Parasite effector proteins target various host cell compartments to alter host processes and promote infection. How effectors cross membrane-rich interfaces to reach these compartments is a major question in effector biology. Growing evidence suggests that effectors use molecular mimicry to subvert host cell machinery for protein sorting. We recently identified CTP1 (chloroplast-targeted protein 1), a candidate effector from the poplar leaf rust fungus Melampsora larici-populina that carries a predicted transit peptide and accumulates in chloroplasts. Here, we show that the CTP1 transit peptide is necessary and sufficient for accumulation in the stroma of chloroplasts, and is cleaved after translocation. CTP1 is part of a Melampsora-specific family of polymorphic secreted proteins whose members translocate and are processed in chloroplasts in a N-terminal signal-dependent manner. Our findings reveal that fungi have evolved effector proteins that mimic plant-specific sorting signals to traffic within plant cells.
The introgression of disease resistance (R) genes encoding immunoreceptors with broad-spectrum recognition into cultivated potato appears to be the most promising approach to achieve sustainable management of late blight caused by the oomycete pathogen Phytophthora infestans. Rpi-blb2 from Solanum bulbocastanum, shows great potential for use in agriculture based on preliminary potato disease trials. Rpi-blb2 confers immunity by recognizing the P. infestans avirulence effector protein AVRblb2 after it is translocated inside the plant cell. This effector belongs to the RXLR class of effectors and is under strong positive selection. Structure-function analyses revealed a key polymorphic amino acid (position 69) in AVRblb2 effector that is critical for activation of Rpi-blb2. In this study, we reconstructed the evolutionary history of the Avrblb2 gene family and further characterized its genetic structure in worldwide populations. Our data indicates that Avrblb2 evolved as a single copy gene in a putative ancestral species of P. infestans and has recently expanded in the Phytophthora species that infect solanaceous hosts. As a consequence, at least four variants of AVRblb2 arose in P. infestans. One of these variants, with a Phe residue at position 69, evades recognition by the cognate resistance gene. Surprisingly, all Avrblb2 variants are maintained in pathogen populations. This suggests a potential benefit for the pathogen in preserving duplicated versions of AVRblb2 possibly because the variants may have different contributions to pathogen fitness in a diversified solanaceous host environment.
Potato late blight, caused by the destructive Irish famine pathogen Phytophthora infestans, is a major threat to global food security1,2. All late blight resistance genes identified to date belong to the coiled-coil, nucleotide-binding, leucine-rich repeat class of intracellular immune receptors3. However, virulent races of the pathogen quickly evolved to evade recognition by these cytoplasmic immune receptors4. Here we demonstrate that the receptor-like protein ELR (elicitin response) from the wild potato Solanum microdontum mediates extracellular recognition of the elicitin domain, a molecular pattern that is conserved in Phytophthora species. ELR associates with the immune co-receptor BAK1/SERK3 and mediates broad-spectrum recognition of elicitin proteins from several Phytophthora species, including four diverse elicitins from P. infestans. Transfer of ELR into cultivated potato resulted in enhanced resistance to P. infestans. Pyramiding cell surface pattern recognition receptors with intracellular immune receptors could maximize the potential of generating a broader and potentially more durable resistance to this devastating plant pathogen.
In a rare gathering, genomics met palaeontology at the 10th New Phytologist Workshop on the ‘Origin and evolution of plants and their interactions with fungi’. An eclectic group of 17 experts met at The Natural History Museum (London, UK) on 9–10 September 2014 to discuss the latest findings on plant interactions with fungi (Eumycota) and oomycetes (Oomycota = Peronosporomycota), with topics ranging from the fossil record and comparative genomics to symbiosis and phytopathology. The discussions were largely disseminated via social media (Box 1). Highly diverse plant–fungal interactions have formed the backbone of land ecosystems and biogeochemical cycles since the Palaeozoic (see Fig. 1 for geological timeframe). As summarized by Christine Strullu-Derrien and Paul Kenrick (The Natural History Museum, London, UK) the first land plants arose c. 470 million years (Myr) ago (Kenrick et al., 2012; Edwards et al., 2014), at which time fungi and oomycetes had already colonized terrestrial ecosystems. Following their terrestrialization, these microbes began to abound within plant fossils (Taylor et al., 2014, and references therein). Ultimately, biological interactions sculpted the genomes of plants, fungi and oomycetes (e.g. Schmidt & Panstruga, 2011; Kohler et al., 2015). Here we illustrate the picture that has emerged from the discussions at the 10th New Phytologist Workshop, and point to some pending questions.
