The life cycles of many organisms are constrained by the seasonality of resources. This is particularly true for leaf-mining herbivorous insects that use deciduous leaves to fuel growth and reproduction even beyond leaf fall. Our results suggest that an intimate association with bacterial endosymbionts might be their way of coping with nutritional constraints to ensure successful development in an otherwise senescent environment. We show that the phytophagous leaf-mining moth Phyllonorycter blancardella(Lepidoptera) relies on bacterial endosymbionts, most likely Wolbachia, to manipulate the physiology of its host plant resulting in the ‘green-island’ phenotype—photosynthetically active green patches in otherwise senescent leaves—and to increase its fitness. Curing leaf-miners of their symbiotic partner resulted in the absence of green-island formation on leaves, increased compensatory larval feeding and higher insect mortality. Our results suggest that bacteria impact green-island induction through manipulation of cytokinin levels. This is the first time, to our knowledge, that insect bacterial endosymbionts have been associated with plant physiology.
The world’s rapidly expanding populations have created a sense of urgency regarding global agricultural output, which needs to expand by at least 70% by the year 2050. Plants will provide a significant proportion of the world’s food supply. This international conference focuses on a group of plant enemies that have an unique style of attack. Instead of simply removing plant tissue, survival, growth and reproduction are enhanced by manipulating the plant to create specialized nutritional resources. This attack strategy can have serious consequences for both natural and agro-ecosystems. Mechanisms of reprogramming host plants remain largely unknown but clearly involve secreted effectors that are applied during attack. Options for defense against reprogrammers include effector-triggered immunity. Historically the phylogenetically diverse plant enemies that reprogram plants have been studied by different groups. This interdisciplinary meeting will bring together the complementary strengths of key international laboratories to discuss advances in our understanding of the enemies that reprogram plants and their associated symbionts, the options that plants have for their defense, and the evolutionary potential of enemies to adapt to plant defense.
Ash dieback is caused by Hymenoscyphus fraxineus, a cryptic species of the putatively harmless Hymenoscyphus albidus. Recently, H. fraxineus was found to be native to East Asia. However, the virulence of Asian H. fraxineus strains on Fraxinus excelsior and the virulence of European H. albidus on hosts other than F. excelsior and Fraxinus mandshurica have not yet been assessed. In a wound inoculation study, the virulence of four H. albidus and four European and Japanese H. fraxineus strains was assessed on F. excelsior and Fraxinus pennsylvanica in a climate chamber. Lesion lengths were measured after approximately three and a half months. No lesions were observed on the negative control or on trees inoculated with H. albidus. In contrast, inoculation with H. fraxineus induced typical symptoms of ash dieback on both tree species. Japanese H. fraxineus strains induced significantly longer lesions compared to European strains. Fraxinus excelsior was highly susceptible and developed lesions averaging lengths of 1·7 and 8·4 cm for European and Japanese strains, respectively. Fraxinus pennsylvanica was less susceptible and developed average lesion lengths of 1·6 and 4·8 cm for European and Japanese strains, respectively. Most strains were successfully reisolated from necrotic lesions or inocula, fulfilling Koch's postulates. The data show that additional introductions of H. fraxineusstrains from the native range to Europe could pose a threat to the conservation of F. excelsior. In addition, introduction of H. fraxineus to North America could potentially have a negative effect on the indigenous F. pennsylvanica.
Pathogen attack sequentially confers pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) after sensing of pathogen patterns and effectors by plant immune receptors, respectively. Reactive oxygen species (ROS) play pivotal roles in PTI and ETI as signaling molecules. Nicotiana benthamiana RBOHB, an NADPH oxidase, is responsible for both the transient PTI ROS burst and the robust ETI ROS burst. Here, we show that RBOHB transactivation mediated by MAPK contributes to R3a/AVR3a-triggered ETI (AVR3a-ETI) ROS burst. RBOHB is markedly induced during the ETI and INF1-triggered PTI (INF1-PTI), but not flg22-tiggered PTI (flg22-PTI). We found that the RBOHB promoter contains a functional W-box in the R3a/AVR3a and INF1 signal-responsive cis-element. Ectopic expression of four phospho-mimicking mutants of WRKY transcription factors, which are MAPK substrates, induced RBOHB, and yeast one-hybrid analysis indicated that these mutants bind to the cis-element. Chromatin immunoprecipitation assays indicated direct binding of the WRKY to the cis-element in plants. Silencing of multiple WRKY genes compromised the upregulation of RBOHB, resulting in impairment of AVR3a-ETI and INF1-PTI ROS bursts, but not the flg22-PTI ROS burst. These results suggest that the MAPK-WRKY pathway is required for AVR3a-ETI and INF1-PTI ROS bursts by activation of RBOHB.
