Norwich Research Park

Norwich, United Kingdom

Norwich Research Park

Norwich, United Kingdom

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Petre B.,Norwich Research Park | Petre B.,French National Institute for Agricultural Research | Kamoun S.,Norwich Research Park
PLoS Biology | Year: 2014

Fungal and oomycete plant parasites are among the most devastating pathogens of food crops. These microbes secrete effector proteins inside plant cells to manipulate host processes and facilitate colonization. How these effectors reach the host cytoplasm remains an unclear and debated area of plant research. In this article, we examine recent conflicting findings that have generated discussion in the field. We also highlight promising approaches based on studies of both parasite and host during infection. Ultimately, this knowledge may inform future broad spectrum strategies for protecting crops from such pathogens. © 2014 Petre, Kamoun.


Patron N.J.,Norwich Research Park
Current Opinion in Plant Biology | Year: 2014

As the speed and accuracy of genome sequencing improves, there are ever-increasing resources available for the design and construction of synthetic DNA parts. These can be used to engineer plant genomes to produce new functions or to elucidate the function of endogenous sequences. Until recently the assembly of amplified or cloned sequences into large and complex designs was a limiting step in plant synthetic biology and biotechnology. A number of new methods for assembling DNA molecules have been developed in the last few years, several of which have been applied to the production of molecules used to modify plant genomes. © 2014 Elsevier Ltd.


Macho A.P.,Norwich Research Park | Zipfel C.,Norwich Research Park
Current Opinion in Microbiology | Year: 2015

During infection, microbes are detected by surface-localized pattern recognition receptors (PRRs), leading to an innate immune response that prevents microbial ingress. Therefore, successful pathogens must evade or inhibit PRR-triggered immunity to cause disease. In the past decade, a number of type-III secretion system effector (T3Es) proteins from plant pathogenic bacteria have been shown to suppress this layer of innate immunity. More recently, the detailed mechanisms of action have been defined for several of these effectors. Interestingly, effectors display a wide array of virulence targets, being able to prevent activation of immune receptors and to hijack immune signaling pathways. Besides being a fascinating example of pathogen-host co-evolution, effectors have also emerged as valuable tools to dissect important biological processes in host cells. © 2014 Elsevier Ltd.


Jones J.D.,Norwich Research Park
Philosophical transactions of the Royal Society of London. Series B, Biological sciences | Year: 2014

Essentially all plant species exhibit heritable genetic variation for resistance to a variety of plant diseases caused by fungi, bacteria, oomycetes or viruses. Disease losses in crop monocultures are already significant, and would be greater but for applications of disease-controlling agrichemicals. For sustainable intensification of crop production, we argue that disease control should as far as possible be achieved using genetics rather than using costly recurrent chemical sprays. The latter imply CO2 emissions from diesel fuel and potential soil compaction from tractor journeys. Great progress has been made in the past 25 years in our understanding of the molecular basis of plant disease resistance mechanisms, and of how pathogens circumvent them. These insights can inform more sophisticated approaches to elevating disease resistance in crops that help us tip the evolutionary balance in favour of the crop and away from the pathogen. We illustrate this theme with an account of a genetically modified (GM) blight-resistant potato trial in Norwich, using the Rpi-vnt1.1 gene isolated from a wild relative of potato, Solanum venturii, and introduced by GM methods into the potato variety Desiree.


Macho A.P.,Norwich Research Park | Zipfel C.,Norwich Research Park
Molecular Cell | Year: 2014

Despite being sessile organisms constantly exposed to potential pathogens and pests, plants are surprisingly resilient to infections. Plants can detect invaders via the recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs). Plant PRRs are surface-localized receptor-like kinases, which comprise a ligand-binding ectodomain and an intracellular kinase domain, or receptor-like proteins, which do not exhibit any known intracellular signaling domain. In this review, we summarize recent discoveries that shed light on the molecular mechanisms underlying ligand perception and subsequent activation of plant PRRs. Notably, plant PRRs appear as central components of multiprotein complexes at the plasma membrane that contain additional transmembrane and cytosolic kinases required for the initiation and specificity of immune signaling. PRR complexes are under tight control by protein phosphatases, E3 ligases, and other regulatory proteins, illustrating the exquisite and complex regulation of these molecular machines whose proper activation underlines a crucial layer of plant immunity. © 2014 Elsevier Inc.


