scholarly journals Functional genomics and mycotoxin discovery in the wheat glume blotch pathogen Stagonospora nodorum

2011 ◽  
Vol 32 (4) ◽  
pp. 156
Author(s):  
Peter S Solomon

Stagonospora nodorum is a fungal pathogen of wheat and is responsible for over $100 million in yield losses in Australia each year. Significant progress has recently been made in understanding how S. nodorum causes disease on wheat. These pathogens, known as a necrotrophs, were thought to secrete a battery of lytic and degradative enzymes during infection. These enzymes would simply degrade host tissue, allowing the infecting pathogen to feed off the lysed cellular contents. Recent studies have shown that this is not so, and that these fungi secrete unique effector proteins during the early stages of infection, which appear to be translocated into wheat cells. Once inside, these proteins interact (either directly or indirectly) with the products of dominant susceptibility loci leading to a localised programmed cell death response. Consequently, it is through an intricate gene-for-gene mechanism involving the interaction of pathogen effector proteins and host dominant susceptibility genes that S. nodorum infects its wheat host, not through a crude secretion of cell lysis enzymes. These findings have been recently reviewed by Oliver and Solomon3. This short article focuses on how modern functional genomics techniques have been exploited to reveal a new dimension to the wheat pathogen S. nodorum.

2010 ◽  
Vol 38 (6) ◽  
pp. 1417-1419 ◽  
Author(s):  
Paul R. Pryor ◽  
Sally A. Raines

Lysosomes form part of our innate immunity and are an important line of defence against microbes, viruses and parasites. Although it is more than 50 years since de Duve discovered lysosomes, it is only in more recent years that we are slowly unravelling the molecular mechanisms involved in the delivery of material to the lysosome. However, successful intracellular pathogens often have a better grip on the mechanisms involved in delivery to the lysosome and can manipulate membrane trafficking pathways to create an intracellular environment that is favourable for replication. By studying pathogen effector proteins that are secreted into the host's cytosol, we can learn about both pathogen-survival mechanisms and further regulatory elements involved in trafficking to the lysosome.


2016 ◽  
Vol 88 (1) ◽  
pp. 13-25 ◽  
Author(s):  
Susan Breen ◽  
Simon J. Williams ◽  
Britta Winterberg ◽  
Bostjan Kobe ◽  
Peter S. Solomon

2010 ◽  
Vol 37 (10) ◽  
pp. 919 ◽  
Author(s):  
Adrienne R. Hardham ◽  
David M. Cahill

Plants constantly come into contact with a diverse range of microorganisms that are potential pathogens, and they have evolved multi-faceted physical and chemical strategies to inhibit pathogen ingress and establishment of disease. Microbes, however, have developed their own strategies to counteract plant defence responses. Recent research on plant–microbe interactions has revealed that an important part of the infection strategies of a diverse range of plant pathogens, including bacteria, fungi and oomycetes, is the production of effector proteins that are secreted by the pathogen and that promote successful infection by manipulating plant structure and metabolism, including interference in plant defence mechanisms. Pathogen effector proteins may function either in the extracellular spaces within plant tissues or within the plant cell cytoplasm. Extracellular effectors include cell wall degrading enzymes and inhibitors of plant enzymes that attack invading pathogens. Intracellular effectors move into the plant cell cytoplasm by as yet unknown mechanisms where, in incompatible interactions, they may be recognised by plant resistance proteins but where, in compatible interactions, they may suppress the plant’s immune response. This article presents a brief overview of our current understanding of the nature and function of effectors produced by oomycete plant pathogens.


2015 ◽  
Vol 100 (3) ◽  
pp. 828-830 ◽  
Author(s):  
Stéphane Bermon ◽  
Eric Vilain ◽  
Patrick Fénichel ◽  
Martin Ritzén

The recent implementation by some major sports-governing bodies of policies governing eligibility of females with hyperandrogenism to compete in women’s sports has raised a lot of attention and is still a controversial issue. This short article addresses two main subjects of controversy: the existing scientific basis supporting performance enhancing of high blood T levels in elite female athletes, and the ethical rationale and considerations about these policies. Given the recently published data about both innate and acquired hyperandrogenic conditions and their prevalence in elite female sports, we claim that the high level of androgens are per se performance enhancing. Regulating women with clinical and biological hyperandrogenism is an invitation to criticism because biological parameters of sex are not neatly divided into only two categories in the real world. It is, however, the responsibility of the sports-governing bodies to do their best to guarantee a level playing field to all athletes. In order not cloud the discussions about the policies on hyperandrogenism in sports, issues of sports eligibility and therapeutic options should always be considered and explained separately, even if they may overlap. Finally, some proposals for refining the existing policies are made in the present article.


Science ◽  
2019 ◽  
Vol 365 (6455) ◽  
pp. 793-799 ◽  
Author(s):  
Shane Horsefield ◽  
Hayden Burdett ◽  
Xiaoxiao Zhang ◽  
Mohammad K. Manik ◽  
Yun Shi ◽  
...  

