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Current Opinion in Microbiology: Interspecific hybridization impacts host range and pathogenicity of filamentous microbes (2016)

Current Opinion in Microbiology: Interspecific hybridization impacts host range and pathogenicity of filamentous microbes (2016) | Plants and Microbes | Scoop.it

Highlights
• Interspecific hybridization is observed within various eukaryotic taxa.
• Globalization enhances the opportunity for hybridization events to occur.
• Hybridization often occurs under particular, often enigmatic, conditions.
• Hybridization affects microbial genome evolution and impacts pathogenicity.
• Stable hybrids are fitter than their parental lineages that may be outcompeted.

Interspecific hybridization is widely observed within diverse eukaryotic taxa, and is considered an important driver for genome evolution. As hybridization fuels genomic and transcriptional alterations, hybrids are adept to respond to environmental changes or to invade novel niches. This may be particularly relevant for organisms that establish symbiotic relationships with host organisms, such as mutualistic symbionts, endophytes and pathogens. The latter group is especially well-known for engaging in everlasting arms races with their hosts. Illustrated by the increased identification of hybrid pathogens with altered virulence or host ranges when compared with their parental lineages, it appears that hybridization is a strong driver for pathogen evolution, and may thus significantly impact agriculture and natural ecosystems.


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Nature Microbiology: Fungal pathogenesis: Host modulation every which way (2016)

Nature Microbiology: Fungal pathogenesis: Host modulation every which way (2016) | Plants and Microbes | Scoop.it

The plant pathogenic fungus Fusarium oxysporum secretes an effector that is similar to a plant peptide hormone, underscoring the variety of mechanisms that plant pathogens have evolved to tamper with host physiology.

 

Plant pathogens cause devastating diseases of crop plants and threaten food security in an era of continuous population growth. Annual losses due to fungal and oomycete diseases amount to enough food calories to feed at least half a billion people. Understanding how plant pathogens infect and colonize plants should help to develop disease-resistant crops. It appears that plant pathogens are sophisticated manipulators of their hosts. They secrete effector molecules that alter host biological processes in a variety of ways, generally promoting the pathogen lifestyle. A new study by Masachis, Segorbe and colleagues describes a new mechanism by which plant pathogens interfere with plant physiology. They discovered that the root-infecting fungus F. oxysporum secretes a peptide similar to the plant regulatory peptide RALF (rapid alkalinization factor) to induce host tissue alkalinization and enhance plant colonization. This study demonstrates that in addition to secreting classical plant hormones (or mimics thereof), fungi have also evolved functional homologues of plant peptides to alter host cellular processes.

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Nature Microbiology: A fungal pathogen secretes plant alkalinizing peptides to increase
infection (2016)

Nature Microbiology: A fungal pathogen secretes plant alkalinizing peptides to increase<br/>                    infection (2016) | Plants and Microbes | Scoop.it

Plant infections caused by fungi are often associated with an increase in the pH of the surrounding host tissue1. Extracellular alkalinization is thought to contribute to fungal pathogenesis, but the underlying mechanisms are poorly understood. Here, we show that the root-infecting fungus Fusarium oxysporum uses a functional homologue of the plant regulatory peptide RALF (rapid alkalinization factor)2,3 to induce alkalinization and cause disease in plants. An upshift in extracellular pH promotes infectious growth of Fusarium by stimulating phosphorylation of a conserved mitogen-activated protein kinase essential for pathogenicity4,5. Fungal mutants lacking a functional Fusarium (F)-RALF peptide failed to induce host alkalinization and showed markedly reduced virulence in tomato plants, while eliciting a strong host immune response. Arabidopsis plants lacking the receptor-like kinase FERONIA, which mediates the RALF-triggered alkalinization response6, displayed enhanced resistance against Fusarium. RALF homologues are found across a number of phylogenetically distant groups of fungi, many of which infect plants. We propose that fungal pathogens use functional homologues of alkalinizing peptides found in their host plants to increase their infectious potential and suppress host immunity.

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New Phytologist: A multilayered regulatory mechanism for the autoinhibition and activation of a plant CC-NB-LRR resistance protein with an extra N-terminal domain (2016)

New Phytologist: A multilayered regulatory mechanism for the autoinhibition and activation of a plant CC-NB-LRR resistance protein with an extra N-terminal domain (2016) | Plants and Microbes | Scoop.it
  • The tomato resistance protein Sw-5b differs from the classical coiled-coil nucleotide-binding leucine-rich repeat (CC-NB-LRR) resistance proteins by having an extra N-terminal domain (NTD). To understand how NTD, CC and NB-LRR regulate autoinhibition and activation of Sw-5b, we dissected the function(s) of each domain.
  • When viral elicitor was absent, Sw-5b LRR suppressed the central NB-ARC to maintain autoinhibition of the NB-LRR segment. The CC and NTD domains independently and additively enhanced the autoinhibition of NB-LRR.
  • When viral elicitor was present, the NB-LRR segment of Sw-5b was specifically activated to trigger a hypersensitive response. Surprisingly, Sw-5b CC suppressed the activation of NB-LRR, whereas the extra NTD of Sw-5b became a positive regulator and fully activated the resistance protein, probably by relieving the inhibitory effects of the CC. In infection assays of transgenic plants, the NB-LRR segment alone was insufficient to confer resistance against Tomato spotted wilt tospovirus; the layers of NTD and CC regulation on NB-LRR were required for Sw-5b to confer resistance.
  • Based on these findings, we propose that, to counter the negative regulation of the CC on NB-LRR, Sw-5b evolved an extra NTD to coordinate with the CC, thus developing a multilayered regulatory mechanism to control autoinhibition and activation.