Monaghan J.,Norwich Research Park | Zipfel C.,Norwich Research Park
Current Opinion in Plant Biology | Year: 2012

A key feature of innate immunity is the ability to recognize and respond to potential pathogens in a highly sensitive and specific manner. In plants, the activation of pattern recognition receptors (PRRs) by pathogen-associated molecular patterns (PAMPs) elicits a defense programme known as PAMP-triggered immunity (PTI). Although only a handful of PAMP-PRR pairs have been defined, all known PRRs are modular transmembrane proteins containing ligand-binding ectodomains. It is becoming clear that PRRs do not act alone but rather function as part of multi-protein complexes at the plasma membrane. Recent studies describing the molecular interactions and protein modifications that occur between PRRs and their regulatory proteins have provided important mechanistic insight into how plants avoid infection and achieve immunity. © 2012 Elsevier Ltd.


Lozano-Duran R.,Norwich Research Park | Zipfel C.,Norwich Research Park
Trends in Plant Science | Year: 2015

A balance between growth and immunity exists in plants. Recently, the growth-promoting hormones brassinosteroids (BR) have emerged as crucial regulators of the growth-immunity trade-off, although the molecular mechanisms underlying this role remained unclear. New evidence obtained from the model plant Arabidopsis thaliana points at an indirect crosstalk between BR signaling and immunity, mediated by the transcription factors BZR1 and HBI1, which suppress immunity upon BR perception. The core transcriptional cascade formed by BZR1 and HBI1 seems to act as a regulatory hub on which multiple signaling inputs impinge, ensuring effective fine-tuning of the trade-off between growth and immunity in a timely and cost-efficient manner. © 2014 Elsevier Ltd.


Zipfel C.,Norwich Research Park
Trends in Immunology | Year: 2014

Plants are constantly exposed to would-be pathogens in their immediate environment. Yet, despite relying on innate immunity only, plants are resistant to most microbes. They employ pattern-recognition receptors (PRRs) for sensitive and rapid detection of the potential danger caused by microbes and pests. Plant PRRs are either surface-localized receptor kinases (RKs) or receptor-like proteins (RLPs) containing various ligand-binding ectodomains that perceive pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). In this review, I summarize our current knowledge of plant PRRs and their ligands, illustrating the multiple molecular strategies employed by plant PRRs to activate innate immune signaling to survive. © 2014 Elsevier Ltd.


Robert-Seilaniantz A.,Norwich Research Park | Grant M.,University of Exeter | Jones J.D.G.,Norwich Research Park
Annual Review of Phytopathology | Year: 2011

Until recently, most studies on the role of hormones in plant-pathogen interactions focused on salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). It is now clear that pathogen-induced modulation of signaling via other hormones contributes to virulence. A picture is emerging of complex crosstalk and induced hormonal changes that modulate disease and resistance, with outcomes dependent on pathogen lifestyles and the genetic constitution of the host. Recent progress has revealed intriguing similarities between hormone signaling mechanisms, with gene induction responses often achieved by derepression. Here, we report on recent advances, updating current knowledge on classical defense hormones SA, JA, and ET, and the roles of auxin, abscisic acid (ABA), cytokinins (CKs), and brassinosteroids in molding plant-pathogen interactions. We highlight an emerging theme that positive and negative regulators of these disparate hormone signaling pathways are crucial regulatory targets of hormonal crosstalk in disease and defense. © 2011 by Annual Reviews. All rights reserved.


Segonzac C.,Norwich Research Park | Zipfel C.,Norwich Research Park
Current Opinion in Microbiology | Year: 2011

The first active layer of plant innate immunity relies on the recognition by surface receptors of molecules indicative of non-self or modified-self. The activation of pattern-recognition receptors (PRRs) by pathogen-associated molecular patterns (PAMPs) is in essence sufficient to stop pathogen invasion through transcriptional reprogramming and production of anti-microbials. The few PRR/PAMP pairs that are characterised provide useful models to study the specificity of ligand-binding and likely activation mechanisms. Both classical and new approaches are still required to identify new bacterial PAMPs. Current genetic screens, functional genomics and biochemical analyses have identified the regulation mechanisms of PRR transcription and biogenesis, provided insights into the composition of PRR complexes at the plasma membrane and highlighted the roles of long-known signalling components in PAMP-triggered immunity (PTI). © 2011 Elsevier Ltd.

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