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Rescooped by Dr.donkey from microbial pathogenesis and plant immunity
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PNAS: Phytophthora effector targets a novel component of small RNA pathway in plants to promote infection

PNAS: Phytophthora effector targets a novel component of small RNA pathway in plants to promote infection | Plant immunity | Scoop.it
A broad range of parasites rely on the functions of effector proteins to subvert host immune response and facilitate disease development. The notorious Phytophthora pathogens evolved effectors with RNA silencing suppression activity to promote infection in plant hosts. Here we report that the Phytophthora Suppressor of RNA Silencing 1 (PSR1) can bind to an evolutionarily conserved nuclear protein containing the aspartate–glutamate–alanine–histidine-box RNA helicase domain in plants. This protein, designated PSR1-Interacting Protein 1 (PINP1), regulates the accumulation of both microRNAs and endogenous small interfering RNAs in Arabidopsis. A null mutation of PINP1 causes embryonic lethality, and silencing of PINP1 leads to developmental defects and hypersusceptibility to Phytophthora infection. These phenotypes are reminiscent of transgenic plants expressing PSR1, supporting PINP1 as a direct virulence target of PSR1. We further demonstrate that the localization of the Dicer-like 1 protein complex is impaired in the nucleus of PINP1-silenced or PSR1-expressing cells, indicating that PINP1 may facilitate small RNA processing by affecting the assembly of dicing complexes. A similar function of PINP1 homologous genes in development and immunity was also observed in Nicotiana benthamiana. These findings highlight PINP1 as a previously unidentified component of RNA silencing that regulates distinct classes of small RNAs in plants. Importantly, Phytophthora has evolved effectors to target PINP1 in order to promote infection.

Via Suayib Üstün, Jim Alfano
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Rescooped by Dr.donkey from Plants and Microbes
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The New Yorker: We Have No Bananas - Can scientists defeat a devastating blight? (2015)

The New Yorker: We Have No Bananas - Can scientists defeat a devastating blight? (2015) | Plant immunity | Scoop.it

Darwin, the capital of Australia’s Northern Territory, is more than a thousand miles northwest of the country’s largest banana plantations, which are centered around Innisfail, on the eastern seaboard. A ramshackle place, Darwin is known for its many impoverished indigenous residents, entertainment attractions like Crocosaurus Cove (where visitors are lowered, via “the Cage of Death,” into a crocodile-filled tank), and, as one local puts it, “not partying, exactly, but certainly drinking.” To Robert Borsato, a fruit farmer, the area looked like an ideal place to grow bananas. In 1996, he began farming a thousand acres in Humpty Doo, which is on the road between Darwin and Kakadu National Park.


To bear fruit, banana plants need at least fourteen consecutive months of frost-free weather, which is why they are not grown commercially in the continental United States. Darwin offered this, and more. As one of Borsato’s workers told me recently, “You came up here and saw the consistency that you’ve got between the blue sky, the sunshine, the water, the fucking soil. You knew you were going to beat everybody else, hands down.” There were a few nuisances: crocodiles wandered onto the property, Asian buffalo trampled young plants, and dingoes chewed the sprinklers. Before long, though, the Darwin Banana Farming Company was growing lush ten-foot plants with as many as a hundred and seventy bananas on each stalk. In 2006, Cyclone Larry decimated ninety per cent of the Innisfail plantations; banana prices soared from ten dollars a carton to a hundred and thirty, and Borsato became a multimillionaire.


More than a thousand kinds of banana can be found worldwide, but Borsato specialized in a variety called Cavendish, which a nineteenth-century British explorer happened upon in a household garden in southern China. Today, the Cavendish represents ninety-nine per cent of the banana export market. The vast majority of banana varieties are not viable for international trade: their bunches are too small, or their skin is too thin, or their pulp is too bland. Although Cavendishes need pampering, they are the only variety that provides farmers with a high yield of palatable fruit that can endure overseas trips without ripening too quickly or bruising too easily. The Cavendish, which is rich in Vitamins B6 and C, has high levels of potassium, magnesium, and fibre; it is also cheap—about sixty cents a pound. In 2008, Americans ate 7.6 billion pounds of Cavendish bananas, virtually all of them imported from Latin America. Each year, we eat as many Cavendish bananas as we do apples and oranges combined. Your supermarket likely sells many varieties of apples, but when you shop for bananas you usually have one option. The world’s banana plantations are a monoculture of Cavendishes.


Several years ago, Borsato noticed a couple of sick-looking plants on a neighbor’s property. The leaves turned a soiled yellow, starting at the edges and rapidly moving inward; necrotic patches appeared and, a few weeks later, the leaves buckled. What had once formed a canopy now dangled around the base of the plant, like a cast-off grass skirt. Inside the plant, the effects were even worse. Something was blocking the plants’ vascular system, causing rot, and tissue that should have been as ivory as the inside of a celery stalk was a putrefying mixture of brown, black, and blood-red. When the plants were cut open, they smelled like garbage, and their roots were so anemic that the plants could barely stay upright.