The tomato I-3 and I-7 genes confer resistance to Fusarium oxysporum f. sp. lycopersici (Fol) race 3 and were introgressed into the cultivated tomato, Solanum lycopersicum, from the wild relative Solanum pennellii. I-3 was identified previously on chromosome 7 and encodes an S-receptor-like kinase, but little was known about I-7. Molecular markers have been developed for the marker-assisted breeding of I-3, but none were available for I-7. We used an RNA-seq and SNP-analysis approach to map I-7 to a small introgression of S. pennellii DNA (ca. 210 kb) on chromosome 8 and identify I-7 as a gene encoding a leucine-rich-repeat receptor-like protein (LRR-RLP), thereby expanding the repertoire of resistance protein classes conferring resistance to Fol. Using an eds1 mutant of tomato we showed that I-7, like many other LRR-RLPs conferring pathogen resistance in tomato, is EDS1 dependent. Using transgenic tomato plants carrying only the I-7 gene for Fol resistance, we found that I-7 also confers resistance to Fol races 1 and 2. Given that Fol race 1 carries Avr1, resistance to Fol race 1 indicates that I-7-mediated resistance, unlike I-2 or I-3-mediated resistance, is not suppressed by Avr1. This suggests Avr1 is not a general suppressor of Folresistance in tomato leading us to hypothesise that Avr1 may be acting against an EDS1-independent pathway for resistance activation. The identification of I-7 has allowed us to develop molecular markers for marker-assisted breeding of both genes currently known to confer Folrace 3 resistance (I-3 and I-7). Given that I-7-mediated resistance is not suppressed by Avr1, I-7 may be a useful addition to I-3 in the tomato breeder's toolbox.
Plant pathogens secrete an arsenal of effector proteins to impair host immunity. Some effectors possess enzymatic activities that can modify their host targets. Previously, we demonstrated that a Phytophthora sojae RXLR effector Avr3b acts as a Nudix hydrolase when expressed in planta; and this enzymatic activity is required for full virulence of P. sojae strain P6497 in soybean (Glycine max). Interestingly, recombinant Avr3b produced by E. coli does not have the hydrolase activity unless it was incubated with plant protein extracts. Here, we report the activation of Avr3b by a prolyl-peptidyl isomerase (PPIase), cyclophilin, in plant cells. Avr3b directly interacts with soybean cyclophilin GmCYP1, which activates the hydrolase activity of Avr3b in a PPIase activity-dependent manner. Avr3b contains a putative Glycine-Proline (GP) motif; which is known to confer cyclophilin-binding in other protein substrates. Substitution of the Proline (P132) in the putative GP motif impaired the interaction of Avr3b with GmCYP1; as a result, the mutant Avr3bP132A can no longer be activated by GmCYP1, and is also unable to promote Phytophthora infection. Avr3b elicits hypersensitive response (HR) in soybean cultivars producing the resistance protein Rps3b, but Avr3bP132A lost its ability to trigger HR. Furthermore, silencing of GmCYP1 rendered reduced cell death triggered by Avr3b, suggesting that GmCYP1-mediated Avr3b maturation is also required for Rps3b recognition. Finally, cyclophilins of Nicotiana benthamiana can also interact with Avr3b and activate its enzymatic activity. Overall, our results demonstrate that cyclophilin is a “helper” that activates the enzymatic activity of Avr3b after it is delivered into plant cells; as such, cyclophilin is required for the avirulence and virulence functions of Avr3b.
Background - Root rot caused by Aphanomyces euteiches is one of the most destructive pea diseases while a distantly related species P. pisi has been recently described as the agent of pea and faba bean root rot. These two oomycete pathogens with different pathogenicity factor repertories have both evolved specific mechanisms to infect pea. However, little is known about the genes and mechanisms of defence against these pathogens in pea. In the present study, the transcriptomic response of pea to these two pathogens was investigated at two time points during early phase of infection using a Medicago truncatula microarray.
