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TheMetaNews: Interview-«J’étais censé avoir "reviewé" quatre articles, c'était faux !» (2019)

TheMetaNews: Interview-«J’étais censé avoir "reviewé" quatre articles, c'était faux !» (2019) | Publications | Scoop.it

Chercheur en pathologie des plantes au Royaume-Uni, Sophien Kamouns’est tout récemment fait pirater son identité par une revue prédatrice.

 

Comment vous êtes-vous rendu compte du piratage de votre identité ?
J’ai reçu un email du Research journal of plant pathologyqui a attiré mon attention car il me remerciait d’avoir "reviewé" des articles pour leur compte. Il y avait le mot de passe de "mon" profil en bas du mail, j’ai donc pu y accéder et réaliser que j’étais censé avoir rendu quatre rapports (très mauvais d'ailleurs), alors que je n’ai jamais travaillé pour cette revue.  

Avez-vous contacté les éditeurs de la revue pour avoir des explications ? 
J’en doutais au départ mais il s’agit de vraies personnes ! Un chercheur aux Etats-Unis, un autre en Chine, les deux assez reconnus. J’en ai parlé à l’administration de mon institut et nous avons décidé que je ne les contacterai pas personnellement, mais d’agir de manière formelle. Une lettre signée de mon institut est en cours de rédaction, à l’attention de la revue, ainsi que des deux éditeurs. C’est également mon employeur qui décidera s’il y a lieu d’engager des poursuites judiciaires.

Quel est le meilleur moyen de lutter contre les revues prédatrices ?
Par la transparence. Je suis pour un système « publish & filter », et non l’inverse, où le peer-review se fait sur des plateformes dédiées comme PREreview, après mise en ligne du preprint. Les maisons d'édition historiques ne sont pas forcément un gage de qualité du peer-review même si les chercheurs se cachent souvent derrière le fait qu'un article est publié dans Nature pour ne pas se poser de questions. Cela peut être très dangereux, comme nous montre le cas de l’article liant vaccination et autisme, qui a finalement été retiré mais 18 ans après sa publication. 

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PNAS: Extracellular proteolytic cascade in tomato activates immune protease Rcr3 (2020)

PNAS: Extracellular proteolytic cascade in tomato activates immune protease Rcr3 (2020) | Publications | Scoop.it

Significance

The secretion of papain-like cysteine proteases (PLCPs) is an important component of the immune response across the plant kingdom. Here we show that immune protease Rcr3, a secreted PLCP of tomato, is activated by secreted subtilisins, which are common serine proteases in plants. Subtilase P69B activates proRcr3 by cleaving after aspartates in the junction between the autoinhibitory prodomain and the protease domain of the Rcr3 precursor, thereby activating Rcr3. Subtilases of a different subfamily facilitate proRcr3 processing in a tobacco relative, indicating that this proteolytic cascade might be common in plants. Thus, pathogens that secrete subtilisin inhibitors may indirectly prevent the activation of immune proteases.

Abstract

Proteolytic cascades regulate immunity and development in animals, but these cascades in plants have not yet been reported. Here we report that the extracellular immune protease Rcr3 of tomato is activated by P69B and other subtilases (SBTs), revealing a proteolytic cascade regulating extracellular immunity in solanaceous plants. Rcr3 is a secreted papain-like Cys protease (PLCP) of tomato that acts both in basal resistance against late blight disease (Phytophthora infestans) and in gene-for-gene resistance against the fungal pathogen Cladosporium fulvum (syn. Passalora fulva). Despite the prevalent model that Rcr3-like proteases can activate themselves at low pH, we found that catalytically inactive proRcr3 mutant precursors are still processed into mature mRcr3 isoforms. ProRcr3 is processed by secreted P69B and other Asp-selective SBTs in solanaceous plants, providing robust immunity through SBT redundancy. The apoplastic effector EPI1 of P. infestans can block Rcr3 activation by inhibiting SBTs, suggesting that this effector promotes virulence indirectly by preventing the activation of Rcr3(-like) immune proteases. Rcr3 activation in Nicotiana benthamiana requires a SBT from a different subfamily, indicating that extracellular proteolytic cascades have evolved convergently in solanaceous plants or are very ancient in the plant kingdom. The frequent incidence of Asp residues in the cleavage region of Rcr3-like proteases in solanaceous plants indicates that activation of immune proteases by SBTs is a general mechanism, illuminating a proteolytic cascade that provides robust apoplastic immunity.