Our conceptual and mechanistic understanding of how plant nucleotide-binding leucine-rich repeat (NLR or NB-LRR) proteins perceive pathogens continues to advance. NLRs are intracellular multidomain proteins that recognize pathogen-derived effectors either directly or indirectly (Jones and Dangl, 2006; van der Hoorn and Kamoun, 2008; Dodds and Rathjen, 2010; Cesari et al., 2014). In the direct model, the NLR protein binds a pathogen effector or serves as a substrate for the effector’s enzymatic activity. In the indirect model, the NLR recognizes modifications of additional host protein(s) targeted by the effector. Such intermediate host protein(s) are often called effector targets (ETs). However, given that effectors can act on multiple host targets, the specific protein that mediates recognition by the NLR may not be the effector’s operative target and may have evolved to function as a decoy dedicated to pathogen detection. This “decoy” model contrasts with the “guard” model in which the NLR perceives the effector via its action on its operative target (van der Hoorn and Kamoun, 2008).
In a recent article, Cesari et al. (2014) elegantly synthesized the literature to propose a novel model of how NLRs recognise effectors termed the “integrated decoy” hypothesis. Based on new data from several pathosystems, it appears that some NLRs recognize pathogen effectors through extraneous domains that have evolved by duplication of an ET followed by fusion into the NLR. This NLR-integrated domain mimics the effector binding/substrate property of the original ET to enable pathogen detection. In addition, these “receptor” or “sensor” NLRs typically partner with NLR proteins with a classic architecture that function as signalling partners required for the resistance response (Eitas and Dangl, 2010; Cesari et al., 2013; Cesari et al., 2014; Williams et al., 2014).
Here, we expand on the Cesari et al. (2014) model and introduce the possibility that NLR-integrated domains do not have to be decoys (as in defective mimics) of the effector’s operative target. Indeed, in addition to binding effectors or serving as their substrates, operative targets carry a biochemical activity that is modulated by the effector. The perturbation of this activity by the effector leads to effector-triggered susceptibility, an activity often related to immunity (Boller and He, 2009; Dodds and Rathjen, 2010; Win et al., 2012). Clearly NLR-integrated domains must retain the “sensor” activity of the ancestral ET, but they could also retain their biochemical activity, continuing to function in the effector-targeted pathway even as an extraneous domain within a classic NLR architecture. At present, this possibility cannot be discounted given that the biochemical activities of the ancestral ETs and their NLR-integrated counterparts are generally unknown. Additionally, when NLR-fusions occurred recently, there may not have been enough time for the integrated ET to lose its original function and evolve into a decoy. We therefore propose to refer to the extraneous domains of classic NLR proteins described by Cesari et al. (2014) as sensor domains (SD), a term that is agnostic to any potential biochemical activities of the integrated module.