Borsato feared that he was seeing the symptoms of a pestilence that had wiped out the Cavendish across Asia: Tropical Race Four. A soil-borne fungus that is known to be harmful only to bananas, it can survive for decades in the dirt, spreading through the transportation of tainted plants, or in infected mud stuck to a tractor’s tire or a rancher’s boot. It cannot be controlled with chemicals. Tropical Race Four appeared in Taiwan in the late eighties, and destroyed roughly seventy per cent of the island’s Cavendish plantations. In Indonesia, more than twelve thousand acres of export bananas were abandoned; in Malaysia, a local newspaper branded the disease “the H.I.V. of banana plantations.” When the fungus reached China and the Philippines, the effect was equally ruinous.


[Fusarium oxysporum f. sp. cubense TR4]


Via Kamoun Lab @ TSL
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Rescooped by Dr.donkey from Plant-Microbe Interaction
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Nuclear processes associated with plant immunity and pathogen susceptibility

Nuclear processes associated with plant immunity and pathogen susceptibility | Plant immunity | Scoop.it
Plants are sessile organisms that have evolved exquisite and sophisticated mechanisms to adapt to their biotic and abiotic environment. Plants deploy receptors and vast signalling networks to detect, transmit and respond to a given biotic threat by inducing properly dosed defence responses. Genetic analyses and, more recently, next-generation -omics approaches have allowed unprecedented insights into the mechanisms that drive immunity. Similarly, functional genomics and the emergence of pathogen genomes have allowed reciprocal studies on the mechanisms governing pathogen virulence and host susceptibility, collectively allowing more comprehensive views on the processes that govern disease and resistance. Among others, the identification of secreted pathogen molecules (effectors) that modify immunity-associated processes has changed the plant–microbe interactions conceptual landscape. Effectors are now considered both important factors facilitating disease and novel probes, suited to study immunity in plants. In this review, we will describe the various mechanisms and processes that take place in the nucleus and help regulate immune responses in plants. Based on the premise that any process required for immunity could be targeted by pathogen effectors, we highlight and describe a number of functional assays that should help determine effector functions and their impact on immune-related processes. The identification of new effector functions that modify nuclear processes will help dissect nuclear signalling further and assist us in our bid to bolster immunity in crop plants.

Via Christophe Jacquet, Guogen Yang
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Jennifer Mach's curator insight, April 13, 8:34 AM

The abstract opens with the classic "plants are sessile organisms" gambit...

Rescooped by Dr.donkey from Plant immunity and legume symbiosis
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A Novel Pyrimidin-Like Plant Activator Stimulates Plant Disease Resistance and Promotes Growth

A Novel Pyrimidin-Like Plant Activator Stimulates Plant Disease Resistance and Promotes Growth | Plant immunity | Scoop.it
Plant activators are chemicals that induce plant defense responses to a broad spectrum of pathogens. Here, we identified a new potential plant activator, 5-(cyclopropylmethyl)-6-methyl-2-(2-pyridyl)pyrimidin-4-ol,named PPA (pyrimidin-type plant activator). Compared with benzothiadiazole S-methyl ester (BTH), a functional analog of salicylic acid (SA), PPA was fully soluble in water and increased fresh weight of rice (Oryza sativa) and Arabidopsis plants at low concentrations. In addition, PPA also promoted lateral root development. Microarray data and real-time PCR revealed that PPA-treated leaves not challenged with pathogen showed up-regulation of genes related to reactive oxygen species (ROS), defenses and SA. During bacterial infection, Arabidopsis plants pretreated with PPA showed dramatically decreased disease symptoms and an earlier and stronger ROS burst, compared with plants pretreated with BTH. Microscopy revealed that H2O2 accumulated in the cytosol, plasma membrane and cell wall around intracellular bacteria, and also on the bacterial cell wall, indicating that H2O2 was directly involved in killing bacteria. The increase in ROS-related gene expression also supported this observation. Our results indicate that PPA enhances plant defenses against pathogen invasion through the plant redox system, and as a water-soluble compound that can promote plant growth, has broad potential applications in agriculture.

Via Christophe Jacquet
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Genome-wide exploration of the molecular evolution and regulatory network of mitogen-activated protein kinase cascades upon multiple stresses in Brachypodium distachyon

Genome-wide exploration of the molecular evolution and regulatory network of mitogen-activated protein kinase cascades upon multiple stresses in Brachypodium distachyon | Plant immunity | Scoop.it

In this study, we have identified MAPKKKs which belong to the biggest gene family of MAPK cascade kinases. We have systematically investigated the evolution of whole MAPK cascade kinase gene family in terms of gene structures, protein structural organization, chromosomal localization, orthologs construction and gene duplication analysis. Our results showed that most BdMAPK cascade kinases were located at the low-CpG-density region, and the clustered members in each group shared similar structures of the genes and proteins. Synteny analysis showed that 62 or 21 pairs of duplicated orthologs were present between B. distachyon and Oryza sativa, or between B. distachyon and Arabidopsis thaliana respectively. Gene expression data revealed that BdMAPK cascade kinases were rapidly regulated by stresses and phytohormones. Importantly, we have constructed a regulation network based on co-expression patterns of the expression profiles upon multiple stresses performed in this study.