 

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eLife: Arabidopsis heterotrimeric G proteins regulate immunity by directly coupling to the FLS2 receptor (2016)

eLife: Arabidopsis heterotrimeric G proteins regulate immunity by directly coupling to the FLS2 receptor (2016) | Plants and Microbes | Scoop.it

The Arabidopsis immune receptor FLS2 perceives bacterial flagellin epitope flg22 to activate defenses through the central cytoplasmic kinase BIK1. The heterotrimeric G proteins composed of the non-canonical Gα protein XLG2, the Gβ protein AGB1, and the Gγ proteins AGG1 and AGG2 are required for FLS2-mediated immune responses through an unknown mechanism. Here we show that in the pre-activation state, XLG2 directly interacts with FLS2 and BIK1, and it functions together with AGB1 and AGG1/2 to attenuate proteasome-mediated degradation of BIK1, allowing optimum immune activation. Following the activation by flg22, XLG2 dissociates from AGB1 and is phosphorylated by BIK1 in the N terminus. The phosphorylated XLG2 enhances the production of reactive oxygen species (ROS) likely by modulating the NADPH oxidase RbohD. The study demonstrates that the G proteins are directly coupled to the FLS2 receptor complex and regulate immune signaling through both pre-activation and post-activation mechanisms.

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Mol Plant Pathol: Bacterial pathogenesis of plants: Future challenges from a microbial perspective (2016)

Mol Plant Pathol: Bacterial pathogenesis of plants: Future challenges from a microbial perspective (2016) | Plants and Microbes | Scoop.it
Plant infection is a complicated process. Upon encountering a plant, pathogenic microorganisms must first adapt to life on the epiphytic surface, and survive long enough to initiate an infection. Responsiveness to the environment is critical throughout infection, with intracellular and community-level signal transduction pathways integrating environmental signals and triggering appropriate responses in the bacterial population. Ultimately, phytopathogens must migrate from the epiphytic surface into the plant tissue using motility and chemotaxis pathways. This migration is coupled to overcoming the physical and chemical barriers to entry into the plant apoplast. Once inside the plant, bacteria use an array of secretion systems to release phytotoxins and protein effectors that fulfil diverse pathogenic functions (Fig. 1)(Phan Tran et al., 2011, Melotto & Kunkel, 2013).

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The Sainsbury Lab's curator insight, May 16, 4:03 AM
Plant infection is a complicated process. Upon encountering a plant, pathogenic microorganisms must first adapt to life on the epiphytic surface, and survive long enough to initiate an infection. Responsiveness to the environment is critical throughout infection, with intracellular and community-level signal transduction pathways integrating environmental signals and triggering appropriate responses in the bacterial population. Ultimately, phytopathogens must migrate from the epiphytic surface into the plant tissue using motility and chemotaxis pathways. This migration is coupled to overcoming the physical and chemical barriers to entry into the plant apoplast. Once inside the plant, bacteria use an array of secretion systems to release phytotoxins and protein effectors that fulfil diverse pathogenic functions (Fig. 1)(Phan Tran et al., 2011, Melotto & Kunkel, 2013).
The Pub Club's curator insight, May 17, 8:23 AM
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Rakesh Yashroy's curator insight, May 18, 9:54 PM
Host-pathogen interface is the real battle field of survival against odds both for animals and plant infections @ https://en.wikipedia.org/wiki/Host-pathogen_interface
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Disqus: Reviews of bioRxiv "Wheat blast disease caused by Pyricularia graminis-tritici sp. nov." (2016)

Disqus: Reviews of bioRxiv "Wheat blast disease caused by Pyricularia graminis-tritici sp. nov." (2016) | Plants and Microbes | Scoop.it

Pierre Gladieux:

 

Thank you very much for sharing your work. I looked at the methods and results and I have a few concerns regarding the validity of species identification.

 

Only the genealogy of the concatenated dataset is shown. The 10 individual gene trees are not presented, so I cannot get an idea of the level of discordance across genealogies. What would be the result of Genealogical Concordance Phylogenetic Species Recognition (http://taylorlab.berkeley.edu/... Table 3 suggests that most of the divergence in the total evidence genealogy is caused by one gene (MPG1). Table 4 shows that there is also exclusive polymorphism at one gene in one of the wheat-infecting lineages. Is it sufficient to conclude that these lineages are reproductively isolated and form distinct phylogenetic species?

 

Mark Farman:

 

Let's see how the proposed new Pgt species maps on a phylogenetic tree based on whole genome data. Below is a neighbor-joining tree built using genetic distances assessed across the whole genome. Gray shaded ovals encompass strains that fall under the proposed Pgt umbrella. Placements seem kind of arbitrary, don't they?