SARM1 (sterile alpha and TIR motif containing 1) is responsible for depletion of nicotinamide adenine dinucleotide in its oxidized form (NAD+) during Wallerian degeneration associated with neuropathies. Plant nucleotide-binding leucine-rich repeat (NLR) immune receptors recognize pathogen effector proteins and trigger localized cell death to restrict pathogen infection. Both processes depend on closely related Toll/interleukin-1 receptor (TIR) domains in these proteins, which, as we show, feature self-association–dependent NAD+ cleavage activity associated with cell death signaling. We further show that SARM1 SAM (sterile alpha motif) domains form an octamer essential for axon degeneration that contributes to TIR domain enzymatic activity. The crystal structures of ribose and NADP+ (the oxidized form of nicotinamide adenine dinucleotide phosphate) complexes of SARM1 and plant NLR RUN1 TIR domains, respectively, reveal a conserved substrate binding site. NAD+ cleavage by TIR domains is therefore a conserved feature of animal and plant cell death signaling pathways.


2020 ◽  
Author(s):  
Nathan Kleczewski ◽  
Christina Cowger ◽  
Hillary Mehl ◽  
Gary Bergstrom ◽  
Carl Bradley ◽  
...  

Plants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 219 ◽  
Author(s):  
Kristin Widyasari ◽  
Mazen Alazem ◽  
Kook-Hyung Kim

Soybean mosaic virus (SMV) occurs in all soybean-growing areas in the world and causes huge losses in soybean yields and seed quality. During early viral infection, molecular interactions between SMV effector proteins and the soybean resistance (R) protein, if present, determine the development of resistance/disease in soybean plants. Depending on the interacting strain and cultivar, R-protein in resistant soybean perceives a specific SMV effector, which triggers either the extreme silent resistance or the typical resistance manifested by hypersensitive responses and induction of salicylic acid and reactive oxygen species. In this review, we consider the major advances that have been made in understanding the soybean–SMV arms race. We also focus on dissecting mechanisms SMV employs to establish infection and how soybean perceives and then responds to SMV attack. In addition, progress on soybean R-genes studies, as well as those addressing independent resistance genes, are also addressed.


2018 ◽  
Vol 19 (2) ◽  
pp. 257-259 ◽  
Author(s):  
Nick C. Snelders ◽  
Graeme J. Kettles ◽  
Jason J. Rudd ◽  
Bart P. H. J. Thomma

2010 ◽  
Vol 107 (5) ◽  
pp. 2349-2354 ◽  
Author(s):  
Mike Wilton ◽  
Rajagopal Subramaniam ◽  
James Elmore ◽  
Corinna Felsensteiner ◽  
Gitta Coaker ◽  
...  

Plant immunity can be induced by two major classes of pathogen-associated molecules. Pathogen- or microbe-associated molecular patterns (PAMPs or MAMPs) are conserved molecular components of microbes that serve as “non-self” features to induce PAMP-triggered immunity (PTI). Pathogen effector proteins used to promote virulence can also be recognized as “non-self” features or induce a “modified-self” state that can induce effector-triggered immunity (ETI). The Arabidopsis protein RIN4 plays an important role in both branches of plant immunity. Three unrelated type III secretion effector (TTSE) proteins from the phytopathogen Pseudomonas syringae, AvrRpm1, AvrRpt2, and AvrB, target RIN4, resulting in ETI that effectively restricts pathogen growth. However, no pathogenic advantage has been demonstrated for RIN4 manipulation by these TTSEs. Here, we show that the TTSE HopF2Pto also targets Arabidopsis RIN4. Transgenic plants conditionally expressing HopF2Pto were compromised for AvrRpt2-induced RIN4 modification and associated ETI. HopF2Pto interfered with AvrRpt2-induced RIN4 modification in vitro but not with AvrRpt2 activation, suggestive of RIN4 targeting by HopF2Pto. In support of this hypothesis, HopF2Pto interacted with RIN4 in vitro and in vivo. Unlike AvrRpm1, AvrRpt2, and AvrB, HopF2Pto did not induce ETI and instead promoted P. syringae growth in Arabidopsis. This virulence activity was not observed in plants genetically lacking RIN4. These data provide evidence that RIN4 is a major virulence target of HopF2Pto and that a pathogenic advantage can be conveyed by TTSEs that target RIN4.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ruth Kristianingsih ◽  
Dan MacLean

Abstract Background Plant pathogens cause billions of dollars of crop loss every year and are a major threat to global food security. Effector proteins are the tools such pathogens use to infect the cell, predicting effectors de novo from sequence is difficult because of the heterogeneity of the sequences. We hypothesised that deep learning classifiers based on Convolutional Neural Networks would be able to identify effectors and deliver new insights. Results We created a training set of manually curated effector sequences from PHI-Base and used these to train a range of model architectures for classifying bacteria, fungal and oomycete sequences. The best performing classifiers had accuracies from 93 to 84%. The models were tested against popular effector detection software on our own test data and data provided with those models. We observed better performance from our models. Specifically our models showed greater accuracy and lower tendencies to call false positives on a secreted protein negative test set and a greater generalisability. We used GRAD-CAM activation map analysis to identify the sequences that activated our CNN-LSTM models and found short but distinct N-terminal regions in each taxon that was indicative of effector sequences. No motifs could be observed in these regions but an analysis of amino acid types indicated differing patterns of enrichment and depletion that varied between taxa. Conclusions Small training sets can be used effectively to train highly accurate and sensitive deep learning models without need for the operator to know anything other than sequence and without arbitrary decisions made about what sequence features or physico-chemical properties are important. Biological insight on subsequences important for classification can be achieved by examining the activations in the model


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