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bioRxiv: The rice NLR pair Pikp-1/Pikp-2 initiates cell death through receptor cooperation rather than negative regulation (2020)

bioRxiv: The rice NLR pair Pikp-1/Pikp-2 initiates cell death through receptor cooperation rather than negative regulation (2020) | Publications | Scoop.it

Plant NLR immune receptors are multidomain proteins that can function as specialized sensor/helper pairs. Paired NLR immune receptors are generally thought to function via negative regulation, where one NLR represses the activity of the second and detection of pathogen effectors relieves this repression to initiate immunity. However, whether this mechanism is common to all NLR pairs is not known. Here, we show that the rice NLR pair Pikp-1/Pikp-2, which confers resistance to strains of the blast pathogen Magnaporthe oryzae (syn. Pyricularia oryzae) expressing the AVR-PikD effector, functions via receptor cooperation, with effector-triggered activation requiring both NLRs to trigger the immune response. To investigate the mechanism of Pikp-1/Pikp-2 activation, we expressed truncated variants of these proteins, and made mutations in previously identified NLR sequence motifs. We found that any domain truncation, in either Pikp-1 or Pikp-2, prevented cell death in the presence of AVR-PikD, revealing that all domains are required for activity. Further, expression of individual Pikp-1 or Pikp-2 domains did not result in cell death. Mutations in the conserved P-loop and MHD sequence motifs in both Pikp-1 and Pikp-2 prevented cell death activation, demonstrating that these motifs are required for the function of the two partner NLRs. Finally, we showed that Pikp-1 and Pikp-2 associate to form homo- and hetero-complexes in planta in the absence of AVR-PikD; on co-expression the effector binds to Pikp-1 generating a tri-partite complex. Taken together, we provide evidence that Pikp-1 and Pikp-2 form a fine-tuned system that is activated by AVR-PikD via receptor cooperation rather than negative regulation. 

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bioRxiv: A complex resistance locus in Solanum americanum recognizes a conserved Phytophthora effector (2020)

bioRxiv: A complex resistance locus in Solanum americanum recognizes a conserved Phytophthora effector (2020) | Publications | Scoop.it

Late blight caused by Phytophthora infestans greatly constrains potato production. Many Resistance (R) genes were cloned from wild Solanum species and/or introduced into potato cultivars by breeding. However, individual R genes have been overcome by P. infestansevolution; durable resistance remains elusive. We positionally cloned a new R gene, Rpi-amr1, from Solanum americanum, that encodes an NRC helper-dependent CC-NLR protein. Rpi-amr1 confers resistance in potato to all 19 P. infestans isolates tested. Using association genomics and long-read RenSeq, we defined eight additional Rpi-amr1 alleles from different S. americanum and related species. Despite only ∼90% identity between Rpi-amr1 proteins, all confer late blight resistance but differentially recognize Avramr1 orthologs and paralogs. We propose that Rpi-amr1 gene family diversity facilitates detection of diverse paralogs and alleles of the recognized effector, enabling broad-spectrum and durable resistance against P. infestans.

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MPMI: A clone resource of Magnaporthe oryzae effectors that share sequence and structural similarities across host-specific lineages (2020)

MPMI: A clone resource of Magnaporthe oryzae effectors that share sequence and structural similarities across host-specific lineages (2020) | Publications | Scoop.it

The blast fungus Magnaporthe oryzae (Syn. Pyricularia oryzae) is a destructive plant pathogen that can infect about 50 species of both wild and cultivated grasses, including important crops such as rice and wheat. M. oryzae is composed of genetically differentiated lineages that tend to infect specific host genera. To date, most studies of M. oryzae effectors have focused on the rice-infecting lineage. We describe a clone resource of 195 effectors of M. oryzae predicted from all the major host-specific lineages. These clones are freely available as Golden Gate compatible entry plasmids. Our aim is to provide the community with an open source effector clone library to be used in a variety of functional studies. We hope that this resource will encourage studies of M. oryzae effectors on diverse host species.

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Plantae: LOCKDOWN CONVERSATIONS How to tide over the Covid-19 pandemic? (2020)

Plantae: LOCKDOWN CONVERSATIONS How to tide over the Covid-19 pandemic? (2020) | Publications | Scoop.it

“Revisit your objectives and expectations. Have a plan”

1. This current lockdown seems to be unprecedented in recent history. How is your lab coping up?  

These are challenging and uncertain times for all of us and for our friends and families. I have encouraged everyone in my lab to regularly check in and update the team on how they are doing and so on. I have also encouraged everyone to make use of the lab network as much as possible to stay connected and seek help as needed. We’ve also continued our lab meeting through Zoom and started a weekly journal club.

2. What pieces of suggestion would you offer early career researchers on utilizing this time?

First, it’s important to appreciate that people respond differently to situations like this. My first advice would be to carefully consider your own mental state and address any anxiety you may experience. I think it’s useless to try to get intellectual work done when you’re in the wrong frame of mind. This is generally true and it’s even more relevant during this time. So, just like an athlete before a sporting event, scientists need to learn to chill and relax.

 

The second point is to revisit your objectives and expectations. Have a plan.

Otherwise, it’s been said elsewhere that researchers can engage in a number of activities that do not require a wet lab: writing, reading, training, computational analyses etc. In biology, everyone has been busy producing data. It’s data, data, data! But if the data isn’t shared and published, it’s generally useless. Now, perhaps there is more time to process and share unpublished datasets. There are many open platforms that allow you to publish datasets and bare-bone mini-publications, which shouldn’t take that long to produce.

 

If the dataset is worth sharing, then anyone who curates it and analyses it should be in a position to publish it (with due credit to everyone involved of course). That still would be a valued and valuable contribution to add to a CV. We have identified such old unpublished datasets in my lab, and we hope that the extra time offered by this situation would allow us to share and release these data in the coming weeks.