How to test whether or not SDs are decoys? We propose a straightforward genetic test that can reject the decoy hypothesis. Isogenic plants either carrying or lacking the NLR-SD can be challenged with a pathogen strain that lacks the matching avirulence effector (Figure 1). There are several possible outcomes. If the NLR-SD isogenic lines do not differ in their response to the pathogen without the matching effector, the result is inconclusive and the null decoy hypothesis cannot be rejected. If the presence of NLR-SD without the known matching effector shows higher levels of resistance, and there are no signs of typical effector-triggered immunity, then the SD is likely to have retained the ET biochemical activity and contributes to basal immunity in a manner analogous to the ancestral ET. An even more interesting result would be if in the absence of the matching effector, the NLR-SD line is more susceptible as has been shown for several ETs (van Schie and Takken, 2014). In this scenario, another (unrecognized) effector might still be targeting the original biochemical activity of the SD domain. It would be conceptually fascinating if an NLR that functions as a resistance (R) gene against certain strains of a pathogen becomes a susceptibility (S) gene when exposed to other strains. Once again, this concept emphasizes how the outcome of plant-pathogen interactions is so critically dependent on the genotypes of the interacting organisms – a gene that has a certain impact in a particular genetic combination can have the exact opposite effect in another (Jones and Dangl, 2006; van der Hoorn and Kamoun, 2008; Dodds and Rathjen, 2010; Win et al., 2012).
Our goal is not to engage in an exercise in semantics. However, we wish to avoid conceptually restrictive terminology and urge the plant-microbe interactions community to test a rich spectrum of models and hypotheses. The proposed sensor domain terminology would accommodate this breadth of ideas. Ultimately, it may very well turn out that the majority, if not all, of the NLR integrated domains have lost their biochemical activities and have evolved into decoys. Also, it is possible that the sensor domain has already evolved into a decoy prior to recombination into a NLR. Nonetheless, further genetic and biochemical experiments are required to determine whether sensor domains of NLR-SDs are decoys or biochemically functional duplicates of their ancestral ETs.
Rust fungi are devastating crop pathogens that deliver effector proteins into infected tissues to modulate plant functions and promote parasitic growth. The genome of the poplar leaf rust fungus Melampsora larici-populina revealed a large catalogue of secreted proteins, some of which have been considered candidate effectors. Unravelling how these proteins function in host cells is key to understanding pathogenicity mechanisms and developing resistant plants. In this study, we used an effectoromics pipeline to select, clone, and express 20 candidate effectors in Nicotiana benthamiana leaf cells to determine their subcellular localisation and identify the plant proteins they interact with. Confocal microscopy revealed that six candidate effectors target the nucleus, nucleoli, chloroplasts, mitochondria and discrete cellular bodies. We also used coimmunoprecipitation and mass spectrometry to identify 606 N. benthamiana proteins that associate with the candidate effectors. Five candidate effectors specifically associated with a small set of plant proteins that may represent biologically relevant interactors. We confirmed the interaction between the candidate effector MLP124017 and the TOPLESS-Related Protein 4 from poplar by in planta coimmunoprecipitation. Altogether, our data enable us to validate effector proteins from M. larici-populina and reveal that these proteins may target multiple compartments and processes in plant cells. It also shows that N. benthamiana can be a powerful heterologous system to study effectors of obligate biotrophic pathogens.
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.
• Cas9 is an RNA-guided DNA endonuclease innate to prokaryotic immune systems. • CRISPR/Cas9 has recently emerged as a powerful genome editing tool. • CRISPR/Cas9 has been successfully applied in many organisms, including model and crop plants. • CRISPR/Cas9 is a cheap, robust and easy to implement technology.
CRISPR/Cas9 is a rapidly developing genome editing technology that has been successfully applied in many organisms, including model and crop plants. Cas9, an RNA-guided DNA endonuclease, can be targeted to specific genomic sequences by engineering a separately encoded guide RNA with which it forms a complex. As only a short RNA sequence must be synthesized to confer recognition of a new target, CRISPR/Cas9 is a relatively cheap and easy to implement technology that has proven to be extremely versatile. Remarkably, in some plant species, homozygous knockout mutants can be produced in a single generation. Together with other sequence-specific nucleases, CRISPR/Cas9 is a game-changing technology that is poised to revolutionise basic research and plant breeding.