Via Elsa Ballini
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Rescooped by Dr.donkey from Trends in MPMI
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Retromer Contributes to Immunity-Associated Cell Death in Arabidopsis

Membrane trafficking is required during plant immune responses, but its contribution to the hypersensitive response (HR), a form of programmed cell death (PCD) associated with effector-triggered immunity, is not well understood. HR is induced by nucleotide binding-leucine-rich repeat (NB-LRR) immune receptors and can involve vacuole-mediated processes, including autophagy. We previously isolated lazarus (laz) suppressors of autoimmunity-triggered PCD in the Arabidopsis thaliana mutant accelerated cell death11 (acd11) and demonstrated that the cell death phenotype is due to ectopic activation of the LAZ5 NB-LRR. We report here that laz4 is mutated in one of three VACUOLAR PROTEIN SORTING35 (VPS35) genes. We verify that LAZ4/VPS35B is part of the retromer complex, which functions in endosomal protein sorting and vacuolar trafficking. We show that VPS35B acts in an endosomal trafficking pathway and plays a role in LAZ5-dependent acd11 cell death. Furthermore, we find that VPS35 homologs contribute to certain forms of NB-LRR protein-mediated autoimmunity as well as pathogen-triggered HR. Finally, we demonstrate that retromer deficiency causes defects in late endocytic/lytic compartments and impairs autophagy-associated vacuolar processes. Our findings indicate important roles of retromer-mediated trafficking during the HR; these may include endosomal sorting of immune components and targeting of vacuolar cargo.

 

 


Via Christophe Jacquet, CP
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Rescooped by Dr.donkey from Plant Immunity And Microbial Effectors
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Nature Communications: Two linked pairs of Arabidopsis TNL resistance genes independently confer recognition of bacterial effector ​AvrRps4 (2015)

Plant immunity requires recognition of pathogen effectors by intracellular NB-LRR immune receptors encoded by Resistance (R) genes. Most R proteins recognize a specific effector, but some function in pairs that recognize multiple effectors. Arabidopsis thaliana TIR-NB-LRR proteins RRS1-R and RPS4together recognize two bacterial effectors, AvrRps4 from Pseudomonas syringae and PopP2 from Ralstonia solanacearum. However, AvrRps4, but not PopP2, is recognized in rrs1/rps4 mutants. We reveal an R gene pair that resembles and is linked to RRS1/RPS4, designated as RRS1B/RPS4B, which confers recognition of AvrRps4 but not PopP2. Like RRS1/RPS4, RRS1B/RPS4B proteins associate and activate defence genes upon AvrRps4 recognition. Inappropriate combinations (RRS1/RPS4B or RRS1B/RPS4) are non-functional and this specificity is not TIR domain dependent. Distinct putative orthologues of both pairs are maintained in the genomes of Arabidopsis thalianarelatives and are likely derived from a common ancestor pair. Our results provide novel insights into paired R gene function and evolution.


Via The Sainsbury Lab, Kamoun Lab @ TSL, IPM Lab
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The Sainsbury Lab's curator insight, March 6, 3:09 PM

Plant immunity requires recognition of pathogen effectors by intracellular NB-LRR immune receptors encoded by Resistance (R) genes. Most R proteins recognize a specific effector, but some function in pairs that recognize multiple effectors. Arabidopsis thaliana TIR-NB-LRR proteins RRS1-R and RPS4together recognize two bacterial effectors, AvrRps4 from Pseudomonas syringae and PopP2 from Ralstonia solanacearum. However, AvrRps4, but not PopP2, is recognized in rrs1/rps4 mutants. We reveal an R gene pair that resembles and is linked to RRS1/RPS4, designated as RRS1B/RPS4B, which confers recognition of AvrRps4 but not PopP2. Like RRS1/RPS4, RRS1B/RPS4B proteins associate and activate defence genes upon AvrRps4 recognition. Inappropriate combinations (RRS1/RPS4B or RRS1B/RPS4) are non-functional and this specificity is not TIR domain dependent. Distinct putative orthologues of both pairs are maintained in the genomes of Arabidopsis thalianarelatives and are likely derived from a common ancestor pair. Our results provide novel insights into paired R gene function and evolution.

Rescooped by Dr.donkey from Plant Immunity And Microbial Effectors
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Perturbation of Maize Phenylpropanoid Metabolism by an AvrE-family Type III Effector from Pantoea stewartii

AvrE-family type III effector proteins share the ability to suppress host defenses, induce disease-associated cell death and promote bacterial growth.

