Viruses interfere with and usurp host machinery and circumvent defense responses to create a suitable cellular environment for successful infection. This is usually achieved through interactions between viral proteins and host factors. Geminiviruses are a group of plant-infecting DNA viruses, of which some contain a betasatellite, known as DNAβ. Here, we report that Cotton leaf curl Multan virus (CLCuMuV) uses its sole satellite-encoded protein βC1 to regulate the plant ubiquitination pathway for effective infection. We found that CLCuMu betasatellite (CLCuMuB) βC1 interacts with NbSKP1, and interrupts the interaction of NbSKP1s with NbCUL1. Silencing of either NbSKP1s or NbCUL1 enhances the accumulation of CLCuMuV genomic DNA and results in severe disease symptoms in plants. βC1 impairs the integrity of SCFCOI1 and the stabilization of GAI, a substrate of the SCFSYL1 to hinder responses to jasmonates (JA) and gibberellins (GA). Moreover, JA treatment reduces viral accumulation and symptoms. These results suggest that CLCuMuB βC1 inhibits the ubiquitination function of SCF E3 ligases through interacting with NbSKP1s to enhance CLCuMuV infection and symptom induction in plants.
Soil microorganisms are central to the provision of food, feed, fiber, and medicine. Engineering of soil microbiomes may promote plant growth and plant health, thus contributing to food security and agricultural sustainability ( 1 , 2 ). However, little is known about most soil microorganisms and their impact on plant health. Disease-suppressive soils offer microbiome-mediated protection of crop plants against infections by soil-borne pathogens. Understanding of the microbial consortia and mechanisms involved in disease suppression may help to better manage plants while reducing fertilizer and pesticide inputs.
Background - The recognition of microbe-associated molecular patterns during infection is central to the mounting of an effective immune response. In spite of their importance, it remains difficult to identify these molecules and the host receptors required for their perception, ultimately limiting our understanding of the role of these molecules in the evolution of host-pathogen relationships.
Results - We employ a comparative genomics screen to identify six new immune eliciting peptides from the phytopathogenic bacterium Pseudomonas syringae. We then perform a reverse genetic screen to identify Arabidopsis thaliana leucine-rich repeat receptor-like kinases required for the recognition of these elicitors. We test the six elicitors on 187 receptor-like kinase knock-down insertion lines using a high-throughput peroxidase-based immune assay and identify multiple lines that show decreased immune responses to specific peptides. From this primary screen data, we focused on the interaction between the xup25 peptide from a bacterial xanthine/uracil permease and the Arabidopsis receptor-like kinase xanthine/uracil permease sensing 1; a family XII protein closely related to two well-characterized receptor-like kinases. We show that xup25 treatment increases pathogenesis-related gene induction, callose deposition, seedling growth inhibition, and resistance to virulent bacteria, all in a xanthine/uracil permease sensing 1-dependent manner. Finally, we show that this kinase-like receptor can bind the xup25 peptide directly. These results identify xup25 as a P. syringae microbe-associated molecular pattern and xanthine/uracil permease sensing 1 as a receptor-like kinase that detects the xup25 epitope to activate immune responses.
Conclusions - The present study demonstrates an efficient method to identify immune elicitors and the plant receptors responsible for their perception. Further exploration of these molecules will increase our understanding of plant-pathogen interactions and the basis for host specificity.
Plants and animals detect bacterial presence through Microbe-Associated Molecular Patterns (MAMPs) which induce an innate immune response. The field of fungal–bacterial interaction at the molecular level is still in its infancy and little is known about MAMPs and their detection by fungi. Exposing Fusarium graminearum to bacterial MAMPs led to increased fungal membrane hyperpolarization, a putative defense response, and a range of transcriptional responses. The fungus reacted with a different transcript profile to each of the three tested MAMPs, although a core set of genes related to energy generation, transport, amino acid production, secondary metabolism, and especially iron uptake were detected for all three. Half of the genes related to iron uptake were predicted MirA type transporters that potentially take up bacterial siderophores. These quick responses can be viewed as a preparation for further interactions with beneficial or pathogenic bacteria, and constitute a fungal innate immune response with similarities to those of plants and animals.
