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Steven H. Spoel

Researcher at University of Edinburgh

Publications -  54
Citations -  9535

Steven H. Spoel is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Proteasome & S-Nitrosylation. The author has an hindex of 30, co-authored 50 publications receiving 8316 citations. Previous affiliations of Steven H. Spoel include Duke University & Utrecht University.

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NPR1 Modulates Cross-Talk between Salicylate- and Jasmonate-Dependent Defense Pathways through a Novel Function in the Cytosol

TL;DR: Analysis of the Arabidopsis mutant npr1 revealed that the antagonistic effect of SA on JA signaling requires the regulatory protein NPR1, indicating that cross-talk between SA and JA is modulated through a novel function of NPR1 in the cytosol.
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Plant Immunity Requires Conformational Charges of NPR1 via S-Nitrosylation and Thioredoxins

TL;DR: It is reported that S-nitrosylation of NPR1 by S-Nitrosoglutathione at cysteine-156 facilitates its oligomerization, which maintains protein homeostasis upon SA induction, and suggest a link between pathogen-triggered redox changes and gene regulation in plant immunity.
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How do plants achieve immunity? Defence without specialized immune cells

TL;DR: Recent developments point towards a multilayered plant innate immune system comprised of self-surveillance, systemic signalling and chromosomal changes that together establish effective immunity.
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NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants

TL;DR: It is shown that the NPR1 paralogues NPR3 and NPR4 are SA receptors that bind SA with different affinities, and that this mutant is defective in pathogen effector-triggered programmed cell death and immunity.
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Regulation of tradeoffs between plant defenses against pathogens with different lifestyles

TL;DR: This work shows that plants tightly control cross-talk between SA- and JA-dependent defenses in a previously unrecognized spatial and pathogen type-specific fashion, which allows them to prevent unfavorable signal interactions and maximize their ability to concomitantly fend off multiple pathogens.