Publications by authors named "Petra Boevink"

Endocytosis is an essential cellular process that uptakes substances into cells at the plasma membrane from the extracellular space and plays a major role in plant development and responses to environmental stimuli. Research has shown that plant membrane-resident proteins are endocytosed and transported into plant endosomes in response to pathogen-secreted elicitors. However, there is no conclusive experimental evidence demonstrating how secreted cytoplasmic effectors from oomycetes and fungi enter host cells during infection.

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Article Synopsis
  • Plants adapt to environmental stress by altering growth and development, with calcium (Ca) playing a crucial role as a secondary messenger in response to these stressors.
  • The bi-directional dual-flow RootChip (bi-dfRC) platform was used to study root growth and defense signaling by simulating salinity stress with sodium chloride (NaCl) treatment, revealing a concentration-dependent calcium burst that spreads from the stele to the root tip.
  • Research also demonstrated that salinity impacts root growth differently depending on root architecture, with varying responses observed and novel insights gained into root force sensing through engineered microfluidic channels.
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Arg-any amino acid-Leu-Arg (RXLR) effectors are central oomycete virulence factors that suppress plant immunity. Relatively little is known about how they are processed post-translationally before delivery into host cells. A range of molecular, cell and biochemical processes were used to investigate proteolytic processing of RXLR and Glu-Glu-Arg (EER) motifs in Phytophthora infestans effectors.

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Chloroplasts regulate plant development and immunity. Here we report that potato chloroplast elongation factors StTuA and StTuB, targeted by Phytophthora infestans RXLR effector Pi22926, positively regulate immunity and growth. Plants expressing Pi22926, or silenced for TuA/B, show increased P.

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Cytoplasmic effectors with an Arg-any amino acid-Arg-Leu (RxLR) motif are encoded by hundreds of genes within the genomes of oomycete spp. and downy mildew pathogens. There has been a dramatic increase in our understanding of the evolution, function, and recognition of these effectors.

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Recent findings demonstrate that cytoplasmic effectors from fungal and oomycete pathogens enter plant cells via clathrin-mediated endocytosis (CME). This raises several questions: Does effector secretion pathway facilitate host uptake? How is CME triggered in host cells? How are the effectors released from endosomal compartments to reach diverse subcellular destinations?

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Recent research demonstrates that undermining interactions between pathogen effectors and their host target proteins can reduce infection. As more effector-target pairs are identified, their structures and interaction surfaces exposed, and there is the possibility of making multiple edits to diverse plant genomes, the desire to convert crops to nonhosts could become reality.

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Filamentous (oomycete and fungal) plant pathogens deliver cytoplasmic effector proteins into host cells to facilitate disease. How RXLR effectors from the potato late blight pathogen Phytophthora infestans enter host cells is unknown. One possible route involves clathrin-mediated endocytosis (CME).

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Plants are resistant to most microbial species due to nonhost resistance (NHR), providing broad-spectrum and durable immunity. However, the molecular components contributing to NHR are poorly characterised. We address the question of whether failure of pathogen effectors to manipulate nonhost plants plays a critical role in NHR.

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Oomycete pathogens secrete hundreds of cytoplasmic RxLR effectors to modulate host immunity by targeting diverse plant proteins. Revealing how effectors manipulate host proteins is pivotal to understanding infection processes and to developing new strategies to control plant disease. Here we show that the Phytophthora infestans RxLR effector Pi22798 interacts in the nucleus with a potato class II knotted-like homeobox (KNOX) transcription factor, StKNOX3.

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The growing concern regarding the potential risks of pesticides and their impact on nontarget organisms stimulates the development and application of alternative, environmentally friendly products. It seems necessary to develop alternatives for conventional products and for those already widely used in organic agriculture, e.g.

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Phytophthora species cause some of the most serious diseases of trees and threaten forests in many parts of the world. Despite the generation of genome sequence assemblies for over 10 tree-pathogenic Phytophthora species and improved detection methods, there are many gaps in our knowledge of how these pathogens interact with their hosts. To facilitate cell biology studies of the infection cycle we examined whether the tree pathogen Phytophthora kernoviae could infect the model plant Nicotiana benthamiana.

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The ability to secrete effector proteins that can enter plant cells and manipulate host processes is a key determinant of what makes a successful plant pathogen. Here, we review intracellular effectors from filamentous (fungal and oomycete) phytopathogens and the host proteins and processes that are targeted to promote disease. We cover contrasting virulence strategies and effector modes of action.