3. How is the cooperation of members in your lab and institute? How do you keep track of their work progress?

It’s the same as always. We continue our weekly lab meeting and that’s our primary forum through which lab members update everyone about their projects. We also have ad-hoc team meetings as needed. The only difference is that this has gone online, but Zoom is working just fine and I’m amazed at how quickly everyone has adjusted to this model.

4. Some journals have come up with guidelines to support researchers in this time of difficulty. What do you think is the role of journals at this time and what more do you think they can do?

I’m much more interested in highlighting the key role of preprint servers in this crisis. First, preprints, such as bioRxiv and medRxiv, have accelerated the dissemination of new COVID-19 research. Second, preprints allow immediate sharing of all those papers that scientists are writing up during lockdowns. I don’t think the classic journal model can cope with a surge in submissions as the system is already overloaded. Many articles will get stuck in the outdated model of journal pre-publication peer review. Just imagine how we would cope without bioRxiv at the moment. All that good science would be held up for months and months for no one to see except for an editor and a few reviewers.

5. Do you think this time might serve as a cooling-off period for researchers from the usual monotony of lab work? If so, how productive do you foresee the immediate future after the restoration of normalcy?

Scientific research should never be monotonous. Who says planning, executing and interpreting experiments can be boring? As my friend and colleague Ken Shirasu likes to remind us, “Science is the ultimate entertainment for humankind.” So just enjoy and cherish being a scientist whether you’re in a lab or at home.

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Zenodo: How to trick a plant pathogen? (2020)

Zenodo: How to trick a plant pathogen? (2020) | Publications | Scoop.it

Plants can get sick too. In fact, they get infected by all types of microbes and little critters. But plants have evolved an effective immune system to fight off pathogen invasion. Amazingly, nearly every single plant cell is able to protect itself and its neighbours against infections. The plant immune system gets switched on when one of its many immune receptors matches a ligand in the pathogen. As a consequence of a long evolutionary history of fighting off pathogens, immune receptors are now encoded by hundreds of genes that populate the majority of plant genomes. Understanding how the plant immune system functions and how it has evolved can give invaluable insights that would benefit modern agriculture and help breeding disease resistant crops.

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YouTube: Don’t perish! A step by step guide to writing a scientific paper (2020)

Sophien Kamoun's presentation to the Norwich research Park PhD student. A step by step guide to writing scientific papers. April 1, 2020.

See slides at https://www.slideshare.net/SophienKamoun/dont-perish-a-step-by-step-guide-to-writing-a-scientific-paper

See summary and notes at https://kamounlab.tumblr.com/post/614297962173120512/dont-perish-a-step-by-step-guide-to-writing-a

This presentation is part of a workshop about writing scientific papers. It describes a 10 step guide for writing papers.

1. Create a folder
2. Write a story line
3. Make list of Figures
4. Finalize Figures
5. Write the Results
6. Write the Intro
7. Write the Discussion
8. Assemble the Abstract
9. Write the Title
10. Post it on bioRxiv

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Journal of Cell Science: The plant–pathogen haustorial interface at a glance (2020)

Journal of Cell Science: The plant–pathogen haustorial interface at a glance (2020) | Publications | Scoop.it

Many filamentous pathogens invade plant cells through specialized hyphae called haustoria. These infection structures are enveloped by a newly synthesized plant-derived membrane called the extrahaustorial membrane (EHM). This specialized membrane is the ultimate interface between the plant and pathogen, and is key to the success or failure of infection. Strikingly, the EHM is reminiscent of host-derived membrane interfaces that engulf intracellular metazoan parasites. These perimicrobial interfaces are critical sites where pathogens facilitate nutrient uptake and deploy virulence factors to disarm cellular defenses mounted by their hosts. Although the mechanisms underlying the biogenesis and functions of these host–microbe interfaces are poorly understood, recent studies have provided new insights into the cellular and molecular mechanisms involved. In this Cell Science at a Glance and the accompanying poster, we summarize these recent advances with a specific focus on the haustorial interfaces associated with filamentous plant pathogens. We highlight the progress in the field that fundamentally underpin this research topic. Furthermore, we relate our knowledge of plant–filamentous pathogen interfaces to those generated by other plant-associated organisms. Finally, we compare the similarities between host–pathogen interfaces in plants and animals, and emphasize the key questions in this research area.


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eLife: An N-terminal motif in NLR immune receptors is functionally conserved across distantly related plant species (2019)

eLife: An N-terminal motif in NLR immune receptors is functionally conserved across distantly related plant species (2019) | Publications | Scoop.it

The molecular codes underpinning the functions of plant NLR immune receptors are poorly understood. We used in vitro Mu transposition to generate a random truncation library and identify the minimal functional region of NLRs. We applied this method to NRC4—a helper NLR that functions with multiple sensor NLRs within a Solanaceae receptor network. This revealed that the NRC4 N-terminal 29 amino acids are sufficient to induce hypersensitive cell death. This region is defined by the consensus MADAxVSFxVxKLxxLLxxEx (MADA motif) that is conserved at the N-termini of NRC family proteins and ~20% of coiled-coil (CC)-type plant NLRs. The MADA motif matches the N-terminal a1 helix of Arabidopsis NLR protein ZAR1, which undergoes a conformational switch during resistosome activation. Immunoassays revealed that the MADA motif is functionally conserved across NLRs from distantly related plant species. NRC-dependent sensor NLRs lack MADA sequences indicating that this motif has degenerated in sensor NLRs over evolutionary time.