Results - Of the 37,976 genes analysed, 574 and 817 were differentially expressed in response to A. euteiches at 6 hpi and 20 hpi, respectively, while 544 and 611 genes were differentially regulated against P. pisi at 6 hpi and 20 hpi, respectively. Differentially expressed genes associated with plant immunity responses were involved in cell wall reinforcement, hormonal signalling and phenylpropanoid metabolism. Activation of cell wall modification, regulation of jasmonic acid biosynthesis and induction of ethylene signalling pathway were among the common transcriptional responses to both of these oomycetes. However, induction of chalcone synthesis and the auxin pathway were specific transcriptional changes against A. euteiches.
Conclusions - Our results demonstrate a global view of differentially expressed pea genes during compatible interactions with P. pisi and A. euteiches at an early phase of infection. The results suggest that distinct signalling pathways are triggered in pea by these two pathogens that lead to common and specific immune mechanisms in response to these two oomycetes. The generated knowledge may eventually be used in breeding pea varieties with resistance against root rot disease.
Aquilegia vulgaris (Ranunculaceae) (Columbine) is a flowering herbaceous perennial native to Europe and widely cultivated in UK gardens. It is an important crop for some commercial nurseries that produce large numbers of potted plants for retail sale in garden centres. In 2008, 100% crop loss due to a bacterial disease was reported by one grower. Subsequently, during a survey of bacterial diseases of herbaceous perennials on commercial nurseries carried out during 2010 (Roberts, 2011), symptoms consisting of black spots or larger lesions with a water-soaked margin were observed on the leaves and stems of plants at two nurseries in different regions of the UK.
In the mid-20th century, an American scientist named Harold Henry Flor helped explain how certain varieties of plants can fight off some plant killers (pathogens), but not others, with a model called the “gene-for-gene” hypothesis. Seventy years later, an international team of scientists describes precisely how a plant senses a pathogen, bringing an unprecedented level of detail to Flor’s model.
“We know that plants have sensors to detect pathogens but we knew little about how they work,” says Professor Banfield from the John Innes Centre (UK).
In a study published in eLife, the team led by Professor Mark Banfield, in collaboration with the Iwate Biotechnology Research Centre (Japan) and The Sainsbury Laboratory (UK), investigated how one sensor protein from rice called Pik binds AVR-Pik, a protein from the rice blast pathogen. This fungus causes the most devastating disease of rice crops. Using X-ray crystallography facilities at Diamond Light Source in Oxfordshire, the team succeeded in imaging the contact points between the plant and pathogen proteins at the molecular level – the first time this has been done for a pair of plant and pathogen proteins that follow the gene-for-gene model.
Dr Abbas Maqbool from the JIC, first author of the study added, “Harold Flor predicted that plant sensors discriminate between different pathogen types, but at the time he had no knowledge of the molecules involved. It is remarkable that his ideas have now crystallized into detailed molecular models.”
Dr Maqbool, Professor Banfield and colleagues went on to discover that the strength at which the Pik sensor binds the pathogen AVR-Pik protein correlates with the strength of the plant’s response. This opens up new avenues for engineering better plant responses against pathogens by building sensors with increased strength of binding to pathogen proteins, and therefore conferring enhanced resistance to disease.
“Once we understand how these plant sensors detect invading pathogens, we can devise strategies to ‘boost’ the plant immune system and help protect rice and other important food crops from disease,” says Professor Banfield.
Background -- Geminiviruses (family Geminiviridae) are small single-stranded (ss) DNA viruses infecting plants. Their virion morphology is unique in the known viral world – two incomplete T = 1 icosahedra are joined together to form twinned particles. Geminiviruses utilize a rolling-circle mode to replicate their genomes. A limited sequence similarity between the three conserved motifs of the rolling-circle replication initiation proteins (RCR Reps) of geminiviruses and plasmids of Gram-positive bacteria allowed Koonin and Ilyina to propose that geminiviruses descend from bacterial replicons.
Results -- Phylogenetic and clustering analyses of various RCR Reps suggest that Rep proteins of geminiviruses share a most recent common ancestor with Reps encoded on plasmids of phytoplasmas, parasitic wall-less bacteria replicating both in plant and insect cells and therefore occupying a common ecological niche with geminiviruses. Capsid protein of Satellite tobacco necrosis virus was found to be the best template for homology-based structural modeling of the geminiviral capsid protein. Good stereochemical quality of the generated models indicates that the geminiviral capsid protein shares the same structural fold, the viral jelly-roll, with the vast majority of icosahedral plant-infecting ssRNA viruses.