Via IPM Lab
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Rescooped by Dr.donkey from TAL effector science
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Molecular recognition of avirulence protein (avrxa5) by eukaryotic transcription factor xa5 of rice - JMGM

Molecular recognition of avirulence protein (avrxa5) by eukaryotic transcription factor xa5 of rice - JMGM | Plant immunity | Scoop.it

(via T. Lahaye, thx)

Dehury et al, 2015

The avirulence gene avrxa5 of bacterial blight pathogen Xanthomonas oryzae pv. oryzae (Xoo) recognized by the resistant rice lines having corresponding resistance (xa5) gene in a gene-for-gene manner. We used a combinatorial approach involving protein-protein docking, molecular dynamics (MD) simulations, and binding free energy calculations to gain novel insights into the gene-for gene mechanism that governs the direct-direct interaction of R-Avr protein,. From the best three binding poses predicted by molecular docking, MD simulations were performed to explore the dynamic binding processes of xa5 and avrxa5. Molecular Mechanics/Poisson Boltzmann Surface Area (MM/PBSA) techniques were employed to calculate the binding free energy and to uncover the thriving force behind the molecular recognition of avrxa5 by eukaryotic transcription factor xa5. Binding free energy analysis revealed van der Waals term as the most constructive component that favors the xa5 and avrxa5 interaction. In addition, hydrogen bonds and essential electrostatic interactions analysis highlighted amino acid residues Lys54/Asp870, Lys56/Ala868, Lys56/Ala866, Lys56/Glu871, Ile59/His862, Gly61/Phe858, His62/Arg841, His62/Leu856, Ser101/Ala872 and Ser105/Asp870 plays pivotal role for the energetically stability of the R-Avr complex. Insights gained from the present study are expected to unveil the molecular mechanisms that define the transcriptional activator mediated transcriptome modification in host plants.


Via dromius
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Rescooped by Dr.donkey from Plant pathogens and pests
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New insight into a complex plant-fungal pathogen interaction : Nature Genetics : Nature Publishing Group

New insight into a complex plant-fungal pathogen interaction : Nature Genetics : Nature Publishing Group | Plant immunity | Scoop.it
The coevolution of plants and microbes has shaped plant mechanisms that detect and repel pathogens. A newly identified plant gene confers partial resistance to a fungal pathogen not by preventing initial infection but by limiting its spread through the plant.

Via Christophe Jacquet
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Plant innate immunity – sunny side up?

Plant innate immunity – sunny side up? | Plant immunity | Scoop.it

Highlights

•Reactive oxygen species (ROS) and calcium signaling are central to plant immunity.

•Surprisingly, ROS and calcium signaling branch via the chloroplast during immunity.

•Light influences the chloroplast branch to alter immunity.

•The chloroplast branch provides environmental feedback on the immune reaction.


Via Steve Marek
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Ten Simple Rules for Finishing Your PhD

Ten Simple Rules for Finishing Your PhD | Plant immunity | Scoop.it

After years of research and with completion in sight, the final year of the PhD often represents the most challenging time of a student's career, in which the ultimate reward is the PhD honor itself. A large investment in time, energy, and motivation is needed, with many tasks to be completed; concluding experiments must be carried out, results interpreted, and a research story mapped out in preparation for writing the final thesis. All the while, administrative obligations need attention (e.g., university credits and mandatory documents), papers may need to be published, students mentored, and due consideration paid to planning for the next career move. Without some form of strategic action plan and the employment of project management skills, students run the risk of becoming overwhelmed and run down or of not meeting their final deadlines. Personal time management and stress resilience are competences that can be developed and honed during this final period of the PhD.

Here, we present ten simple rules on how to deal with time issues and conflict situations when facing the last year of a PhD in science. The rules focus on defining research goals in advance and designing a plan of action. Moreover, we discuss the importance of managing relationships with supervisors and colleagues, as well as early career planning.


Via Francis Martin, Jean-Michel Ané, Guogen Yang
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A Noncanonical Role for the CKI-RB-E2F Cell-Cycle Signaling Pathway in Plant Effector-Triggered Immunity

A Noncanonical Role for the CKI-RB-E2F Cell-Cycle Signaling Pathway in Plant Effector-Triggered Immunity | Plant immunity | Scoop.it
Highlights



The nuclear membrane protein CPR5 inhibits effector-triggered immunity (ETI)


CPR5 inhibits ETI via interaction with cyclin-dependent kinase inhibitors (CKIs)


CKIs are released from CPR5 upon ETI induction and are required for PCD and immunity


CKIs induce immunity through RB hyperphosphorylation and E2F overactivation

Summary

Effector-triggered immunity (ETI), the major host defense mechanism in plants, is often associated with programmed cell death (PCD). Plants lack close homologs of caspases, the key mediators of PCD in animals. So although the NB-LRR receptors involved in ETI are well studied, how they activate PCD and confer disease resistance remains elusive. We show that the Arabidopsis nuclear envelope protein, CPR5, negatively regulates ETI and the associated PCD through a physical interaction with cyclin-dependent kinase inhibitors (CKIs). Upon ETI induction, CKIs are released from CPR5 to cause overactivation of another core cell-cycle regulator, E2F. In cki and e2f mutants, ETI responses induced by both TIR-NB-LRR and CC-NB-LRR classes of immune receptors are compromised. We further show that E2F is deregulated during ETI, probably through CKI-mediated hyperphosphorylation of retinoblastoma-related 1 (RBR1). This study demonstrates that canonical cell-cycle regulators also play important noncanonical roles in plant immunity.