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Plant Physiology: NRC4 gene cluster is not essential for bacterial flagellin-triggered immunity (2019)

Plant Physiology: NRC4 gene cluster is not essential for bacterial flagellin-triggered immunity (2019) | Publications | Scoop.it

Plants utilise cell surface pattern recognition receptors (PRRs) and intracellular nucleotide-binding domain leucine-rich repeat containing receptors (NLRs) to fend off invading pathogens (Dodds and Rathjen, 2010; Win et al., 2012). Both types of immune receptors detect pathogen molecules directly or indirectly to activate complex immune responses and disease resistance (Kourelis and van der Hoorn, 2018). Although PRR- and NLR-triggered immunity are generally thought to activate distinct pathways, they can induce similar outputs such as production of reactive oxygen species (ROS) and hypersensitive cell death (Peng et al., 2018). Both PRR- and NLR-activated pathways involve calcium-dependent protein kinases, mitogen-activate protein kinases (MAPKs), phytohormone signalling, and transcriptional reprogramming (Peng et al., 2018). However, whether these two pathways converge at some point to potentiate and strengthen the immune response remains unclear. A recent study suggested that the tomato NLR helper NRC4 positively regulates the ROS burst induced by the bacterial flagellin peptide flg22 (Leibman-Markus et al. 2018b). We took advantage of the CRISPR/Cas9 system to knock out multiple NRC genes in tomato and Nicotiana benthamiana. Although these mutants failed to respond to the NRC-dependent NLRs, they remained unaltered in flg22-induced responses. We conclude that the NRC genes are not essential for flg22-induced responses in tomato and N. benthamiana.


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bioRxiv: Genomic rearrangements generate hypervariable mini-chromosomes in host-specific lineages of the blast fungus (2020)

bioRxiv: Genomic rearrangements generate hypervariable mini-chromosomes in host-specific lineages of the blast fungus (2020) | Publications | Scoop.it

Supernumerary mini-chromosomes–a unique type of genomic structural variation–have been implicated in the emergence of virulence traits in plant pathogenic fungi. However, the mechanisms that facilitate the emergence and maintenance of mini-chromosomes across fungi remain poorly understood. In the blast fungus Magnaporthe oryzae, mini-chromosomes have been first described in the early 1990s but, until very recently, have been overlooked in genomic studies. Here we investigated structural variation in four isolates of the blast fungus M. oryzae from different grass hosts and analyzed the sequences of mini-chromosomes in the rice, foxtail millet and goosegrass isolates. The mini-chromosomes of these isolates turned out to be highly diverse with distinct sequence composition. They are enriched in repetitive elements and have lower gene density than core-chromosomes. We identified several virulence-related genes in the mini-chromosome of the rice isolate, including the polyketide synthase Ace1 and the effector gene AVR-Pik. Macrosynteny analyses around these loci revealed structural rearrangements, including inter-chromosomal translocations between core- and mini-chromosomes. Our findings provide evidence that mini-chromosomes independently emerge from structural rearrangements of core-chromosomes and might contribute to adaptive evolution of the blast fungus.

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TheMetaNews: Interview-«J’étais censé avoir "reviewé" quatre articles, c'était faux !» (2019)

TheMetaNews: Interview-«J’étais censé avoir "reviewé" quatre articles, c'était faux !» (2019) | Publications | Scoop.it

Chercheur en pathologie des plantes au Royaume-Uni, Sophien Kamouns’est tout récemment fait pirater son identité par une revue prédatrice.

 

Comment vous êtes-vous rendu compte du piratage de votre identité ?
J’ai reçu un email du Research journal of plant pathologyqui a attiré mon attention car il me remerciait d’avoir "reviewé" des articles pour leur compte. Il y avait le mot de passe de "mon" profil en bas du mail, j’ai donc pu y accéder et réaliser que j’étais censé avoir rendu quatre rapports (très mauvais d'ailleurs), alors que je n’ai jamais travaillé pour cette revue.  

Avez-vous contacté les éditeurs de la revue pour avoir des explications ? 
J’en doutais au départ mais il s’agit de vraies personnes ! Un chercheur aux Etats-Unis, un autre en Chine, les deux assez reconnus. J’en ai parlé à l’administration de mon institut et nous avons décidé que je ne les contacterai pas personnellement, mais d’agir de manière formelle. Une lettre signée de mon institut est en cours de rédaction, à l’attention de la revue, ainsi que des deux éditeurs. C’est également mon employeur qui décidera s’il y a lieu d’engager des poursuites judiciaires.