 

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bioRxiv: Wheat blast disease caused by Pyricularia graminis-tritici sp. nov. (2016)

bioRxiv: Wheat blast disease caused by Pyricularia graminis-tritici sp. nov. (2016) | Plants and Microbes | Scoop.it

Pyricularia oryzae is a species complex that causes blast disease on more than 50 species of poaceous plants. Pyricularia oryzae has a worldwide distribution as a rice (Oryza) pathogen and in the last century emerged as an important wheat (Triticum) pathogen in southern Brazil. Presently, P. oryzae pathotype Oryza is considered the rice blast pathogen, whereas P. oryzae pathotype Triticum is the wheat blast pathogen. In this study we investigated whether the Oryza and Triticum pathotypes of P. oryzae were distinct at the species level. We also describe a new Pyricularia species causing blast on several other poaceous hosts in Brazil, including wheat. We conducted phylogenetic analyses using 10 housekeeping loci from an extensive sample (N = 128) of sympatric populations of P. oryzae adapted to rice, wheat and other poaceous hosts found in or near wheat fields. The Bayesian phylogenetic analysis grouped the isolates into two major monophyletic clusters (I and II) with high Bayesian probabilities (P = 0.99). Cluster I contained isolates obtained from wheat as well as other Poaceae hosts (P = 0.98). Cluster II was divided into three host-associated clades (Clades 1, 2 and 3; P > 0.75). Clade 1 contained isolates obtained from wheat and other poaceous hosts, Clade 2 contained exclusively wheat-derived isolates, and Clade 3 comprised isolates associated only with rice. Our interpretation was that cluster I and cluster II correspond to two distinct species: Pyricularia graminis-tritici sp. nov. (Pgt), newly described in this study, and Pyricularia oryzae (Po). The host-associated clades found in P. oryzae Cluster II correspond to P. oryzae pathotype Triticum (PoT; Clades 1 and 2), and P. oryzae pathotype Oryza (PoO; Clade 3). No morphological or cultural differences were observed among these species, but a distinctive pathogenicity spectrum was observed. Pgt and PoT were pathogenic and highly aggressive on Triticum aestivum (wheat), Hordeum vulgare (barley), Urochloa brizantha (signal grass) and Avena sativa (oats). PoO was highly virulent on the original rice host (Oryza sativa), and also on wheat, barley, and oats, but not on signal grass. We concluded that blast disease on wheat and its associated Poaceae hosts in Brazil is caused by multiple Pyricularia species: the newly described Pyricularia graminis-tritici sp. nov., and the known P. oryzae pathotypes Triticum and Oryza. To our knowledge, P. graminis-tritici sp. nov. is still restricted to Brazil, but obviously represents a serious threat to wheat cultivation globally.

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Nature Biotech: Accelerated cloning of a potato late blight–resistance gene using RenSeq and SMRT sequencing (2016)

Nature Biotech: Accelerated cloning of a potato late blight–resistance gene using RenSeq and SMRT sequencing (2016) | Plants and Microbes | Scoop.it

Global yields of potato and tomato crops have fallen owing to potato late blight disease, which is caused by Phytophthora infestans. Although most commercial potato varieties are susceptible to blight, many wild potato relatives show variation for resistance and are therefore a potential source of Resistance to P. infestans (Rpi) genes. Resistance breeding has exploited Rpi genes from closely related tuber-bearing potato relatives, but is laborious and slow1, 2, 3. Here we report that the wild, diploid non-tuber-bearing Solanum americanum harbors multiple Rpi genes. We combine resistance (R) gene sequence capture (RenSeq)4 with single-molecule real-time (SMRT) sequencing (SMRT RenSeq) to clone Rpi-amr3i. This technology should enable de novo assembly of complete nucleotide-binding, leucine-rich repeat receptor (NLR) genes, their regulatory elements and complex multi-NLR loci from uncharacterized germplasm. SMRT RenSeq can be applied to rapidly clone multiple R genes for engineering pathogen-resistant crops.


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The Sainsbury Lab's curator insight, April 26, 4:21 AM
Global yields of potato and tomato crops have fallen owing to potato late blight disease, which is caused by Phytophthora infestans. Although most commercial potato varieties are susceptible to blight, many wild potato relatives show variation for resistance and are therefore a potential source of Resistance to P. infestans (Rpi) genes. Resistance breeding has exploited Rpi genes from closely related tuber-bearing potato relatives, but is laborious and slow1, 2, 3. Here we report that the wild, diploid non-tuber-bearing Solanum americanum harbors multiple Rpi genes. We combine resistance (R) gene sequence capture (RenSeq)4 with single-molecule real-time (SMRT) sequencing (SMRT RenSeq) to clone Rpi-amr3i. This technology should enable de novo assembly of complete nucleotide-binding, leucine-rich repeat receptor (NLR) genes, their regulatory elements and complex multi-NLR loci from uncharacterized germplasm. SMRT RenSeq can be applied to rapidly clone multiple R genes for engineering pathogen-resistant crops.
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Github: The origin of wheat blast in Bangladesh (2016)

Github: The origin of wheat blast in Bangladesh (2016) | Plants and Microbes | Scoop.it

via Daniel Croll and Bruce McDonald

What did we find out?
  1. The wheat blast outbreak in Bangladesh was not caused by a mutated rice blast strain. We found that the strains isolated from Bangladesh grouped very tightly with all known wheat blast strains from Brazil and not with any known rice blast strains.

  2. The wheat blast strains in Bangladesh are genetically very similar to wheat blast strains previously identified in Brazil. The genetically most similar strains were collected in Brazilian wheat fields and on associated weeds Eleusine indica (goose grass) and Cenchrus echinatus collected in Brazil.

  3. One of the genetically closest strains known from Brazil is PY0925. The genome sequence and annotation can be downloaded here. We made the genome sequence of an additional Brazilian wheat blast strain available. This is strain 205 isolated in São Borja (RS, Brazil) and is slightly more distant to the Bangladesh blast strains. Download the genomegene models and protein sequences.

  4. The high similarity among the wheat blast strains from Bangladesh and Brazil suggests that wheat blast was introduced into Bangladesh from Brazil. Many fungal diseases can be transmitted via grains and previous research indicated that wheat blast can be seed-transmitted. A transmission of the disease from Brazil is plausible because Bangladesh is one of the largest Asian importers of wheat and Brazil is one of the major suppliers of wheat to Bangladesh.