Via Christophe Jacquet, Guogen Yang
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Introgression of blast resistance genes into the elite variety mr263 through marker-assisted backcrossing

Introgression of blast resistance genes into the elite variety mr263 through marker-assisted backcrossing | Plant immunity | Scoop.it
The improved MR263-BR-3-2, MR263-BR-4-3, MR263-BR-13-1 and MR263-BR-26-4 lines carrying the Pi-7(t), Pi-d (t), Pir2-3(t) genes and qLN2 QTL were developed using the SSR markers RM5961 and RM263 (linked to the blast resistance genes and QTL) for foreground selection and a collection of 65 polymorphic SSR markers for background selection in backcrossed and selfed generations. A background analysis revealed that the highest rate of recurrent parent genome recovery was 96.0% in MR263-BR-4-3 and 94.1% in MR263-BR-3-2.

Via Elsa Ballini
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Rescooped by Dr.donkey from microbial pathogenesis and plant immunity
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eLife: Natural genetic variation in Arabidopsis thaliana defense metabolism genes modulates field fitness (2015)

eLife: Natural genetic variation in Arabidopsis thaliana defense metabolism genes modulates field fitness (2015) | Plant immunity | Scoop.it

Natural populations persist in complex environments, where biotic stressors, such as pathogen and insect communities, fluctuate temporally and spatially. These shifting biotic pressures generate heterogeneous selective forces that can maintain standing natural variation within a species. To directly test if genes containing causal variation for the Arabidopsis thaliana defensive compounds, glucosinolates (GSL) control field fitness and are therefore subject to natural selection, we conducted a multi-year field trial using lines that vary in only specific causal genes. Interestingly, we found that variation in these naturally polymorphic GSL genes affected fitness in each of our environments but the pattern fluctuated such that highly fit genotypes in one trial displayed lower fitness in another and that no GSL genotype or genotypes consistently out-performed the others. This was true both across locations and within the same location across years. These results indicate that environmental heterogeneity may contribute to the maintenance of GSL variation observed within Arabidopsis thaliana.


Via Kamoun Lab @ TSL, Jim Alfano
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Rescooped by Dr.donkey from Trends in MPMI
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The future of the postdoc

The future of the postdoc | Plant immunity | Scoop.it
There is a growing number of postdocs and few places in academia for them to go. But change could be on the way.

Via Niklaus Grunwald, CP
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Rescooped by Dr.donkey from Plant immunity and legume symbiosis
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Frontiers | Vacuolar processing enzyme in plant programmed cell death | Plant Physiology

Frontiers | Vacuolar processing enzyme in plant programmed cell death | Plant Physiology | Plant immunity | Scoop.it
Vacuolar processing enzyme (VPE) is a cysteine proteinase originally identified as the proteinase responsible for the maturation and activation of vacuolar proteins in plants, and it is known to be an ortholog of animal asparaginyl endopeptidase (AEP/VPE/legumain). VPE has been shown to exhibit enzymatic properties similar to that of caspase 1, which is a cysteine protease that mediates the programmed cell death (PCD) pathway in animals. Although there is limited sequence identity between VPE and caspase 1, their predicted three-dimensional structures revealed that the essential amino-acid residues for these enzymes form similar pockets for the substrate peptide YVAD. In contrast to the cytosolic localization of caspases, VPE is localized in vacuoles. VPE provokes vacuolar rupture, initiating the proteolytic cascade leading to PCD in the plant immune response. It has become apparent that the VPE-dependent PCD pathway is involved not only in the immune response, but also in the responses to a variety of stress inducers and in the development of various tissues. This review summarizes the current knowledge on the contribution of VPE to plant PCD and its role in vacuole-mediated cell death, and it also compares VPE with the animal cell death executor caspase 1.

Via Christophe Jacquet
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Brachypodium as an emerging model for cereal–pathogen interactions

Brachypodium as an emerging model for cereal–pathogen interactions | Plant immunity | Scoop.it
Abstract

Background Cereal diseases cause tens of billions of dollars of losses annually and have devastating humanitarian consequences in the developing world. Increased understanding of the molecular basis of cereal host–pathogen interactions should facilitate development of novel resistance strategies. However, achieving this in most cereals can be challenging due to large and complex genomes, long generation times and large plant size, as well as quarantine and intellectual property issues that may constrain the development and use of community resources. Brachypodium distachyon (brachypodium) with its small, diploid and sequenced genome, short generation time, high transformability and rapidly expanding community resources is emerging as a tractable cereal model.