Quel est le meilleur moyen de lutter contre les revues prédatrices ?
Par la transparence. Je suis pour un système « publish & filter », et non l’inverse, où le peer-review se fait sur des plateformes dédiées comme PREreview, après mise en ligne du preprint. Les maisons d'édition historiques ne sont pas forcément un gage de qualité du peer-review même si les chercheurs se cachent souvent derrière le fait qu'un article est publié dans Nature pour ne pas se poser de questions. Cela peut être très dangereux, comme nous montre le cas de l’article liant vaccination et autisme, qui a finalement été retiré mais 18 ans après sa publication. 

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Zenodo: How to select a PhD lab? (2019)

Zenodo: How to select a PhD lab? (2019) | Publications | Scoop.it

I regularly get this question from predocs. How do I select a PhD lab? How do I decide on a good supervisor? Should I select a lab based on a project? Below is a hodgepodge of the answers I generally give.

 

Click here for the Arabic version on Arabixiv.

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mBio: Divergent Evolution of PcF/SCR74 Effectors in Oomycetes Is Associated with Distinct Recognition Patterns in Solanaceous Plants (2020)

mBio: Divergent Evolution of PcF/SCR74 Effectors in Oomycetes Is Associated with Distinct Recognition Patterns in Solanaceous Plants (2020) | Publications | Scoop.it

Plants deploy cell surface receptors known as pattern-recognition receptors (PRRs) that recognize non-self molecules from pathogens and microbes to defend against invaders. PRRs typically recognize microbe-associated molecular patterns (MAMPs) that are usually widely conserved, some even across kingdoms. Here, we report an oomycete-specific family of small secreted cysteine-rich (SCR) proteins that displays divergent patterns of sequence variation in the Irish potato famine pathogen Phytophthora infestans. A subclass that includes the conserved effector PcF from Phytophthora cactorum activates immunity in a wide range of plant species. In contrast, the more diverse SCR74 subclass is specific to P. infestans and tends to trigger immune responses only in a limited number of wild potato genotypes. The SCR74 response was recently mapped to a G-type lectin receptor kinase (G-LecRK) locus in the wild potato Solanum microdontum subsp. gigantophyllum. The G-LecRK locus displays a high diversity in Solanum host species compared to other solanaceous plants. We propose that the diversification of the SCR74 proteins in P. infestans is driven by a fast coevolutionary arms race with cell surface immune receptors in wild potato, which contrasts the presumed slower dynamics between conserved apoplastic effectors and PRRs. Understanding the molecular determinants of plant immune responses to these divergent molecular patterns in oomycetes is expected to contribute to deploying multiple layers of disease resistance in crop plants.


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YTRB Interview Series: Sophien Kamoun...à la poursuite de l'émerveillement perpétuel (2020)

Invité du jour, Pr. Sophien Kamoun, Group Leader au Sainsbury Laboratory, Norwich, UK, et expert mondialement connu des plant pathogens, entre autre...nous parle de sa philosophie de la science...

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Microbiology Resource Announcements: Genome Sequences of Plant-Associated Rhodococcus sp. Isolates from Tunisia (2020)

Microbiology Resource Announcements: Genome Sequences of Plant-Associated Rhodococcus sp. Isolates from Tunisia (2020) | Publications | Scoop.it

The draft genome sequences of plant-associated Rhodococcus spp. from Tunisia are reported here. Two Rhodococcus fascians strains were obtained from almond rootstocks, and one Rhodococcus kroppenstedtii strain was obtained from a pistachio tree. The fourth Rhodococcus sp. strain was isolated from an ornamental plant.


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bioRxiv: A vector system for fast-forward in vivo studies of the ZAR1 resistosome in the model plant Nicotiana benthamiana (2020)

bioRxiv: A vector system for fast-forward in vivo studies of the ZAR1 resistosome in the model plant Nicotiana benthamiana (2020) | Publications | Scoop.it

Nicotiana benthamiana has emerged as a complementary experimental system to Arabidopsis. It enables fast-forward in vivo analyses primarily through transient gene expression and is particularly popular in the study of plant immunity. Recently, our understanding of NLR plant immune receptors has greatly advanced following the discovery of Arabidopsis ZAR1 resistosome. Here, we describe a novel vector system of 52 plasmids that enables functional studies of the ZAR1 resistosome in N. benthamiana. We showed that ZAR1 stands out among the coiled coil class of NLRs for being highly conserved across distantly related dicot plant species and confirmed NbZAR1 as the N. benthamiana ortholog of Arabidopsis ZAR1. NbZAR1 triggers autoimmune cell death in N. benthamiana and this activity is dependent on a functional N-terminal alpha1 helix. C-terminally tagged NbZAR1 remains functional in N. benthamiana thus enabling cell biology and biochemical studies in this plant system. We conclude that the NbZAR1 open source plasmids form an additional experimental system to Arabidopsis for in planta resistosome studies.


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Biologist: “The mobilization of our country’s scientists has been impressive” (2020)

Biologist: “The mobilization of our country’s scientists has been impressive” (2020) | Publications | Scoop.it

Professor Sophien Kamoun, group leader at the Sainsbury Laboratory, discusses how he and his colleagues have pivoted from studying plant pathogens to tracing a human pathogen at the heart of a global emergency, and how scientists unable to access wet labs can still contribute to research.