Background. Understanding how plants and pathogens modulate gene expression during the host-pathogen interaction is key to uncovering the molecular mechanisms that regulate disease progression. Recent advances in sequencing technologies have provided new opportunities to decode the complexity of such interactions. In this study, we used an RNA-based sequencing approach (RNA-seq) to assess the global expression profiles of the wheat yellow rust pathogen Puccinia striiformis f. sp. tritici (PST) and its host during infection.
Results. We performed a detailed RNA-seq time-course for a susceptible and a resistant wheat host infected with PST. This study (i) defined the global gene expression profiles for PST and its wheat host, (ii) substantially improved the gene models for PST, (iii) evaluated the utility of several programmes for quantification of global gene expression for PST and wheat, and (iv) identified clusters of differentially expressed genes in the host and pathogen. By focusing on components of the defence response in susceptible and resistant hosts, we were able to visualise the effect of PST infection on the expression of various defence components and host immune receptors.
Conclusions. Our data showed sequential, temporally coordinated activation and suppression of expression of a suite of immune-response regulators that varied between compatible and incompatible interactions. These findings provide the framework for a better understanding of how PST causes disease and support the idea that PST can suppress the expression of defence components in wheat to successfully colonize a susceptible host.
Funding for academic research in the United States has declined to a 40-year low in real terms, and other countries are experiencing similar declines. This persistent shortage of support threatens to create a "lost generation" of researchers – talented scientists who either leave the profession entirely, or who stay but acquire the cynicism and short-term thinking that hinders progress. While all researchers are being affected by the decline in funding, early-career researchers such as postdoctoral fellows and new investigators are being hit hardest.
To address this issue, we created Academics for the Future of Science, an organization dedicated to giving a voice to early-career researchers. As part of our effort to engage and educate these researchers (Academics for the Future of Science, 2015) we have solicited stories, especially from postdocs and new investigators, about their experiences in the current funding climate. Each account that follows highlights a different but equally pernicious problem facing early-career researchers.
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.
Recent evidence suggests that the ubiquitin-proteasome system (UPS) is involved in several aspects of plant immunity and a range of plant pathogens subvert the UPS to enhance their virulence. Here, we show that proteasome activity is strongly induced during basal defense in Arabidopsis and mutant lines defective in proteasome subunits RPT2a and RPN12a support increased bacterial growth of virulent Pseudomonas syringae DC3000 (Pst), strains in local leaves. Both proteasome subunits are required for PTI events such as production of reactive oxygen species and mitogen-activated protein kinases signaling as well as for defense gene expression. Furthermore, analysis of bacterial growth after a secondary infection of systemic leaves revealed that the establishment of systemic-acquired resistance (SAR) is impaired in proteasome mutants, suggesting that the proteasome plays an important role in defense priming and SAR. In addition, we show that Pst inhibits proteasome activity in a type-III secretion dependent manner. A systematic screen for type-III effector proteins from Pst for their ability to interfere with proteasome activity revealed HopM1, HopAO1, HopA1 and HopG1 as candidates. Identification of proteins interacting with HopM1 by mass-spectrometry indicate that HopM1 resides in a complex together with several E3 ubiquitin ligases and proteasome subunits, supporting the hypothesis that HopM1 associates with the proteasome leading to its inhibition. We conclude that the proteasome is an essential component of the plant immune system and that some pathogens have developed a general strategy to overcome proteasome-mediated defense.