Conclusion -- We propose a plasmid-to-virus transition scenario, where a phytoplasmal plasmid acquired a capsid-coding gene from a plant RNA virus to give rise to the ancestor of geminiviruses.
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 and mitochondria. Here, we show that the CTP1 transit peptide is necessary and sufficient for accumulation in the stroma of chloroplasts. CTP1 is part of a Melampsora-specific family of polymorphic secreted proteins. Two members of that family, CTP2 and CTP3, also translocate in chloroplasts in a N-terminal signal-dependent manner. CTP1, CTP2 and CTP3 are cleaved when they accumulate in chloroplasts, while they remain intact when they do not translocate into chloroplasts. Our findings reveal that fungi have evolved effector proteins that mimic plant-specific sorting signals to traffic within plant cells.
The oomycete genus Phytophthora contains a large number of plant pathogens that cause significant damage to natural and agricultural systems. Until recently species have been distinguished using a limited set of morphological characters. The development of DNA-based technologies has revealed much broader and more complex diversity than previously recognised, and has led to the recent description of many new species. This review looks at the underlying mechanisms for the generation of diversity within the genus. The intercontinental movement and transplantation of infected plant material partially explains the appearance of new species in unexpected places. However, it is also likely that novel species arise as a result of the hybridisation and rapid evolution of introduced species under episodic selection pressures. Hybrid progeny may possess equal or greater virulence than parent species, thereby posing an increasing risk to our natural environment and agricultural production systems. These discoveries amplify the threats posed by the introduction of plant pathogens into new environments, and expose a crucial weakness in current evidence-based biosecurity regimes. Further work is required to identify hybrids, anticipate and understand the occurrence of hybridisation, and to implement appropriate quarantine and risk management measures.
Thousands of putative biosynthetic genes in Arabidopsis thaliana have no known function, which suggests that there are numerous molecules contributing to plant fitness that have not yet been discovered1, 2. Prime among these uncharacterized genes are cytochromes P450 upregulated in response to pathogens3, 4. Here we start with a single pathogen-induced P450 (ref. 5), CYP82C2, and use a combination of untargeted metabolomics and coexpression analysis to uncover the complete biosynthetic pathway to 4-hydroxyindole-3-carbonyl nitrile (4-OH-ICN), a previously unknown Arabidopsis metabolite. This metabolite harbours cyanogenic functionality that is unprecedented in plants and exceedingly rare in nature6, 7; furthermore, the aryl cyanohydrin intermediate in the 4-OH-ICN pathway reveals a latent capacity for cyanogenic glucoside biosynthesis8, 9 in Arabidopsis. By expressing 4-OH-ICN biosynthetic enzymes in Saccharomyces cerevisiae and Nicotiana benthamiana, we reconstitute the complete pathway in vitro and in vivo and validate the functions of its enzymes. Arabidopsis 4-OH-ICN pathway mutants show increased susceptibility to the bacterial pathogen Pseudomonas syringae, consistent with a role in inducible pathogen defence. Arabidopsis has been the pre-eminent model system10, 11 for studying the role of small molecules in plant innate immunity12; our results uncover a new branch of indole metabolism distinct from the canonical camalexin pathway, and support a role for this pathway in the Arabidopsis defence response13. These results establish a more complete framework for understanding how the model plant Arabidopsis uses small molecules in pathogen defence.
Plants and animals rely on immune receptors, known as nucleotide-binding domain and leucine-rich repeat containing proteins (NB-LRR or NLR), to defend against invading pathogens and activate immune responses. How NLR receptors respond to pathogens is inadequately understood. We previously reported single-residue mutations that expand the response of the potato immune receptor R3a to AVR3aEM, a stealthy effector from the late blight oomycete pathogen Phytophthora infestans. I2, another NLR that mediates resistance to the wilt causing fungus Fusarium oxysporum f. sp. lycopersici, is the tomato ortholog of R3a. We transferred previously identified R3a mutations to I2 to assess the degree to which the resulting I2 mutants have an altered response. We discovered that wild-type I2 protein responds weakly to AVR3a. One mutant in the N-terminal coiled-coil domain, I2I141N, appeared sensitized and displayed markedly increased response to AVR3a. Remarkably, I2I141N conferred partial resistance to P. infestans. Further, I2I141N has an expanded response spectrum to F. oxysporum f. sp. lycopersici effectors compared to the wild-type I2 protein. Our results suggest that synthetic immune receptors can be engineered to confer resistance to phylogenetically divergent pathogens and indicate that knowledge gathered for one NLR could be exploited to improve NLRs from other plant species.