  5. Other Asian countries that received wheat from Brazil, including Thailand, Philippines and Vietnam should increase surveillance efforts to learn if wheat blast has entered into their wheat fields.

 

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SlideShare: The recent emergence of wheat blast in Brazil (2015)

An update on current knowledge of the wheat blast pathogen in Brazil. Presented by Bruce McDonald at the Fungal Genetics Conference, Asilomar, March, 2015.

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8th International Geminivirus Symposium, New Delhi, 7-10 November, 2016

8th International Geminivirus Symposium, New Delhi, 7-10 November, 2016 | Plants and Microbes | Scoop.it

The 8th International Geminivirus Symposium and the 6th International ssDNA Comparative Virology Workshop will be held in association with Indian Virological Society from 7th-10th November, 2016 at Vivanta by Taj, Dwarka, New Delhi, India. The symposium will present an excellent platform to discuss and share the latest developments in the subject of geminiviruses and ssDNA viruses of plants, animals and human beings. There will be facilities for commercial organizations to showcase their products to an international audience. Concessional rates for registration will be made available for PhD students and post-doctoral fellows.

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#ECFG13 13th European Conference on Fungal Genetics, Paris, April 2016

#ECFG13 13th European Conference on Fungal Genetics, Paris, April 2016 | Plants and Microbes | Scoop.it

Welcome to 13th European Conference on Fungal Genetics!   
 
The aim of ECFG13 is to showcase recent advances in fungal genetics and molecular biology, including cellular biology, evolutionary genomics, biotic intercations, systems and synthetic biology, ecogenomics and biotechnology. The program includes keynote lectures, 6 plenary sessions, 9 concurrent sessions, and 2 poster sessions for more informal discussions. These sessions will be complemented with satellite meetings, which will be held prior to the main conference. The conference will provide an interdisciplinary forum for scientists to present and discuss the most recent innovations, trends and issues in the field of fungal genetics and molecular biology.The conference will be held in Paris, France, a city with many attractions, in the setting of the Center of Science and Industry (La Cité des Sciences et de l'Industrie) in La Villette Park. The organizing committee looks forward to welcoming you in 2016 to enjoy springtime and some exciting science!    

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Science: Nuclear-localized cyclic nucleotide–gated channels mediate symbiotic calcium oscillations (2016)

Science: Nuclear-localized cyclic nucleotide–gated channels mediate symbiotic calcium oscillations (2016) | Plants and Microbes | Scoop.it

Nuclear-associated Ca2+ oscillations mediate plant responses to beneficial microbial partners—namely, nitrogen-fixing rhizobial bacteria that colonize roots of legumes and arbuscular mycorrhizal fungi that colonize roots of the majority of plant species. A potassium-permeable channel is known to be required for symbiotic Ca2+ oscillations, but the calcium channels themselves have been unknown until now. We show that three cyclic nucleotide–gated channels in Medicago truncatula are required for nuclear Ca2+ oscillations and subsequent symbiotic responses. These cyclic nucleotide–gated channels are located at the nuclear envelope and are permeable to Ca2+. We demonstrate that the cyclic nucleotide–gated channels form a complex with the postassium-permeable channel, which modulates nuclear Ca2+ release. These channels, like their counterparts in animal cells, might regulate multiple nuclear Ca2+ responses to developmental and environmental conditions.


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BMC Genomics: Host specialization of the blast fungus Magnaporthe oryzae is associated with dynamic gain and loss of genes linked to transposable elements (2016)

BMC Genomics: Host specialization of the blast fungus Magnaporthe oryzae is associated with dynamic gain and loss of genes linked to transposable elements (2016) | Plants and Microbes | Scoop.it

Background. Magnaporthe oryzae (anamorph Pyricularia oryzae) is the causal agent of blast disease of Poaceae crops and their wild relatives. To understand the genetic mechanisms that drive host specialization of M. oryzae, we carried out whole genome resequencing of four M. oryzae isolates from rice (Oryza sativa), one from foxtail millet (Setaria italica), three from wild foxtail millet S. viridis, and one isolate each from finger millet (Eleusine coracana), wheat (Triticum aestivum) and oat (Avena sativa), in addition to an isolate of a sister species M. grisea, that infects the wild grass Digitaria sanguinalis.

 

Results. Whole genome sequence comparison confirmed that M. oryzae Oryza and Setaria isolates form a monophyletic and close to another monophyletic group consisting of isolates from Triticum and Avena. This supports previous phylogenetic analysis based on a small number of genes and molecular markers. When comparing the host specific subgroups, 1.2–3.5 % of genes showed presence/absence polymorphisms and 0–6.5 % showed an excess of non-synonymous substitutions. Most of these genes encoded proteins whose functional domains are present in multiple copies in each genome. Therefore, the deleterious effects of these mutations could potentially be compensated by functional redundancy. Unlike the accumulation of nonsynonymous nucleotide substitutions, gene loss appeared to be independent of divergence time. Interestingly, the loss and gain of genes in pathogens from the Oryza and Setaria infecting lineages occurred more frequently when compared to those infecting Triticum and Avena even though the genetic distance between Oryza and Setaria lineages was smaller than that between Triticum and Avena lineages. In addition, genes showing gain/loss and nucleotide polymorphisms are linked to transposable elements highlighting the relationship between genome position and gene evolution in this pathogen species.

 

Conclusion. Our comparative genomics analyses of host-specific M. oryzae isolates revealed gain and loss of genes as a major evolutionary mechanism driving specialization to Oryza and Setaria. Transposable elements appear to facilitate gene evolution possibly by enhancing chromosomal rearrangements and other forms of genetic variation.