Plants protect themselves against a variety of invading pathogenic organisms via sophisticated defence mechanisms. These responses include deployment of specialized antimicrobial compounds, such as phytoalexins, that rapidly accumulate at pathogen infection sites. However, the extent to which these compounds contribute to species-level resistance and their spectrum of action remain poorly understood. Capsidiol, a defense related phytoalexin, is produced by several solanaceous plants including pepper and tobacco during microbial attack. Interestingly, capsidiol differentially affects growth and germination of the oomycete pathogensPhytophthora infestans and Phytophthora capsici, although the underlying molecular mechanisms remain unknown. In this study we revisited the differential effect of capsidiol on P. infestans and P. capsici, using highly pure capsidiol preparations obtained from yeast engineered to express the capsidiol biosynthetic pathway. Taking advantage of transgenicPhytophthora strains expressing fluorescent markers, we developed a fluorescence-based method to determine the differential effect of capsidiol on Phytophtora growth. Using these assays, we confirm major differences in capsidiol sensitivity between P. infestans and P. capsiciand demonstrate that capsidiol alters the growth behaviour of both Phytophthora species. Finally, we report intraspecific variation within P. infestans isolates towards capsidiol tolerance pointing to an arms race between the plant and the pathogens in deployment of defence related phytoalexins.
Filamentous plant pathogens such as the late blight pathogenPhytophthora infestans form digit-like infection structures called haustoria inside plant cells. Haustoria enable the pathogen to feed on its host, and secrete effector proteins that modulate the physiology of the host cell to facilitate infection. Haustoria are enveloped by a specialized plant-derived membrane (the extrahaustorial membrane) the biogenesis of which is poorly understood. In this issue, Bozkurt et al. http://www.plantphysiol.org/content/165/3/1005 used the plant membrane microdomain protein REMORIN1.3, known to accumulate around P. infestans haustoria, to reveal discrete extrahaustorial domains labeled by REMORIN1.3 and P. infestans effector AVRblb2. SYNAPTOTAGMIN1, another previously identified perihaustorial protein, localized to subdomains which are mainly not labeled by REMORIN1.3 and AVRblb2. Functional characterization of REMORIN1.3 revealed that it is a susceptibility factor that promotes infection by P. infestans. This activity, and REMORIN1.3 recruitment to the EHM, require REM1.3 membrane-binding domain. These results implicate REMORIN1.3 membrane microdomains in plant susceptibility to an oomycete pathogen. The cover shows Nicotiana benthamiana epidermal cells expressing fluorescently labeled REMORIN1.3 (blue) infected by P. infestans expressing the red fluorescent protein (red). Cover image credits: Sylvain Raffaele.
Nonhost resistance (NHR) is a plant immune response to resist most pathogens. The molecular basis of NHR is poorly understood, but recognition of pathogen effectors by immune receptors, a response known as effector-triggered immunity, has been proposed as a component of NHR.
We performed transient expression of 54 Phytophthora infestansRXLR effectors in pepper (Capsicum annuum) accessions. We used optimized heterologous expression methods and analyzed the inheritance of effector-induced cell death in an F2 population derived from a cross between two pepper accessions.
Pepper showed a localized cell death response upon inoculation with P. infestans, suggesting that recognition of effectors may contribute to NHR in this system. Pepper accessions recognized as many as 36 effectors. Among the effectors, PexRD8 and Avrblb2 induced cell death in a broad range of pepper accessions. Segregation of effector-induced cell death in an F2 population derived from a cross between two pepper accessions fit 15 : 1, 9 : 7 or 3 : 1 ratios, depending on the effector.
Our genetic data suggest that a single or two independent/complementary dominant genes are involved in the recognition of RXLR effectors. Multiple loci recognizing a series of effectors may underpin NHR of pepper to P. infestans and confer resistance durability.
NRP Doctoral Training Programme Summer Conference 2015 The Assembly House, Norwich, Thursday 18th June
We’re in the business of generating and communicating knowledge. We communicate knowledge through publications, which come in many different forms. World class outputs stand the test of time and make a difference. We evaluate publications on their own merit and using article-level metrics; we shouldn’t use journals as a proxy. Are we heading towards a new reward culture? You can make it happen!