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spp. secrete vast arrays of effector molecules during infection to aid in host colonization. The crinkling and necrosis (CRN) protein family forms an extensive repertoire of candidate effectors that accumulate in the host nucleus to perturb processes required for immunity.

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Ubiquitination is a post-translational modification that regulates many processes in plants. Several ubiquitin E3 ligases act as either positive or negative regulators of immunity by promoting the degradation of different substrates. StPUB17 is an E3 ligase that has previously been shown to positively regulate immunity to bacteria, fungi and oomycetes, including the late blight pathogen .

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An understanding of the cell biology underlying the burgeoning molecular genetic and genomic knowledge of oomycete pathogenicity is essential to gain the full context of how these pathogens cause disease on plants. An intense research focus on secreted Phytophthora effector proteins, especially those containing a conserved N-terminal RXLR motif, has meant that most cell biological studies into Phytophthora diseases have focussed on the effectors and their host target proteins. While these effector studies have provided novel insights into effector secretion and host defence mechanisms, there remain many unanswered questions about fundamental processes involved in spore biology, host penetration and haustorium formation and function.

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The potato blight agent Phytophthora infestans secretes a range of RXLR effectors to promote disease. Recent evidence indicates that some effectors suppress early pattern-triggered immunity (PTI) following perception of microbe-associated molecular patterns (MAMPs). Phytophthora infestans effector PiSFI3/Pi06087/PexRD16 has been previously shown to suppress MAMP-triggered pFRK1-Luciferase reporter gene activity.

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Oomycetes such as the potato blight pathogen Phytophthora infestans deliver RXLR effectors into plant cells to manipulate host processes and promote disease. Knowledge of where they localize inside host cells is important in understanding their function. Fifty-two P.

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The oomycete potato blight pathogen secretes a diverse set of proteins to manipulate host plant immunity. However, there is limited knowledge about how and where they are secreted during infection. Here we used the endoplasmic reticulum (ER)-to-Golgi secretion pathway inhibitor brefeldin A (BFA) in combination with liquid chromatography-electrospray tandem mass spectrometry (LC-MS/MS) to identify extracellular proteins from that were conventionally secreted from -cultured hyphae.

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Plant pathogens deliver effectors into plant cells to suppress immunity. Whereas many effectors inactivate positive immune regulators, other effectors associate with negative regulators of immunity: so-called susceptibility (S) factors. Little is known about how pathogens exploit S factors to suppress immunity.

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Pathogens secrete effector proteins to interfere with plant innate immunity, in which Ca /calmodulin (CaM) signalling plays key roles. Thus far, few effectors have been identified that directly interact with CaM for defence suppression. Here, we report that SFI5, an RXLR effector from Phytophthora infestans, suppresses microbe-associated molecular pattern (MAMP)-triggered immunity (MTI) by interacting with host CaMs.

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Plant pathogens deliver effectors to manipulate processes in their hosts, creating a suitable environment for invasion and proliferation. Yet, little is known about the host proteins that are targeted by effectors from filamentous pathogens. Here, we show that stable transgenic expression in potato () and transient expression in of the arginine-any amino acid-leucine-arginine effector Pi17316 enhances leaf colonization by the late blight pathogen Expression of Pi17316 also attenuates cell death triggered by the pathogen-associated molecular pattern Infestin1 (INF1), indicating that the effector suppresses pattern-triggered immunity.

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This article comments on: 2017. Plant extracellular vesicles are incorporated by a fungal pathogen and inhibit its growth. Journal of Experimental Botany 5485–5495.

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The potato blight pathogen Phytophthora infestans secretes effector proteins that are delivered inside (cytoplasmic) or can act outside (apoplastic) plant cells to neutralize host immunity. Little is known about how and where effectors are secreted during infection, yet such knowledge is essential to understand and combat crop disease. We used transient Agrobacterium tumefaciens-mediated in planta expression, transformation of P.

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An emerging area in plant research focuses on antagonism between regulatory systems governing growth and immunity. Such cross talk represents a point of vulnerability for pathogens to exploit. AVR2, an RXLR effector secreted by the potato blight pathogen , interacts with potato BSL1, a putative phosphatase implicated in growth-promoting brassinosteroid (BR) hormone signaling.

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