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Arjen ten Have's curator insight, May 25, 9:55 AM
So for all of you that keep thinking of transposable elements and alike as mere selfish genes that do not contribute to the other replicators of its host, maybe you should read this. Bummer that this happens in a pathogen.
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PLOS Pathogens: Direct and Indirect Targeting of PP2A by Conserved Bacterial Type-III Effector Proteins (2016)

PLOS Pathogens: Direct and Indirect Targeting of PP2A by Conserved Bacterial Type-III Effector Proteins (2016) | Plants and Microbes | Scoop.it

Bacterial AvrE-family Type-III effector proteins (T3Es) contribute significantly to the virulence of plant-pathogenic species of Pseudomonas, Pantoea, Ralstonia, Erwinia, Dickeya and Pectobacterium, with hosts ranging from monocots to dicots. However, the mode of action of AvrE-family T3Es remains enigmatic, due in large part to their toxicity when expressed in plant or yeast cells. To search for targets of WtsE, an AvrE-family T3E from the maize pathogen Pantoea stewartii subsp. stewartii, we employed a yeast-two-hybrid screen with non-lethal fragments of WtsE and a synthetic genetic array with full-length WtsE. Together these screens indicate that WtsE targets maize protein phosphatase 2A (PP2A) heterotrimeric enzyme complexes via direct interaction with B’ regulatory subunits. AvrE1, another AvrE-family T3E from Pseudomonas syringae pv. tomato strain DC3000 (Pto DC3000), associates with specific PP2A B’ subunit proteins from its susceptible host Arabidopsis that are homologous to the maize B’ subunits shown to interact with WtsE. Additionally, AvrE1 was observed to associate with the WtsE-interacting maize proteins, indicating that PP2A B’ subunits are likely conserved targets of AvrE-family T3Es. Notably, the ability of AvrE1 to promote bacterial growth and/or suppress callose deposition was compromised in Arabidopsis plants with mutations of PP2A genes. Also, chemical inhibition of PP2A activity blocked the virulence activity of both WtsE and AvrE1 in planta. The function of HopM1, a Pto DC3000 T3E that is functionally redundant to AvrE1, was also impaired in specific PP2A mutant lines, although no direct interaction with B’ subunits was observed. These results indicate that sub-component specific PP2A complexes are targeted by bacterial T3Es, including direct targeting by members of the widely conserved AvrE-family.


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fundoshi's curator insight, May 20, 6:17 AM
Hop好きだけど いよいよ応用には今後しばらく結びつかないのかなって感でてきた気がする
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Truth in Olive Oil: The Strange Case of Italian Olive Oil (2016)

Truth in Olive Oil: The Strange Case of Italian Olive Oil (2016) | Plants and Microbes | Scoop.it

When news of xylella hit in 2013, I immediately thought: Scam. In Puglia, ancient olive trees are protected by law from being cut down or otherwise removed. As you can imagine, this law has been unpopular with certain businesses, like real estate developers and road-builders. The areas affected by xylella were, by strange chance, extraordinarily beautiful landscapes – ripe for posh new hotels. The emergency plan which a handful of authorities drew up shortly after the announcement of the xylella epidemic in Puglia was trenchant: cut down all the infected trees, along with a goodly number of their neighbors in case they too had been blighted. Ecco fatto: suddenly there would be more elbow (or hotel) room in several lovely seaside locales in Puglia.

 

Which of course is only one interpretation of the facts. On the other hand, I'm no agronomist, and as reports of the seriousness of the xylella infection echoed in the press, I began to think I'd jumped to a hasty and cynical conclusion. (For more views on the xylella story, see this independent blog.) Developments over the last few months, however, suggest I may have been right all along. A 2015 report on mafia infiltration of Italian agriculture, written by a team led by the renowned anti-mafia prosecutor Gian Carlo Caselli, dedicated a 9-page sub-chapter to what it called “The Strange Case of Xylella Fastidiosa,” echoing Robert Louis Stevenson’s novella of Jekyll and Hyde. The report noted that xylella broke out shortly after an international agronomy conference had been held in Bari in 2010, though the infection appeared not in olive trees near Bari, but in the Gallipoli area – precisely where hordes of troublesome grandfather trees were holding up plans for a perfectly lovely new mega-resort. Cue yet another criminal investigation: in mid-December, prosecutors led by Cataldo Motta, chief magistrate in Lecce, charged ten agronomists and other public “experts” who’d launched the xylella jihad with a range of misdeeds, among which are spreading plant disease, making false official statements, and destroying and disfiguring natural landscapes. (Italian and English.) The Lecce prosecutors also blocked further eradication of ancient olive trees, at least for the time being.

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PLOS Pathogens: Fungal Genomics Challenges the Dogma of Name-Based Biosecurity (2016)

PLOS Pathogens: Fungal Genomics Challenges the Dogma of Name-Based Biosecurity (2016) | Plants and Microbes | Scoop.it

A paradigm shift is needed to overcome these serious shortcomings in biosecurity. Risk assessments should target the genes of pathogens rather than their names. Genomic research over the last decade has paved the way towards gene-based biosecurity. Detailed information about fungal genomes can help predict risks posed by undescribed pathogens through (i) prediction of lifestyle, e.g., biotrophic and saprotrophic fungi can be distinguished from nectrotrophic and hemibiotrophic fungi, and saprotrophic fungi can be distinguished from pathogens. In time, protein families that exist in effective pathogens will be discovered and may be predictive for organisms that have an unknown ecology or life strategy. Software for rapid analysis of bacterial genomic data to screen for pathogenic proteins has been designed, and similar tools and databases will be developed for fungal pathogens. (ii) Identification of potential pathogenicity factors, i.e., factors necessary for disease development that suppress or manipulate host-cell physiology to the advantage of a pathogen, but which are not essential for a pathogen to complete its life cycle. One example is disease effector proteins, which are likely expressed by all plant pathogens and may target similar defensive proteins in their hosts . Effector genes do not have conserved motifs in fungi, and identifiers in the genome, such as diversifying selection, will be crucial to identify these genes that may be a clue to pathogenicity. (iii) Identification of transposable elements or high mutation rates, which are implicated in the evolution of pathogenicity genes in fungi.