Pathogens utilize effectors to suppress basal plant defense known as PTI (Pathogen-associated molecular pattern-triggered immunity). However, our knowledge of PTI suppression by filamentous plant pathogens, i.e. fungi and oomycetes, remains fragmentary. Previous work revealed that the co-receptor BAK1/SERK3 contributes to basal immunity against the potato 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 cell death by binding the plant E3 ligase CMPG1. In contrast, AVR3aKI-Y147del, a deletion mutant of the C-terminal tyrosine of AVR3a, fails to bind CMPG1 and does not suppress INF1-mediated cell death. Here, we studied the extent to which AVR3a and its variants perturb additional BAK1/SERK3-dependent PTI responses in N. benthamiana using the elicitor/receptor pair flg22/FLS2 as a model. We found that all tested variants of AVR3a suppress defense responses triggered by flg22 and reduce internalization of activated FLS2. Moreover, we discovered that AVR3a associates with the Dynamin-Related Protein 2 (DRP2), a plant GTPase implicated in receptor-mediated endocytosis. Interestingly, silencing of DRP2 impaired ligand-induced FLS2 internalization but did not affect internalization of the growth receptor BRI1. Our results suggest that AVR3a associates with a key cellular trafficking and membrane-remodeling complex involved in immune receptor-mediated endocytosis. We conclude that AVR3a is a multifunctional effector that can suppress BAK1/SERK3-mediated immunity through at least two different pathways.
Nonhost resistance (NHR) is the most prevalent form of plant immunity. In Arabidopsis, NHR requires membrane-localized ATP-binding cassette (ABC) transporter PENETRATION (PEN) 3. Upon perception of pathogen-associated molecular patterns, PEN3 becomes phosphorylated, suggestive of PEN3 regulation by post-translational modification. Here, we investigated the PEN3 protein interaction network.
We probed the Arabidopsis protein microarray AtPMA-5000 with the N-terminal cytoplasmic domain of PEN3. Several of the proteins identified to interact with PEN3 in vitro represent cellular Ca2+ sensors, including calmodulin (CaM) 3, CaM7 and several CaM-like proteins, pointing to the importance of Ca2+ sensing to PEN3-mediated NHR.
We demonstrated co-localization of PEN3 and CaM7, and we confirmed PEN3–CaM interaction in vitro and in vivo by PEN3 pull-down with CaM Sepharose, CaM overlay assay and bimolecular fluorescence complementation. We also show that just like in pen3, NHR to the nonadapted fungal pathogens Phakopsora pachyrhizi and Blumeria graminis f.sp. hordei is compromised in the Arabidopsis cam7and pen3 cam7 mutants.
Our study discloses CaM7 as a PEN3-interacting protein crucial to Arabidopsis NHR and emphasizes the importance of Ca2+ sensing to plant immunity.
Development of resistant crops is the most effective way to control plant diseases to safeguard food and feed production. Disease resistance is commonly based on resistance genes, which generally mediate the recognition of small proteins secreted by invading pathogens. These proteins secreted by pathogens are called ‘avirulence’ proteins. Their identification is important for being able to assess the usefulness and durability of resistance genes in agricultural settings.
We have used genome sequencing of a set of strains of the melon wilt fungus Fusarium oxysporum f. sp. melonis (Fom), bioinformatics-based genome comparison and genetic transformation of the fungus to identify AVRFOM2, the gene that encodes the avirulence protein recognized by the melon Fom-2 gene.
Both an unbiased and a candidate gene approach identified a single candidate for the AVRFOM2 gene. Genetic complementation of AVRFOM2 in three different race 2 isolates resulted in resistance of Fom-2-harbouring melon cultivars. AvrFom2 is a small, secreted protein with two cysteine residues and weak similarity to secreted proteins of other fungi.
The identification of AVRFOM2 will not only be helpful to select melon cultivars to avoid melon Fusarium wilt, but also to monitor how quickly a Fom population can adapt to deployment of Fom-2-containing cultivars in the field.