Scope Recent research reviewed here has demonstrated that brachypodium is either susceptible or partially susceptible to many of the major cereal pathogens. Thus, the study of brachypodium–pathogen interactions appears to hold great potential to improve understanding of cereal disease resistance, and to guide approaches to enhance this resistance. This paper reviews brachypodium experimental pathosystems for the study of fungal, bacterial and viral cereal pathogens; the current status of the use of brachypodium for functional analysis of cereal disease resistance; and comparative genomic approaches undertaken using brachypodium to assist characterization of cereal resistance genes. Additionally, it explores future prospects for brachypodium as a model to study cereal–pathogen interactions.

Conclusions The study of brachypodium–pathogen interactions appears to be a productive strategy for understanding mechanisms of disease resistance in cereal species. Knowledge obtained from this model interaction has strong potential to be exploited for crop improvement.

Via Christophe Jacquet, Guogen Yang
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NIK1-mediated translation suppression functions as a plant antiviral immunity mechanism

Plants and plant pathogens are subject to continuous co-evolutionary pressure for dominance, and the outcomes of these interactions can substantially impact agriculture and food security. In virus–plant interactions, one of the major mechanisms for plant antiviral immunity relies on RNA silencing, which is often suppressed by co-evolving virus suppressors, thus enhancing viral pathogenicity in susceptible hosts. In addition, plants use the nucleotide-binding and leucine-rich repeat (NB-LRR) domain-containing resistance proteins, which recognize viral effectors to activate effector-triggered immunity in a defence mechanism similar to that employed in non-viral infections. Unlike most eukaryotic organisms, plants are not known to activate mechanisms of host global translation suppression to fight viruses. Here we demonstrate in Arabidopsis that the constitutive activation of NIK1, a leucine-rich repeat receptor-like kinase (LRR-RLK) identified as a virulence target of the begomovirus nuclear shuttle protein (NSP), leads to global translation suppression and translocation of the downstream component RPL10 to the nucleus, where it interacts with a newly identified MYB-like protein, L10-INTERACTING MYB DOMAIN-CONTAINING PROTEIN (LIMYB), to downregulate translational machinery genes fully. LIMYB overexpression represses ribosomal protein genes at the transcriptional level, resulting in protein synthesis inhibition, decreased viral messenger RNA association with polysome fractions and enhanced tolerance to begomovirus. By contrast, the loss of LIMYB function releases the repression of translation-related genes and increases susceptibility to virus infection. Therefore, LIMYB links immune receptor LRR-RLK activation to global translation suppression as an antiviral immunity strategy in plants.


Via hunter chen
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Rescooped by Dr.donkey from Plant Biology Teaching Resources (Higher Education)
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Resources for academic writing and publishing

 

I led a workshop on academic writing and publishing last week, and this is a list of resources I gave to the participants. It's not an exhaustive list, so if you have any favorites let me know and I'll add them!


Links and resources

 

General writing resources

 

Strunk, W. Jr. (1999).The Elements of Style. http://www.bartleby.com/141/

 

 

 

Guidelines and lessons for good scientific writing

 

Cargill, M., and O’Connor, P. (2011). Writing Scientific Research Articles: Strategy and Steps. Wiley. http://eu.wiley.com/WileyCDA/WileyTitle/productCd-1444356216.html

 

Doumont, J., ed. (2010). English Communication for Scientists. Cambridge, MA: NPG Education. http://www.nature.com/wls/ebooks/english-communication-for-scientists-14053993/contents (Free ebook - very useful)

 

Duke University Graduate School. Scientific Writing Resource.  https://cgi.duke.edu/web/sciwriting/index.php Short, online course for graduate students with examples and worksheets

 

Editorial (2010). Scientific writing 101. Nat Struct Mol Biol. 17: 139-139. http://www.nature.com/nsmb/journal/v17/n2/full/nsmb0210-139.html

 

European Association of Science Editors. EASE Toolkit for Authors. http://www.ease.org.uk/publications/ease-toolkit-authors

 

Nature Scitable Effective Writing. http://www.nature.com/scitable/topicpage/effective-writing-13815989

 

Nature Scitable Scientific Papers. http://www.nature.com/scitable/topicpage/scientific-papers-13815490

 

Lichtfouse, E. (2013). Scientific Writing for Impact Factor Journals. Nova Scientific Publishers, Inc. (New York).