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Elsa Ballini's curator insight, May 13, 6:58 AM
How can we change risk assessments for wheat blast?
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OpenWheatBlast: Phylogenomic analyses reveal that the 2016 outbreak of « wheat blast » in Bangladesh is caused by a South American wheat-infecting lineage of Magnaporthe oryzae (2016)

OpenWheatBlast: Phylogenomic analyses reveal that the 2016 outbreak of « wheat blast » in Bangladesh is caused by a South American wheat-infecting lineage of Magnaporthe oryzae (2016) | Plants and Microbes | Scoop.it

Knowledge of pathogen populations, lineages, species, and their reproductive mode is an obligatory step to answer a host of questions common to all emerging diseases: is the disease due to a change in the environment that promotes disease, to the spread of a new pathogen, or to the emergence of a new lineage of an existing pathogen? What are the genomic changes and eco-evolutionary factors underlying disease emergence?


Here, our goal was to determine if « wheat blast » isolates recently collected in Bangladesh were related to Magnaporthe oryzae lineages infecting cereals and grasses using a phylogenomic approach. We also outline avenues for future research on the origins of wheat blast.

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News: Californian sudden oak death epidemic 'unstoppable' (2016)

News: Californian sudden oak death epidemic 'unstoppable' (2016) | Plants and Microbes | Scoop.it

New research shows the sudden oak death epidemic in California cannot now be stopped, but that its tremendous ecological and economic impacts could have been greatly reduced if control had been started earlier. The research also identifies new strategies to enhance control of future epidemics, including identifying where and how to fell trees, as “there will be a next time.”


Sudden oak death — caused by Phytophthora ramorum, a fungus-like pathogen related to potato blight — has killed millions of trees over hundreds of square kilometres of forest in California. First detected near San Francisco in 1995, it spread north through coastal California, devastating the region’s iconic oak and tanoak forests. In 2002 a strain of the pathogen appeared in the south west of England, affecting shrubs but not oaks, since English species of oak are not susceptible. In 2009 the UK strain started killing larch — an important tree crop — and has since spread widely across the UK.


In a study published in PNAS, researchers from the University of Cambridge have used mathematical modelling to show that stopping or even slowing the spread of Phytophthora ramorum in California is now not possible, and indeed has been impossible for a number of years.


Treating trees with chemicals is not practical or cost-effective on the scales that would be necessary for an established forest epidemic. Currently the only option for controlling the disease is to cut down infected trees, together with neighbouring trees that are likely to be infected but may not yet show symptoms. “By comparing the performance of a large number of potential strategies, modelling can tell us where and how to start chopping down trees to manage the disease over very large areas,” explains Nik Cunniffe, lead author from Cambridge’s Department of Plant Sciences.


The authors say that preventing the disease from spreading to large parts of California could have been possible if management had been started in 2002. Before 2002 not enough was known about the pathogen to begin managing the disease. Their modelling also offers new strategies for more effectively controlling inevitable future epidemics.

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Jessie Uehling's curator insight, May 3, 12:54 PM
how sad: News: Californian sudden oak death epidemic 'unstoppable' (2016) Lots of big changes for California's ecosystems in the near future 
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Nature Biotech: A pigeonpea gene confers resistance to Asian soybean rust in soybean (2016)

Nature Biotech: A pigeonpea gene confers resistance to Asian soybean rust in soybean (2016) | Plants and Microbes | Scoop.it

Asian soybean rust (ASR), caused by the fungus Phakopsora pachyrhizi, is one of the most economically important crop diseases, but is only treatable with fungicides, which are becoming less effective owing to the emergence of fungicide resistance. There are no commercial soybean cultivars with durable resistance to P. pachyrhizi, and although soybean resistance loci have been mapped, no resistance genes have been cloned. We report the cloning of a P. pachyrhizi resistance gene CcRpp1 (Cajanus cajan Resistance against Phakopsora pachyrhizi 1) from pigeonpea (Cajanus cajan) and show that CcRpp1 confers full resistance to P. pachyrhizi in soybean. Our findings show that legume species related to soybean such as pigeonpea, cowpea, common bean and others could provide a valuable and diverse pool of resistance traits for crop improvement.