Cover caption: The sculpture by Rowan Gillespie is one of the many Great Famine memorials around the world. It depicts figures walking towards emigration ships on the Dublin Quayside. Photo courtesy of Michael Seidl.
Following the 2011 earthquake and tsunami that affected Japan, >20,000 ha of rice paddy field was inundated with seawater, resulting in salt contamination of the land. As local rice landraces are not tolerant of high salt concentrations, we set out to develop a salt-tolerant rice cultivar. We screened 6,000 ethyl methanesulfonate (EMS) mutant lines of a local elite cultivar, 'Hitomebore', and identified a salt-tolerant mutant that we name hitomebore salt tolerant 1 (hst1). In this Correspondence, we report how we used our MutMap method to rapidly identify a loss-of-function mutation responsible for the salt tolerance of hst1 rice. The salt-tolerant hst1 mutant was used to breed a salt-tolerant variety named 'Kaijin', which differs from Hitomebore by only 201 single-nucleotide polymorphisms (SNPs). Field trials showed that it has the same growth and yield performance as the parental line under normal growth conditions. Notably, production of this salt-tolerant mutant line ready for delivery to farmers took only two years using our approach.
Background Emerging and re-emerging pathogens imperil public health and global food security. Responding to these threats requires improved surveillance and diagnostic systems. Despite their potential, genomic tools have not been readily applied to emerging or re-emerging plant pathogens such as the wheat yellow (stripe) rust pathogen Puccinia striiformis f. sp. tritici (PST). This is due largely to the obligate parasitic nature of PST, as culturing PST isolates for DNA extraction remains slow and tedious. Results To counteract the limitations associated with culturing PST, we developed and applied a field pathogenomics approach by transcriptome sequencing infected wheat leaves collected from the field in 2013. This enabled us to rapidly gain insights into this emerging pathogen population. We found that the PST population across the United Kingdom, UK, underwent a major shift in recent years. Population genetic structure analyses revealed four distinct lineages that correlated to the phenotypic groups determined through traditional pathology-based virulence assays. Furthermore, the genetic diversity between members of a single population cluster for all 2013 PST field samples was much higher than that displayed by historical UK isolates, revealing a more-diverse population of PST. Conclusions Our field pathogenomics approach uncovered a dramatic shift in the PST population in the UK, likely due to a recent introduction of a diverse set of exotic PST lineages. The methodology described herein accelerates genetic analysis of pathogen populations and circumvents the difficulties associated with obligate plant pathogens. In principle, this strategy can be widely applied to a variety of plant pathogens.
Intracellular immune receptors of the nucleotide-binding leucine-rich repeat (NB-LRR or NLR) proteins often function in pairs, with "helper" proteins required for the activity of "sensors" that mediate pathogen recognition. The NLR helper NRC1 (NB-LRR protein required for HR-associated cell death 1) has been described as a signalling hub required for the cell death mediated by both cell surface and intracellular immune receptors in the model plant Nicotiana benthamiana. However, this work predates the availability of the N. benthamiana genome and whether NRC1 is indeed required for the reported phenotypes has not been confirmed. Here, we investigated the NRC family of solanaceous plants using a combination of genome annotation, phylogenetics, gene silencing and genetic complementation experiments. We discovered that a paralog of NRC1, we termed NRC3, is required for the hypersensitive cell death triggered by the disease resistance protein Pto but not Rx and Mi-1.2. NRC3 may also contribute to the hypersensitive cell death triggered by the receptor-like protein Cf-4. Our results highlight the importance of applying genetic complementation to validate gene function in RNA silencing experiments.
I’m a proponent of open science. Science is continuously in flux. Our knowledge, theories and concepts are continuously evolving. The essence of science is to capture new information, integrate it into current models and regurgitate more elaborate concepts. Therefore science cannot thrive without a vibrant culture of discussion and debate. Open science widens the net. Anyone can access the data and comment on it. A tweet by someone you don’t know could lead you to think differently about your science and help you to develop new concepts. We move from elitist old boy clubs to an open door party. This is healthy for science.
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.