The first US caged field studies of a genetically modified (GM) insect for use in agriculture began in July in upstate New York. The GM diamondback moth developed by Oxitec, a spin-out from Oxford University, headquartered in Milton Park, UK, is intended as a tool for crop growers to control infestations without chemical insecticides. Cornell entomologist Anthony Shelton has started testing the transgenic moths, which carry an autocidal gene that causes the insects' female progeny to die before reaching reproductive stage. The results of these trials, and of a handful of others in the works, will provide an indication whether the approach has commercial potential in agriculture and will provide a barometer of attitudes to the release of GM insects that lack a compelling trait for consumers.
Diamondback moths, Plutella xylostella, are an invasive species and a global nemesis of brassica vegetables such as broccoli, cabbage, kale, Brussels sprouts and the field crop canola. Diamondback moths cost the global economy an estimated $4–5 billion annually in damaged crops and pest control methods. “The damage the diamondback moth can do is incredible. I've seen whole fields wiped out,” says Shelton. The moth has also evolved resistance to over 90 insecticide ingredients, forcing farmers to increase pesticide use, further exacerbating resistance.
Oxitec's solution to this pest is the OX4319L moth. The genetically engineered insect contains a synthetic 'self-limiting' gene encoding tetracycline repressible transcription activator variant (tTAV). At high expression levels this protein ties up cells' transcriptional machinery, shutting down cell function and eventually killing the insect. The tTAV protein also binds and induces the tetracycline operator (tetO) sequences, which in turn increases expression of tTAV. The more tTAV binds to tetO, the more tTAV is produced—a positive feedback system. The moths also carry a fluorescent marker gene (DsRed2) that gives the insects color under a certain wavelength of green light, enabling them to be distinguished from wild pests.
Background: Direct targets for plant NLR proteins in immune signalling are largely unknown.
Results: The Rx1 NLR protein of potato binds and distorts DNA following pathogen perception resulting in immune activation.
Conclusion: DNA is a direct signalling target for a plant NLR immune receptor.
Significance: Plant NLR receptors might regulate immune transcriptional responses by directly interacting with plant chromatin.
Plant NLR proteins enable cells to respond to pathogen attack. Several NLRs act in the nucleus, however, conserved nuclear targets that support their role in immunity are unknown. Previously we noted a structural homology between the NB domain of NLRs and DNA replication origin-binding Cdc6/Orc1 proteins. Here we show that the NB-ARC domain of the Rx1 NLR of potato binds nucleic acids. Rx1 induces ATP-dependent bending and melting of DNA in vitro dependent upon a functional P-loop. In situ full-length Rx1 binds nuclear DNA following activation by its cognate pathogen-derived effector protein, the coat protein of potato virus X. In line with its obligatory nucleocytoplasmic distribution, DNA-binding was only observed when Rx1 was allowed to freely translocate between both compartments and was activated in the cytoplasm. Immune activation induced by an unrelated NLR-effector pair did not trigger a Rx1-DNA interaction. DNA-binding is therefore not merely a consequence of immune activation. These data establish a role for DNA distortion in Rx1 immune signalling and defines DNA as a molecular target of an activated NLR.
Background - Powdery mildew, caused by the obligate biotrophic fungus Blumeria graminis, is a major problem in cereal production as it can reduce quality and yield. B. graminis has evolved eight distinct formae speciales (f.sp.) which display strict host specialization. In the last decade, powdery mildew has emerged on triticale, the artificial intergeneric hybrid between wheat and rye. This emergence is probably triggered by a host range expansion of the wheat powdery mildew B. graminis f.sp. tritici. To gain more precise information about the evolutionary processes that led to this host range expansion, we pursued a combined pathological and genetic approach.
Results - B. graminis isolates were sampled from triticale, wheat and rye from different breeding regions in Europe. Pathogenicity tests showed that isolates collected from triticale are highly pathogenic on most of the tested triticale cultivars. Moreover, these isolates were also able to infect several wheat cultivars (their previous hosts), although a lower aggressiveness was observed compared to isolates collected from wheat. Phylogenetic analysis of nuclear gene regions identified two statistically significant clades, which to a certain extent correlated with pathogenicity. No differences in virulence profiles were found among the sampled regions, but the distribution of genetic variation demonstrated to be geography dependent. A multilocus haplotype network showed that haplotypes pathogenic on triticale are distributed at different sites in the network, but always clustered at or near the tips of the network.
Conclusions - This study reveals a genetic structure in B. graminis with population differentiation according to geography and host specificity. In addition, evidence is brought forward demonstrating that the host range expansion of wheat isolates to the new host triticale occurred recently and multiple times at different locations in Europe.
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.