 

Moreira, A., and Haahtela, T. (2011). How to write a scientific paper--and win the game scientists play! Rev. Port. Pneumol. 17:146-149. doi: 10.1016/j.rppneu.2011.03.007. http://www.elsevier.pt/en/linkresolver/320/how-to-write-scientific-paper-and-win/90020266

 

Plaxco, K.W. (2010). The art of writing science. Protein Science 19: 2261 – 2266. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009394/pdf/pro0019-2261.pdf

 

Rogers, Silvia M. (2014). Mastering Scientific and Medical Writing: A Self-Help Guide. Springer. http://www.springer.com/medicine/book/978-3-642-39445-4https://moodle.swarthmore.edu/pluginfile.php/179173/mod_resource/content/1/Good%20versus%20poor%20scientific%20writing%20from%20Silvia%20Rogers.pdf

 

Writing Center University of Wisconsin. (2014) The Writers Handbook: Reverse Outlines. http://writing.wisc.edu/Handbook/ReverseOutlines.html

 

 

 

Guidance from journals

 

J Exp Bot: http://www.oxfordjournals.org/our_journals/exbotj/for_authors/

 

Nature: http://www.nature.com/authors/author_resources/how_write.html

 

Plant Cell: http://www.plantcell.org/site/misc/ifora.xhtml

 

 

 

Figures preparation and ethical issues

 

Blatt, M. and Martin, C. (2013). Manipulation and Misconduct in the Handling of Image Data. Plant Physiology. 163: 3-4. http://www.plantphysiol.org/content/163/1/3.short

 

Cromey, D.W. (2010). Avoiding twisted pixels: ethical guidelines for the appropriate use and manipulation of scientific digital images. Sci. Eng. Ethics 16: 639–667

 

Rossner, M., and Yamada, K.M. (2004). What’s in a picture? The temptation of image manipulation. J. Cell Biol 166: 11–15. http://jcb.rupress.org/content/166/1/11.short

 

 

 

Peer Review Guidelines and Policies, Post-publication peer review

 

Bastian, H. (2014) A Stronger Post-Publication Culture Is Needed for Better Science. PLoS Med 11(12): e1001772. doi:10.1371/journal.pmed.1001772

 

F1000Research: http://blog.f1000research.com/2014/07/08/what-is-post-publication-peer-review/

 

F1000: http://journal.frontiersin.org/Journal/10.3389/fncom.2012.00063/full

 

Mole. (2007). Rebuffs and rebuttals I: how rejected is rejected? J Cell Sci. 120: 1143-1144. http://hwmaint.jcs.biologists.org/cgi/reprint/120/7/1143

 

Nature: http://www.nature.com/authors/policies/peer_review.html

 

Office of Research Integrity. (US Dept of Health and Human Services) The Lab. http://ori.hhs.gov/THELAB

 

Office of Research Integrity. Research Clinic Case Book. http://ori.hhs.gov/rcr-casebook-stories-about-researchers-worth-discussing

 

Science: http://www.sciencemag.org/site/feature/contribinfo/review.xhtml

 

PLOS ONE:www.plosone.org/static/reviewerGuidelines

 

Provenzale, J.M. and Stanley, R.J. (2006). A Systematic Guide to Reviewing a Manuscript. J. Nuclear Med.Techn.. 34: 92-99. http://tech.snmjournals.org/content/34/2/92.full.pdf+html

 

Times Higher Education: http://www.timeshighereducation.co.uk/news/can-post-publication-peer-review-endure/2016895.article

 

 

 

Readability

 

RavenBlog (2010). Ultimate list of online content readability tests. http://blog.raventools.com/ultimate-list-of-online-content-readability-tests/

 

 

 

Communicating more broadly

 

Kuehne, L.M., et al. (2014). Practical science communication strategies for graduate students. Conservation Biology. 28: 1225–1235. .DOI: 10.1111/cobi.12305

 

Osterrieder, A. (2013). The value and use of social media as communication tool in the plant sciences. Plant Methods. 9: 26. http://www.plantmethods.com/content/9/1/26

 

 



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AckerbauHalle's curator insight, February 3, 10:49 AM

Großartige Literatursammlung für wissenschaftliches Schreiben. 

Bibhya Sharma's curator insight, February 3, 8:58 PM

Very helpful for teachers and researchers. 

Andres Zurita's curator insight, February 4, 12:53 PM
Outstanding source of fine material! Thanks Mary!
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Frontiers | To die or not to die? Lessons from lesion mimic mutants | Plant Physiology

Frontiers | To die or not to die? Lessons from lesion mimic mutants | Plant Physiology | Plant immunity | Scoop.it
Programmed cell death (PCD) is a ubiquitous genetically regulated process consisting in an activation of finely controlled signaling pathways that lead to cellular suicide. Although some aspects of PCD control appear evolutionary conserved between plants, animals and fungi, the extent of conservation remains controversial. Over the last decades, identification and characterization of several lesion mimic mutants (LMM) has been a powerful tool in the quest to unravel PCD pathways in plants. Thanks to progress in molecular genetics, mutations causing the phenotype of a large number of LMM and their related suppressors were mapped, and the identification of the mutated genes shed light on major pathways in the onset of plant PCD such as (i) the involvements of chloroplasts and light energy, (ii) the roles of sphingolipids and fatty acids, (iii) a signal perception at the plasma membrane that requires efficient membrane trafficking, (iv) secondary messengers such as ion fluxes and ROS and (v) the control of gene expression as the last integrator of the signaling pathways.