Plant disease resistance occurs as a hypersensitive response (HR) at the site of attempted pathogen invasion. This specific event is initiated in response to recognition of pathogen-associated molecular pattern (PAMP) and subsequent PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI). Both PTI and ETI mechanisms are tightly connected with reactive oxygen species (ROS) production and disease resistance that involves distinct biphasic ROS production as one of its pivotal plant immune responses. This unique oxidative burst is strongly dependent on the resistant cultivars because a monophasic ROS burst is a hallmark of the susceptible cultivars. However, the cause of the differential ROS burst remains unknown. In the study here, we revealed the plausible underlying mechanism of the differential ROS burst through functional understanding of the Magnaporthe oryzae (M. oryzae) AVR effector, AVR-Pii. We performed yeast two-hybrid (Y2H) screening using AVRPii as bait and isolated rice NADP-malic enzyme2 (Os-NADP-ME2) as the rice target protein. To our surprise, deletion of the rice Os-NADP-ME2 gene in a resistant rice cultivar disrupted innate immunity against the rice blast fungus. Malic enzyme activity and inhibition studies demonstrated that AVR-Pii proteins specifically inhibit in vitro NADP-ME activity. Overall, we demonstrate that rice blast fungus, M. oryzae attenuates the host ROS burst via AVR-Pii-mediated inhibition of Os-NADP-ME2, which is indispensable in ROS metabolism for the innate immunity of rice. This characterization of the regulation of the host oxidative burst will help to elucidate how the products of AVR genes function associated with virulence of the pathogen.
Rice blast is one of the most destructive diseases affecting rice worldwide. The adoption of host resistance has proven to be the most economical and effective approach to control rice blast. In recent years, sequence-specific nucleases (SSNs) have been demonstrated to be powerful tools for the improvement of crops via gene-specific genome editing, and CRISPR/Cas9 is thought to be the most effective SSN. Here, we report the improvement of rice blast resistance by engineering a CRISPR/Cas9 SSN (C-ERF922) targeting the OsERF922 gene in rice. Twenty-one C-ERF922-induced mutant plants (42.0%) were identified from 50 T0 transgenic plants. Sanger sequencing revealed that these plants harbored various insertion or deletion (InDel) mutations at the target site. We showed that all of the C-ERF922-induced allele mutations were transmitted to subsequent generations. Mutant plants harboring the desired gene modification but not containing the transferred DNA were obtained by segregation in the T1 and T2 generations. Six T2 homozygous mutant lines were further examined for a blast resistance phenotype and agronomic traits, such as plant height, flag leaf length and width, number of productive panicles, panicle length, number of grains per panicle, seed setting percentage and thousand seed weight. The results revealed that the number of blast lesions formed following pathogen infection was significantly decreased in all 6 mutant lines compared with wild-type plants at both the seedling and tillering stages. Furthermore, there were no significant differences between any of the 6 T2 mutant lines and the wild-type plants with regard to the agronomic traits tested. We also simultaneously targeted multiple sites within OsERF922 by using Cas9/Multi-target-sgRNAs (C-ERF922S1S2 and C-ERF922S1S2S3) to obtain plants harboring mutations at two or three sites. Our results indicate that gene modification via CRISPR/Cas9 is a useful approach for enhancing blast resistance in rice.
.Until recently it was not possible to engineer novel recognition specificities of classical plant immune receptors to completely unrelated effectors. In a recent publication, Kim et al. engineered a plant effector target to inc rease novel recognition specificities by trapping unrela ted pathogen-derived proteases in their act .
RESISTANCE TO PSEUDOMONAS SYRINGAE 5 (RPS5) is a plant immune receptor of the Nucleotide-binding, leucine-rich repeat (NLR) type which perceives the Pseudomonas syringae Type-III effector AvrPphB, a papain-like cysteine protease belonging to the Peptidase C58 family . The perception of AvrPphB by RPS5 requires one additional host-derived factor known as AVRPPHB SUSCEPTIBLE 1 (PBS1), which belongs to Subfamily VII of Receptor-like Cytoplasmic Kinases (RLCK VII). Upon bacterial infection, PBS1, which binds to RPS5 in its pre-activation state, is cleaved by AvrPphB. PBS1 cleavage exposes a five amino acid loop in PBS1 that is believed to activate RPS5, triggering an immune response characterized by the hypersensitive response (HR), a form of programmed cell death . Interestingly, RPS5-mediated immune signaling requires both PBS1 fragments, and the conformational change induced by cleavage can be mimicked by insertion of five amino acids in the AvrPphB cleavage site . Therefore, perception of AvrPphB follows a mouse-trap mechanism where cleavage of PBS1 (bait) sets off the trap and activates RPS5, triggering immune responses..