Can you describe what your role involved before the COVID-19 pandemic and how your focus has changed because of the pandemic?

I normally investigate topics related to plant pathology and plant immunity. The COVID-19 pandemic hasn’t changed the focus of my research, but I was tasked within our laboratory to coordinate projects on innovations that could rapidly scale-up diagnostics.

 

Please tell us about any COVID-19 related projects you have been involved with and what they have achieved so far.

We used a bottom-up approach, which fits best with the ethos of The Sainsbury Laboratory. First we made an open call for ideas and volunteers in late March. I was truly impressed by the willingness of many of our scientists—from students to team leaders—to contribute their expertise and know-how.

Two teams immediately came together and sprung into action. One team has focused on implementing the Cas13a/SHERLOCK method for SARS-CoV-2 detection, while the second one is working on adapting “toehold switch” detection to this coronavirus. At the moment we are still testing these protocols with synthetic controls and haven’t yet worked with clinical samples.

 

We’re interested in how science works during a crisis, and how scientists have responded to these unprecedented circumstances. What have you done differently owing to this being an urgent, emergency situation?

First, it’s important to appreciate that people respond differently to a crisis like this. My first advice to everyone in my team and my collaborators was to carefully consider their own mental state and address any anxiety they may experience. I personally find exercise, meditation music and connecting with friends and family to be very helpful in relieving stress. It’s rather useless to try to get intellectual work done when you’re in the wrong frame of mind. This is true at any time but it’s even more relevant during this situation. So just like athletes before a sporting event, scientists need to learn to chill and relax.

 

The second advice is to revisit objectives and expectations. I advised my team to have a plan. What are your revised goals? How realistic are they? What would it take to achieve them?

Perhaps there is also a silver lining in this crisis. In biology, everyone has been busy producing huge amounts of data. But if the data isn’t shared and published, it’s generally useless. Now that we are kept away from the wet labs, perhaps there is more time to process and share unpublished datasets. If you have such data, then this is the time to curate it and share it. There are many open platforms that allow you to publish datasets and barebone mini-publications, which shouldn’t take that long to produce.

 

The prevailing paradigm in biology is that those who produce the data are expected to publish it. But why should that always be the case? If the dataset is worth sharing, then anyone who curates it and analyses it should be in a position to publish it (with due credit to everyone involved of course). That still would be a valued and valuable contribution to add to a CV. We have identified such old unpublished datasets in my lab, and we hope that any extra time offered by this situation would allow us to share and release these data in the coming weeks.

 

How are you communicating information from your work so that it can be utilised around the world?

Beyond the typical channels, social media continues to serve as a key medium for communicating and disseminating information. Many scientists are on Twitter and I have been posting more frequently on Facebook to reach out to scientists in developing countries given that they tend to be more active on this platform. For instance, Facebook has proven important for sharing knowledge with communities and help groups in Tunisia, my country of origin.

 

It’s also worth highlighting the key role that preprint servers have played in this crisis. First, preprints, such as bioRxiv and medRxiv, have accelerated the dissemination of new COVID-19 research. Second, preprints allow immediate sharing of all those papers that scientists are writing up during lockdowns. As an affiliate for bioRxiv, I get to see and approve submitted papers, and there has been up to 200 papers in the queue. I don’t think the classic journal model can cope with such a surge in submissions as the system is overloaded. Just imagine how we would cope without bioRxiv at the moment! All that good science that would be held up for months and months for no one to see.

 

Can you talk us through some of the challenges of working during these strange times, for example the adaptations required to keep yourself and staff safe; trying to source in-demand equipment and reagents; or the effect on non-COVID research projects/departmental business?

 

The Sainsbury Laboratory and other Institutes on the Norwich Research Park reacted proactively to the crisis. I think the fact that we have a lot of contact with colleagues in China made us more attuned to the scale of the problem. We implemented social distancing and reduced occupancy policies early, in the week of March 9th.

 

We have made our own hand-sanitiser and distributed it widely. Some of our staff arranged to collect and distribute PPE to the hospital, including masks received from collaborators in China. In addition, several members of our Laboratory have volunteered at the Norfolk and Norwich University Hospitals to help scale-up COVID-19 diagnostics.

 

The laboratory is currently closed except for essential maintenance work and the COVID-19 projects. Most of the other work that is currently taking place is either computational or focused on analysing and publishing previously generated data. All meetings have moved to online platforms.

 

How would you describe the bioscience sector’s interaction with public health bodies and Government?

I think the sector has fully engaged with the crisis. The mobilization of our country’s scientists has been impressive, as evidenced for example by the number of volunteers. However, like many of my colleagues, I was surprised by the government’s initial response – the general impression I had is that there was a period of laisser-faire before robust measures were implemented. It seemed imprudent to me that as Lombardy went into lockdown, you couldn’t take a train from Milan to Rome but you could fly from Milan to Heathrow with absolutely no checks whatsoever upon arrival.

 

I was also stunned by the infamous press briefing of Thursday March 12th when the mitigation strategy of herd immunity was announced. Fortunately, the scientific community reacted strongly, and I was very impressed by the broad pushback. I agree with the view that, in due time, we must investigate what happened to be better prepared for the next pandemic.