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.
To test the efficacy of CRISPR/Cas9 in tomato, we chose to target a gene that, when function was disrupted, would result in a distinctive, immediately recognizable phenotype early in the plant tissue culture phase of Agrobacterium-mediated transformation. A CRISPR/Cas9 construct was designed to target neighboring sequences in the second exon of the tomato homolog of Arabidopsis ARGONAUTE7 (SlAGO7), because loss-of-function mutations are recessive and result in plants whose typical compound flat leaves become needle-like, or “wiry” (Fig. 1) (Lesley, 1928; Yifhar et al., 2012). SlAGO7 is required for the biogenesis of a class of small RNAs known as trans-acting short interfering RNAs (ta-siRNAs), which regulate organ polarity through post-transcriptional silencing of AUXIN RESPONSE FACTOR (ARF) genes (Husbands et al., 2009). Strong alleles of slago7 thus produce lower levels of ta-siRNAs and reduced ARF mRNA degradation, resulting in the first leaves of mutant plants having leaflets without petioles, and later formed leaves lacking laminae (Fig. 1C). These distinctive phenotypes allowed us to immediately identify first generation transformed (T0) plants in which both alleles of SlAGO7 might be mutated.
Oomycetes form a deep lineage of eukaryotic organisms that includes a large number of plant pathogens that threaten natural and managed ecosystems. We undertook a survey to query the community for their ranking of plant pathogenic oomycete species based on scientific and economic importance. In total, we received 263 votes from 62 scientists in 15 countries for a total of 33 species. The Top 10 species and their ranking are: (1) Phytophthora infestans; (2, tied) Hyaloperonospora arabidopsidis; (2, tied) Phytophthora ramorum; (4) Phytophthora sojae; (5) Phytophthora capsici; (6) Plasmopara viticola; (7) Phytophthora cinnamomi; (8, tied) Phytophthora parasitica; (8, tied) Pythium ultimum; and (10) Albugo candida. The article provides an introduction to these 10 taxa and a snapshot of current research. We hope that the list will serve as a benchmark for future trends in oomycete research.
See also [link below]:
Top 10 plant-parasitic nematodes in molecular plant pathology Top 10 plant viruses in molecular plant pathology Top 10 plant pathogenic bacteria in molecular plant pathology The Top 10 fungal pathogens in molecular plant pathology
The world's human population continues to expand and is predicted to reach ~9 billion by 2040, up from its current level of just over 7 billion. Some estimate that with this rate of population growth, accommodating the increased demand for food will require the world's agricultural production to increase 50% by 2030. The planet's water resources are also under pressure. As Pamela Ronald highlights in her accompanying Essay, the amount of fresh water available per person has decreased 4-fold in the last 60 years and of the water that is available, ~70% is already used for agriculture. Thus, agricultural production must be intensified to feed more people with less water on the same amount of land (given that little undeveloped arable land remains and what does is being lost to urbanization, desertification, and environmental damage). Furthermore, pathogens that cause devastating crop losses continue to spread in the face of increased global commerce and climate change. Given these challenges, there is a pressing need for plant research to produce solutions to ensure food security in a sustainable and safe way. The need is acute in both developed countries and in the less developed parts of the world, where many people endure chronic malnutrition and suffer the long term consequences on their health and well being. Plant scientists, therefore, urgently need to increase the productivity, pathogen resistance, and sustainability of existing crops, and are challenged to domesticate new crops.
Sharing your scoops to your social media accounts is a must to distribute your curated content. Not only will it drive traffic and leads through your content, but it will help show your expertise with your followers.
How to integrate my topics' content to my website?
Integrating your curated content to your website or blog will allow you to increase your website visitors’ engagement, boost SEO and acquire new visitors. By redirecting your social media traffic to your website, Scoop.it will also help you generate more qualified traffic and leads from your curation work.
Distributing your curated content through a newsletter is a great way to nurture and engage your email subscribers will developing your traffic and visibility.
Creating engaging newsletters with your curated content is really easy.