RAB5 is a small GTPase that acts in endosomal trafficking. In addition to canonical RAB5 members that are homologous to animal RAB5, land plants harbor plant-specific RAB5, the ARA6 group, which regulates distinct trafficking events from canonical RAB5 GTPases. Here, we report that plant RAB5, both canonical and plant-specific members, accumulate at the interface between host plants and biotrophic fungal and oomycete pathogens. Biotrophic fungi and oomycetes colonize living plant tissues by establishing specialized infection hyphae, the haustorium, within host plant cells. We found that Arabidopsis thaliana ARA6/RABF1, a plant-specific RAB5, is localized to the specialized membrane that surrounds the haustorium, the extrahaustorial membrane (EHM), formed by the A. thaliana-adapted powdery mildew fungus Golovinomyces orontii. Whereas the conventional RAB5 ARA7/RABF2b was also localized to the EHM, endosomal SNARE and RAB5-activating proteins were not, which suggests that the EHM has modified endosomal characteristic. The recruitment of host RAB5 to the EHM was shared by the barley-adapted powdery mildew fungus Blumeria graminis f.sp. hordei and oomycete Hyaloperonospora arabidopsidis, but the extrahyphal membrane surrounding the hypha of the hemibiotrophic fungus Colletotrichum higginsianum at the biotrophic stage was devoid of RAB5. The localization of RAB5 to the EHM appears to correlate with the functionality of the haustorium. Our discovery sheds light on a novel relationship between plant RAB5 and obligate biotrophic pathogens.
Bacterial Blight (BB) and Bacterial Leaf Streak (BLS) are important rice diseases caused, respectively, by Xanthomonas oryzae pv. oryzae (Xoo) and Xanthomonas oryzae pv. oryzicola (Xoc). In both bacteria, Transcription Activator-Like (TAL) effectors are major virulence determinants that act by transactivating host genes downstream of Effector-Binding Elements (EBEs) bound in a sequence specific manner. Resistance to Xoo is mostly related to TAL effectors action, either by polymorphisms that prevent induction of susceptibility (S) genes or by executor (R) genes with EBEs embedded in their promoter and that induce cell death and resistance. For Xoc, no resistance sources are known in rice. Here, we investigated whether the recognition of effectors by nucleotide-binding and leucine rich repeat domain immune receptors (NLRs), the most widespread resistance mechanism in plants, is also able to stop BB and BLS. In one instance, transgenic rice lines harboring the AVR1-CO39 effector gene from the rice blast fungus Magnaporthe oryzae, under the control of an inducible promoter, were challenged with transgenic Xoo and Xoc strains carrying a TAL effector designed to transactivate the inducible promoter. This induced AVR1-CO39 expression and triggered BB and BLS resistance when the corresponding Pi-CO39 resistance locus was present. In a second example, transactivation of an auto-active NLR by Xoo-delivered designer TAL effectors resulted in BB resistance, demonstrating that NLR-triggered immune responses efficiently control Xoo. This forms the foundation for future BB and BLS disease control strategies whereupon endogenous TAL effectors will target synthetic promoter regions of Avr or NLR executor genes.
The wheat blast fungus recently hit Bangladesh. Could you briefly outline how it is being tackled by plant pathologists? Wheat blast has just emerged this last February in Bangladesh – its first report in Asia. It could spread to neighboring countries and become a major threat to wheat production in South Asia. Thus, we had to act fast. We used an Open Science approach to mobilize collaborators in Bangladesh and the wider blast fungus community, and managed to identify the pathogen strain in just a few weeks. It turned out that the Bangladeshi outbreak was caused by a clone related to the South American lineage of the pathogen. Now that we know the enemy, we can proceed to put in place an informed response plan. It’s challenging but at least we know the nature of the pathogen – a first step in any response plan to a disease outbreak.