Looking forward, I hope that there will be a better appreciation of the importance of curiosity-driven fundamental research. Let’s reflect on the fact that COVID-19 diagnostics are based on PCR—a method that was discovered through a scientist’s creative exploration of an idea, not through top-down impact driven research.

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PNAS: Pathogen manipulation of chloroplast function triggers a light-dependent immune recognition (2020)

PNAS: Pathogen manipulation of chloroplast function triggers a light-dependent immune recognition (2020) | Publications | Scoop.it

In plants and animals, nucleotide-binding leucine-rich repeat (NLR) proteins are intracellular immune sensors that recognize and eliminate a wide range of invading pathogens. NLR-mediated immunity is known to be modulated by environmental factors. However, how pathogen recognition by NLRs is influenced by environmental factors such as light remains unclear. Here, we show that the agronomically important NLR Rpi-vnt1.1 requires light to confer disease resistance against races of the Irish potato famine pathogen Phytophthora infestans that secrete the effector protein AVRvnt1. The activation of Rpi-vnt1.1 requires a nuclear-encoded chloroplast protein, glycerate 3-kinase (GLYK), implicated in energy production. The pathogen effector AVRvnt1 binds the full-length chloroplast-targeted GLYK isoform leading to activation of Rpi-vnt1.1. In the dark, Rpi-vnt1.1–mediated resistance is compromised because plants produce a shorter GLYK—lacking the intact chloroplast transit peptide—that is not bound by AVRvnt1. The transition between full-length and shorter plant GLYK transcripts is controlled by a light-dependent alternative promoter selection mechanism. In plants that lack Rpi-vnt1.1, the presence of AVRvnt1 reduces GLYK accumulation in chloroplasts counteracting GLYK contribution to basal immunity. Our findings revealed that pathogen manipulation of chloroplast functions has resulted in a light-dependent immune response.

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bioRxiv: The Irish potato famine pathogen subverts host vesicle trafficking to channel starvation-induced autophagy to the pathogen interface (2020)

bioRxiv: The Irish potato famine pathogen subverts host vesicle trafficking to channel starvation-induced autophagy to the pathogen interface (2020) | Publications | Scoop.it

Eukaryotic cells deploy autophagy to eliminate invading microbes. In turn, pathogens have evolved effector proteins to counteract antimicrobial autophagy. How and why adapted pathogens co-opt autophagy for their own benefit is poorly understood. The Irish famine pathogen Phythophthora infestans secretes the effector protein PexRD54 that selectively activates an unknown plant autophagy pathway, while antagonizing antimicrobial autophagy. Here we show that PexRD54 induces autophagosome formation by bridging small GTPase Rab8a-decorated vesicles with autophagic compartments labelled by the core autophagy protein ATG8CL. Rab8a is required for pathogen-triggered and starvation-induced but not antimicrobial autophagy, revealing that specific trafficking pathways underpin selective autophagy. We discovered that Rab8a contributes to basal immunity against P. infestans, but PexRD54 diverts a sub-population of Rab8a vesicles to lipid droplets that associate with autophagosomes. These are then diverted towards pathogen feeding structures that are accommodated within the host cells. We propose that PexRD54 mimics starvation-induced autophagy by channeling host endomembrane trafficking towards the pathogen interface possibly to acquire nutrients. This work reveals that effectors can interconnect independent host compartments to stimulate complex cellular processes that benefit the pathogen.


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Zenodo: Ten things we learned in 2010-2019 (aside from everything else) (2020)

Zenodo: Ten things we learned in 2010-2019 (aside from everything else) (2020) | Publications | Scoop.it

He who has studied himself is his own master. –Sri Lankan proverb.

 

By the time this gets posted, you’ll probably be sick and tired of all those retrospective articles looking back at the 2010-2019 decade. I feel your pain. But hey, we’re still early in the new decade and I have a good reason for writing this. This last decade has been such an exhilarating period of exploration and discovery for me, my team and my collaborators that I just can’t resist the urge to write this post. The decade took us through unexpected research paths that I would have never imagined ten years ago. As I’m drafting these words during my holidays break in Sri Lanka—in between tasting the local milk rice curries and soaking the soft Indian ocean December sunshine—I’m reflecting on the local proverb above and I’m using it as my lame excuse to offer you yet another list of decadal achievements.

 

Please note that this is my personal highly biased perspective on ten things we have learned in 2010-2019. This list is by no means meant to be comprehensive review of advances in our research field but rather a reflection of my own personal take on the scientific topics we investigate.

 

2010. Two-speed genomes, everywhere?
2011. WY fold—commonalities amid diversity.
2011. The haustorial interface—where it all happens?
2013. Genome editing made easy.
2013. Field pathogenomics—just sequence it!
2013. Going back to the past to better prepare for the future.
2014. Effector adaptation after jumping hosts.
2015. The beauty of a protein complex structure.
2017. Do NLRs work in pairs—it’s more complicated!
2019. The coming of age of the plant resistosome. 

