Publications by authors named "Jakub Rzemieniewski"
Plant endogenous signaling peptides shape growth, development and adaptations to biotic and abiotic stress. Here, we identify C-TERMINALLY ENCODED PEPTIDEs (CEPs) as immune-modulatory phytocytokines in Arabidopsis thaliana. Our data reveals that CEPs induce immune outputs and are required to mount resistance against the leaf-infecting bacterial pathogen Pseudomonas syringae pv.
View Article and Find Full Text PDFRegulation of pattern-triggered immunity and growth by phytocytokines.
Curr Opin Plant Biol
August 2022
Article Synopsis
- Endogenous signalling peptides are crucial for plant growth, development, and responses to stress, functioning as both growth regulators and immune-modulatory agents.
- Recent studies have identified phytocytokines, which are peptides that also serve as danger signals, playing a dual role in both plant immunity and development.
- This review emphasizes the complex interactions between peptide signalling pathways that regulate various aspects of a plant's life, particularly in growth and pattern-triggered immunity (PTI).
Plants utilise intracellular nucleotide-binding, leucine-rich repeat (NLR) immune receptors to detect pathogen effectors and activate local and systemic defence. NRG1 and ADR1 "helper" NLRs (RNLs) cooperate with enhanced disease susceptibility 1 (EDS1), senescence-associated gene 101 (SAG101) and phytoalexin-deficient 4 (PAD4) lipase-like proteins to mediate signalling from TIR domain NLR receptors (TNLs). The mechanism of RNL/EDS1 family protein cooperation is not understood.
View Article and Find Full Text PDFPlant nucleotide binding/leucine-rich repeat (NLR) immune receptors are activated by pathogen effectors to trigger host defenses and cell death. Toll-interleukin 1 receptor domain NLRs (TNLs) converge on the ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) family of lipase-like proteins for all resistance outputs. In Arabidopsis () TNL-mediated immunity, EDS1 heterodimers with PHYTOALEXIN DEFICIENT4 (PAD4) transcriptionally induced basal defenses.
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