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Steve Marek's curator insight, January 30, 12:01 PM

Lesion mimic mutants show there are many ways for a cell to die.

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PLOS Pathogens: An Iron-Mimicking, Trojan Horse-Entering Fungi—Has the Time Come for Molecular Imaging of Fungal Infections?

PLOS Pathogens: An Iron-Mimicking, Trojan Horse-Entering Fungi—Has the Time Come for Molecular Imaging of Fungal Infections? | Plant immunity | Scoop.it

Despite recent advancements in the diagnosis and management of fungal infections [1], invasive fungal diseases remain a major cause of morbidity and mortality in immunocompromised patients and are major drivers of elevated healthcare costs [2]. In this context, early diagnosis is a key factor. However, current diagnostic approaches, including laboratory tests and computer tomography, have limitations, especially in terms of sensitivity and specificity [3]. Therefore, empirical therapy has often evolved as the standard of care, irrespective of the immediate and long-term consequences in terms of cost, development of drug resistance, or toxicity [4].

 

An exceptional challenge is the development of imaging modalities providing not only high specificity and sensitivity but also localization of the infection site. In particular, nuclear medicine imaging techniques using radiolabelled probes (radiotracers) have the potential to specifically target the underlying pathophysiological mechanisms of the pathogen leading to molecular localization of the infection site in patients.


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Gilbert Faure au nom de l'ASSIM's curator insight, January 30, 4:59 AM

for diagnosis of fungal infections in immunocompromised patients

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Insights into the origin and evolution of plant hormone signaling machinery

Insights into the origin and evolution of plant hormone signaling machinery | Plant immunity | Scoop.it

"Our multi-species genome-wide analysis reveals: i) AUX, CK and SL signaling pathways originated in charophyte lineages; ii) ABA, JA, and SA signaling pathways arose in the last common ancestor of land plants; iii) the GA signaling evolved after the divergence of bryophytes from land plants; iv) the canonical BR signaling originated before the emergence of angiosperms but likely after the split of gymnosperms and angiosperms; v) the origin of the canonical ETH signaling pathway postdates shortly the emergence of angiosperms. Our findings might have important implications in understanding the molecular mechanisms underlying the emergence of land plants"


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Mary Williams's curator insight, January 8, 5:36 AM

This is a pretty fabulous paper - I'm sure it'll find many uses, not the least being the one-page figure that summarizes all of the hormone signaling pathways. The figure shown here examines the presence or absence of signaling gene homologs in green algal species.

Jorge Lozano-Juste's curator insight, January 8, 7:15 PM

Nice!

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The top 100 papers: NATURE magazine explores the most-cited research papers of all time

The top 100 papers: NATURE magazine explores the most-cited research papers of all time | Plant immunity | Scoop.it

The discovery of high-temperature superconductors, the determination of DNA’s double-helix structure, the first observations that the expansion of the Universe is accelerating — all of these breakthroughs won Nobel prizes and international acclaim. Yet none of the papers that announced them comes anywhere close to ranking among the 100 most highly cited papers of all time.

 

Citations, in which one paper refers to earlier works, are the standard means by which authors acknowledge the source of their methods, ideas and findings, and are often used as a rough measure of a paper’s importance. Fifty years ago, Eugene Garfield published the Science Citation Index (SCI), the first systematic effort to track citations in the scientific literature. To mark the anniversary, Nature asked Thomson Reuters, which now owns the SCI, to list the 100 most highly cited papers of all time. (See the full list at Web of Science Top 100.xls or the interactive graphic, below.) The search covered all of Thomson Reuter’s Web of Science, an online version of the SCI that also includes databases covering the social sciences, arts and humanities, conference proceedings and some books. It lists papers published from 1900 to the present day.

 

The exercise revealed some surprises, not least that it takes a staggering 12,119 citations to rank in the top 100 — and that many of the world’s most famous papers do not make the cut. A few that do, such as the first observation1 of carbon nanotubes (number 36) are indeed classic discoveries. But the vast majority describe experimental methods or software that have become essential in their fields.

 

The most cited work in history, for example, is a 1951 paper2 describing an assay to determine the amount of protein in a solution. It has now gathered more than 305,000 citations — a recognition that always puzzled its lead author, the late US biochemist Oliver Lowry.


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Plant hormones

Plant hormones | Plant immunity | Scoop.it

Selected articles related to plant hormones associated with root development will now be reported in my new Scoop it topic, that you can follow at this address :

 

http://www.scoop.it/t/plant-hormones-by-christophe-jacquet

 


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