 

To cite: Kamoun, S. Ten things we learned in 2010-2019 (aside from everything else). Zenodo. http://doi.org/10.5281/zenodo.3613856

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bioRxiv: Intra-strain elicitation and suppression of plant immunity by Ralstonia solanacearum type-III effectors in Nicotiana benthamiana (2019)

bioRxiv: Intra-strain elicitation and suppression of plant immunity by Ralstonia solanacearum type-III effectors in Nicotiana benthamiana (2019) | Publications | Scoop.it

Effector proteins delivered inside plant cells are powerful weapons for bacterial pathogens, but this exposes the pathogen to potential recognition by the plant immune system. Therefore, effector acquisition must be balanced for a successful infection. Ralstonia solanacearum is an aggressive pathogen with a large repertoire of secreted effectors. One of these effectors, RipE1, is conserved in most R. solanacearum strains sequenced to date. In this work, we found that RipE1 triggers immunity in N. benthamiana, which requires the immune regulator SGT1, but not EDS1 or NRCs. Interestingly, RipE1-triggered immunity induces the accumulation of salicylic acid (SA) and the overexpression of several genes encoding phenylalanine-ammonia lyases (PALs), suggesting that the unconventional PAL-mediated pathway is responsible for the observed SA biosynthesis. Surprisingly, RipE1 recognition also induces the expression of jasmonic acid (JA)-responsive genes and JA biosynthesis, suggesting that both SA and JA may act cooperatively in response to RipE1. Finally, we found that RipE1 expression leads to the accumulation of glutathione in plant cells, which precedes the activation of immune responses. R. solanacearum encodes another effector, RipAY, which is known to inhibit immune responses by degrading cellular glutathione. Accordingly, we show that RipAY inhibits RipE1-triggered immune responses. This work shows a strategy employed by R. solanacearum to counteract the perception of its effector proteins by the plant immune system.


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bioRxiv: Cleavage of a pathogen apoplastic protein by plant subtilases activates immunity (2019)

bioRxiv: Cleavage of a pathogen apoplastic protein by plant subtilases activates immunity (2019) | Publications | Scoop.it

The plant apoplast is a harsh environment in which hydrolytic enzymes, especially proteases, accumulate during pathogen infection. However, the defense functions of most apoplastic proteases remains largely elusive. Here, we show that a newly identified small cysteine-rich secreted protein PC2 from the potato late blight pathogen Phytophthora infestans induces immunity in Solanum plant species only after cleavage by plant apoplastic subtilisin-like proteases, such as tomato P69B. A minimal 61-amino-acid core peptide carrying two key cysteines and widely conserved among most oomycete species is sufficient for PC2 activity. Kazal-like protease inhibitors, such as EPI1 produced by P. infestans can prevent PC2 cleavage and dampen PC2 elicited host immunity. This study reveals that cleavage of pathogen proteins to release immunogenic peptides is an important function of apoplastic proteases but that pathogens interfere with these functions using protease inhibitor effectors.


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bioRxiv: Recently expanded clonal lineages of the rice blast fungus display distinct patterns of presence/absence of effector genes (2020)

bioRxiv: Recently expanded clonal lineages of the rice blast fungus display distinct patterns of presence/absence of effector genes (2020) | Publications | Scoop.it

Background Understanding the mechanisms and timescales of plant pathogen outbreaks requires a detailed genome-scale analysis of their population history. The fungus Magnaporthe (Syn. Pyricularia) oryzae —the causal agent of blast disease of cereals— is among the most destructive plant pathogens to world agriculture and a major threat to the production of rice, wheat and other cereals. Although M. oryzae is a multihost pathogen that infects more than 50 species of cereals and grasses, all rice-infecting isolates belong to a single genetically defined lineage. Here, we combined multiple genomics datasets to reconstruct the genetic history of the rice-infecting lineage of M. oryzae based on 131 isolates from 21 countries.

 

Results The global population of the rice blast fungus consists of a diverse set of individuals and three well-defined genetic groups. Multiple population genetic tests revealed that the rice-infecting lineage of the blast fungus probably originated from a recombining diverse group in South East Asia followed by three independent clonal expansions that took place over the last ∼200 years. Patterns of allele sharing identified a subpopulation from the recombining diverse group that introgressed with one of the clonal lineages before its global expansion. Remarkably, the four genetic lineages of the rice blast fungus vary in the number and patterns of presence/absence of candidate effector genes. In particular, clonal lineages carry a reduced repertoire of effector genes compared with the diverse group, and specific combinations of effector presence/absence define each of the pandemic clonal lineages.

 

Conclusions Our analyses reconstruct the genetic history of the rice-infecting lineage of M. oryzae revealing three clonal lineages associated with rice blast pandemics. Each of these lineages displays a specific pattern of presence/absence of effector genes that may have shaped their adaptation to the rice host and their evolutionary history.

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YouTube: Beyond single genes: receptor networks underpin plant immunity (2019)

Keynote lecture by Sophien Kamoun, The Sainsbury Laboratory, at Plant Genomes in a Changing Environment 2019 organised by Wellcome Genome Campus Advanced Courses and Scientific Conferences