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The Sainsbury Lab's curator insight, April 26, 4:45 AM
Asian soybean rust (ASR), caused by the fungus Phakopsora pachyrhizi, is one of the most economically important crop diseases, but is only treatable with fungicides, which are becoming less effective owing to the emergence of fungicide resistance. There are no commercial soybean cultivars with durable resistance to P. pachyrhizi, and although soybean resistance loci have been mapped, no resistance genes have been cloned. We report the cloning of a P. pachyrhizi resistance gene CcRpp1 (Cajanus cajan Resistance against Phakopsora pachyrhizi 1) from pigeonpea (Cajanus cajan) and show that CcRpp1 confers full resistance to P. pachyrhizi in soybean. Our findings show that legume species related to soybean such as pigeonpea, cowpea, common bean and others could provide a valuable and diverse pool of resistance traits for crop improvement.
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Nature Biotech: Rapid cloning of disease-resistance genes in plants using mutagenesis and sequence capture (2016)

Nature Biotech: Rapid cloning of disease-resistance genes in plants using mutagenesis and sequence capture (2016) | Plants and Microbes | Scoop.it

Wild relatives of domesticated crop species harbor multiple, diverse, disease resistance (R) genes that could be used to engineer sustainable disease control. However, breeding R genes into crop lines often requires long breeding timelines of 5–15 years to break linkage between R genes and deleterious alleles (linkage drag). Further, when R genes are bred one at a time into crop lines, the protection that they confer is often overcome within a few seasons by pathogen evolution1. If several cloned R genes were available, it would be possible to pyramid R genes2 in a crop, which might provide more durable resistance1. We describe a three-step method (MutRenSeq)-that combines chemical mutagenesis with exome capture and sequencing for rapid R gene cloning. We applied MutRenSeq to clone stem rust resistance genes Sr22 and Sr45 from hexaploid bread wheat. MutRenSeq can be applied to other commercially relevant crops and their relatives, including, for example, pea, bean, barley, oat, rye, rice and maize.


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The Sainsbury Lab's curator insight, April 26, 4:14 AM
Wild relatives of domesticated crop species harbor multiple, diverse, disease resistance (R) genes that could be used to engineer sustainable disease control. However, breeding R genes into crop lines often requires long breeding timelines of 5–15 years to break linkage between R genes and deleterious alleles (linkage drag). Further, when R genes are bred one at a time into crop lines, the protection that they confer is often overcome within a few seasons by pathogen evolution1. If several cloned R genes were available, it would be possible to pyramid R genes2 in a crop, which might provide more durable resistance1. We describe a three-step method (MutRenSeq)-that combines chemical mutagenesis with exome capture and sequencing for rapid R gene cloning. We applied MutRenSeq to clone stem rust resistance genes Sr22 and Sr45 from hexaploid bread wheat. MutRenSeq can be applied to other commercially relevant crops and their relatives, including, for example, pea, bean, barley, oat, rye, rice and maize.
Neelam Redekar's curator insight, April 29, 8:19 AM
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Nature News: Devastating wheat fungus appears in Asia for first time (2016)

Nature News: Devastating wheat fungus appears in Asia for first time (2016) | Plants and Microbes | Scoop.it

Fields are ablaze in Bangladesh, as farmers struggle to contain Asia’s first outbreak of a fungal disease that periodically devastates crops in South America. Plant pathologists warn that wheat blast could spread to other parts of south and southeast Asia, and are hurrying to trace its origins.

 

Efforts are also under way to find wheat genes that confer resistance to the disease.

 

First detected in February and confirmed with genome sequencing by Kamoun’s lab this month, the wheat-blast outbreak has already caused the loss of more than 15,000 hectares of crops in Bangladesh. “It’s really an explosive, devastating disease,” says plant pathologist Barbara Valent of Kansas State University in Manhattan, Kansas. “It’s really critical that it be controlled in Bangladesh.”

 

After rice, wheat is the second most cultivated grain in Bangladesh, which has a population of 156 million people. More broadly, inhabitants of south Asia grow 135 million tonnes of wheat each year.

 

Wheat blast is caused by the fungus Magnaporthe oryzae. Since 1985, when scientists discovered it in Brazil’s Paraná state, the disease has raced across South America.

 

The fungus is better known as a pathogen of rice. But unlike in rice, where M. oryzae attacks the leaves, the fungus strikes the heads of wheat, which are difficult for fungicides to reach. A 2009 outbreak in wheat cost Brazil one-third of that year’s crop. “There are regions in South America where they don’t grow wheat because of the disease,” Valent says. Wheat blast was spotted in Kentucky in 2011, but vigorous surveillance helped to stop it spreading in the United States.

 

In South America, the disease tends to take hold in hot and humid spells. Such conditions are present in Bangladesh, and the disease could migrate across south and southeast Asia, say plant pathologists. In particular, itcould spread over the Indo-Gangetic Plain through Bangladesh, northern India and eastern Pakistan, warn scientists at the Bangladesh Agricultural Research Institute (BARI) in Nashipur.

 

Bangladeshi officials are burning government-owned wheat fields to contain the fungus, and telling farmers not to sow seeds from infected plots. The BARI hopes to identify wheat varieties that are more tolerant of the fungus and agricultural practices that can keep it at bay, such as crop rotation and seed treatment.

 

It is unknown how wheat blast got to Bangladesh. One possibility is that a wheat-infecting strain was brought in from South America, says Nick Talbot, a plant pathologist at the University of Exeter, UK. Another is that an M. oryzae strain that infects south Asian grasses somehow jumped to wheat, perhaps triggered by an environmental shift: that is what happened in Kentucky, when a rye-grass strain infected wheat.

 

To tackle the question, this month Kamoun’s lab sequenced a fungus sample from Bangladesh. The strain seems to be related to those that infect wheat in South America, says Kamoun, but data from other wheat-infecting strains and strains that plague other grasses are needed to pinpoint the outbreak’s origins conclusively.

 

The Open Wheat Blast website might help. Kamoun has uploaded the Bangladeshi data, and Talbot has deposited M. oryzae sequences from wheat in Brazil. Talbot hopes that widely accessible genome data could help to combat the outbreak. Researchers could use them to screen seeds for infection or identify wild grasses that can transmit the fungus to wheat fields.