A recent study by Kroj et al. (New Phytologist, 2016) surveyed nucleotide binding-leucine rich repeat (NLR) proteins from plant genomes for the presence of extraneous integrated domains that may serve as decoys or sensors for pathogen effectors. They reported that a FAM75 domain of unknown function occurs near the C-terminus of the potato late blight NLR protein R3a. Here, we investigated in detail the domain architecture of the R3a protein, its potato paralog R3b, and their tomato ortholog I2. We conclude that the R3a, R3b, and I2 proteins do not carry additional domains besides the classic NLR modules, and that the FAM75 domain match is likely a false positive among computationally predicted NLR-integrated domains.
Fig. 5 Highly polymorphic in the effector genes between and within the host-specific subgroups of M. oryzae. a The percentage of genes showing loss, outlier values of dN/dS when dN/dS was included or excluded for each functional category. The black and gray bars indicate the percentage of genes showing loss or outlier values of dN/dS and the others, respectively. These percentages were calculated when we used 70-15 strain genome as the reference. b Distribution of presence and absence of genes encoding the known effectors in M. oryzae and M. grisea. Heat map shows breadth coverage of genes. The blue and yellow panels indicate absence and presence polymorphisms, respectively. The tree indicates the relationship among the tested pathogens based on Fig. 1b
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.
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.
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.
There’s a chance to use cutting-edge technology to save native Hawaiian birds from the mosquitoes that are driving them to extinction.
Hawaii’s fourth-largest island, says Paxton, a scientist with the U.S. Geological Survey, is seeing a sudden, rapid decline in native birds. The prime suspect is avian malaria. It’s being spread by mosquitoes and it kills rare birds such as the 'i'iwi, a bright red honeycreeper with a curvy Dr. Seuss beak. Surveys carried out on the island’s rugged, roadless interior are finding fewer birds than ever before. Extinction for some species looks imminent.
So now a group of government officials, conservationists, and scientists in Hawaii are seriously looking at a high-tech solution: genetically modified mosquitoes. They say the modified bugs, whose offspring die quickly, thereby reducing mosquito populations, could be the best chance to save Hawaii’s endangered birds. If these discussions move forward, one idea would be to release millions of genetically modified bugs to drive mosquitoes off of Kauai’s plateau and maybe right out of the entire archipelago.
What’s certain is that genetically modified organisms are political dynamite on Hawaii. Some districts have passed ordinances to ban biotech crops from being planted. No one knows how Hawaiians would react to GM mosquitoes, but lately, mosquito technology has been winning positive attention as a potential high-tech fix for human diseases such as Zika. One company, Oxitec, is testing GM mosquitoes in Brazil and hopes to do so in Florida. Because of a genetic addition to their DNA, those bugs have offspring that die prematurely. Release enough of them and the number of mosquitoes can drop drastically, although they don’t disappear altogether.
While fighting human disease gets the attention and the funding, conservation could end up being just as important a use of advanced biotechnology. At the San Diego Zoo, there are plans to save the northern white rhinoceros by cloning animals from frozen tissues. Scientists have created a genetically modified American chestnut tree resistant to the blight that’s mostly wiped them out.
The wheat blast outbreak in Bangladesh [ProMED-mail post http://promedmail.org/post/20160411.4150953] 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. - 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_ [burr grass] collected in Brazil. - One of the genetically closest strains known from Brazil is PY0925. An additional Brazilian wheat blast strain, 205, is slightly more distant to the Bangladesh blast strains. - 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. - Other Asian countries that received wheat from Brazil, including Thailand, Philippines, and Viet Nam, should increase surveillance efforts to learn if wheat blast has entered into their wheat fields.
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.
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.
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 genome, gene models and protein sequences.
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.
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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