumed? Leaf survival is in large part due to two processes: firstly, leaf-eating organisms fall prey to predators (top-down pressure on the herbivore); secondly, leaves defend themselves (bottom-up pressure on the herbivore). Remarkably, these two types of event are often linked; they are controlled and coordinated by plants and the molecular mechanisms that underlie this are now beginning to emerge.
This novel text focuses exclusively on the leaf, on the herbivorous organisms that attack leaves, and the mechanisms that plants use to defend these vital organs. It begins with an assessment of the scale of herbivory, before examining direct physical and chemical defences on leaf surfaces and within the leaf itself. Although some leaf defences are easily seen, most operate at the molecular level and are therefore invisible to the naked eye. Many of these recently elucidated mechanisms are described. Throughout the book, perspectives from both the laboratory and the field are combined. A central feature of the work is its emphasis on the coevolution of leaf defences and the digestive tracts of animals including humans, making the book of relevance in understanding the role of leaf defences in agriculture.
Leaf Defence is suitable for senior undergraduate and graduate students taking courses in plant science, as well as a broader audience of biologists and biochemists seeking a comprehensive and authoritative overview of this exciting and emerging topic.
Readership: Senior undergraduate and graduate students taking courses in plant science, as well as a broader audience of biologists and biochemists seeking a comprehensive and authoritative overview of this exciting and emerging topic.
• Appressorium development is linked to cell cycle checkpoints controlling morphogenesis. • Ras GTPase signalling acts upstream of cAMP and MAP kinase pathways for appressorium development. • Melanin is not exclusively associated with appressorium turgor generation. • Septin-mediated actin re-modelling is essential for appressorium function. • Focal secretion of effectors occurs during appressorium infection.
Many plant pathogenic fungi have the capacity to breach the intact cuticles of their plant hosts using specialised infection cells called appressoria. These cells exert physical force to rupture the plant surface, or deploy enzymes in a focused way to digest the cuticle and plant cell wall. They also provide the means by which focal secretion of effectors occurs at the point of plant infection. Development of appressoria is linked to re-modelling of the actin cytoskeleton, mediated by septin GTPases, and rapid cell wall differentiation. These processes are regulated by perception of plant cell surface components, and starvation stress, but also linked to cell cycle checkpoints that control the overall progression of infection-related development.
A rise in resistance to current antifungals necessitates strategies to identify alternative sources of effective fungicides. We report the discovery of poacic acid, a potent antifungal compound found in lignocellulosic hydrolysates of grasses. Chemical genomics using Saccharomyces cerevisiae showed that loss of cell wall synthesis and maintenance genes conferred increased sensitivity to poacic acid. Morphological analysis revealed that cells treated with poacic acid behaved similarly to cells treated with other cell wall-targeting drugs and mutants with deletions in genes involved in processes related to cell wall biogenesis. Poacic acid causes rapid cell lysis and is synergistic with caspofungin and fluconazole. The cellular target was identified; poacic acid localized to the cell wall and inhibited β-1,3-glucan synthesis in vivo and in vitro, apparently by directly binding β-1,3-glucan. Through its activity on the glucan layer, poacic acid inhibits growth of the fungi Sclerotinia sclerotiorum and Alternaria solani as well as the oomycete Phytophthora sojae. A single application of poacic acid to leaves infected with the broad-range fungal pathogen S. sclerotiorumsubstantially reduced lesion development. The discovery of poacic acid as a natural antifungal agent targeting β-1,3-glucan highlights the potential side use of products generated in the processing of renewable biomass toward biofuels as a source of valuable bioactive compounds and further clarifies the nature and mechanism of fermentation inhibitors found in lignocellulosic hydrolysates.
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