 

Rapid data sharing is becoming more common in health emergencies, such as the outbreak of Zika virus in the Americas. Kamoun and Talbot say that their field should follow suit. “The plant-pathology community has a responsibility to allow data to be used to combat diseases that are happening now, and not worry too much about whether they may or may not get a Nature paper out of it,” says Talbot.

 

Last month, Valent’s team reported the first gene variant known to confer wheat-blast resistance (C. D. Cruz et al. Crop Sci. http://doi.org/bfk7; 2016), and field trials of crops that bear the resistance gene variant have begun in South America. But plant pathologists say that finding one variant is not enough: wheat strains must be bred with multiple genes for resistance, to stop M. oryzae quickly overcoming their defences.

 

The work could help in the Asian crisis, says Talbot. “What I would hope for out of this sorry situation,” he says, “is that there will be a bigger international effort to identify resistance genes.”

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News: Scientists issue rallying cry for wheat blast research (2016)

News: Scientists issue rallying cry for wheat blast research (2016) | Plants and Microbes | Scoop.it

A team of scientists in the UK and Bangladesh are turning to the combined knowledge of the global scientific community to address an emerging threat to Asian agriculture.

 

The target is the fearsome fungal disease wheat blast. The pathogen was spotted in Bangladesh in February this year—its first report in Asia. Wheat is the second major food source in Bangladesh, after rice. The blast disease has, so far, caused up to 90% yield losses in more than 15,000 hectares. Scientists fear that the pathogen could spread further to other wheat growing areas in South Asia.

 

The UK and Bangladeshi teams are making raw genetic data for the wheat blast pathogen available on a new website—http://www.wheatblast.net—and inviting others to do the same. Professor Sophien Kamoun, of The Sainsbury Laboratory in Norwich, who is leading the project, said that a wide cultural change is needed for scientists to optimally address new threats to food security.

 

"I have a beef with the way that research is typically done. We need a fundamentally new approach to sharing genetic data for emerging plant diseases," he said. "We need to generate and make data public more rapidly and seek input from a larger crowd because, collectively, we are better able to answer questions."

 

Professor Kamoun, with colleagues at The Genome Analysis Centre and John Innes Centre in Norwich, and with Professor Tofazzal Islam's Team of Bangabndhu Sheikh Mujubur Rahman Agricultural University (BSMRAU) in Bangladesh, is hoping that the wheatblast.net website, together with an accompanying Facebook page, will provide a hub for information, collaboration and comment. They are basing the site on their successful Open Ash Dieback website, which brought scientists together in the fight against ash dieback disease.

 

The blast fungus normally infects rice and over 50 types of grasses. Occasionally, a blast fungus strain would jump from one host to another resulting in a new disease. Such a "host jump" to wheat has happened in Brazil in the 1980s. The wheat blast pathogen is now rife in South America, where it infects up to 3 million hectares and causes serious crop losses.

 

Prof Kamoun and colleagues are working with Professor Tofazzal Islam's team, of the Department of Biotechnology of BSMRAU in Gazipur, Bangladesh. They hope that the genetic data will help determine whether the Bangladeshi wheat-infecting strain has evolved independently from local grass-infecting fungi or was somehow introduced into the country.

 

Professor Tofazzal Islam said "This pathogen causes a destructive disease on rice and it would be disastrous if the same situation arises now in wheat. Genomic and post-genomic research should clarify the origin of the wheat strain and guide measures for disease management. Prompt responses are needed from the scientific community and the government of Bangladesh for addressing this national crisis to ensure increasing wheat production, which is linked with future food and nutritional security of the nation."

 

The group of scientists includes Dr Diane Saunders at The Genome Analysis Centre and John Innes Centre who developed a technique last year, known as Field Pathogenomics. To date, Field Pathogenomics has been applied to track another fungal crop disease - yellow rust. The method generates highly-specific genetic information directly from diseased wheat samples to determine the identity of the pathogen strain that's associated with an epidemic. Application of this method to wheat blast should unmask the pathogen in Bangladesh and contribute to a response plan.

 

The recent wheat blast epidemic in Bangladesh has prompted Professor Nick Talbot, University of Exeter, to post on the wheatblast.net website a set of genetic data generated by his group from worldwide populations of the wheat and rice blast fungus. Prof Talbot said "In an emergency like this one, the community must come together to share data and compare notes. Only then, we will determine the true identity of the pathogen and put in place effective measures in a timely fashion."

 

Professor Neil Hall, Director of The Genome Analysis Centre said: "It is critical in emerging crises like this that scientific data is rapidly generated and made available as soon as possible. Having an open-access site has already galvanized open exchange of information for the ash dieback disease. The scientific community needs to rally behind open science to respond to recurrent threats to global food security."

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Nature Biotechnology: Plant immunity switched from bacteria to virus (2016)

Nature Biotechnology: Plant immunity switched from bacteria to virus (2016) | Plants and Microbes | Scoop.it

Each year, staple crops around the world suffer massive losses in yield owing to the destruc- tive effects of pathogens. Improving the disease resistance of crops by boosting their immunity has been a key objective of agricultural bio- tech ever since the discovery of plant immune receptors in the 1990s. Nucleotide-binding leucine-rich repeat (NLR) proteins, a family of intracellular immune receptors that recog- nize pathogen molecules, are promising targets for enhancing pathogen resistance. In a recent paper in Science, Kim et al.1 describe a clever twist on this approach in which the host target protein for the pathogen effector is engineered rather than the NLR protein itself (Fig. 1).

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