N-glycosylation facilitates the activation of a plant cell-surface receptor.

Plant receptor kinases (RKs) are critical for transmembrane signalling involved in various biological processes including plant immunity. MALE DISCOVERER1-INTERACTING RECEPTOR-LIKE KINASE 2 (MIK2) is a unique RK that recognizes a family of immunomodulatory peptides called SERINE-RICH ENDOGENOUS PEPTIDEs (SCOOPs) and activates pattern-triggered immunity responses. However, the precise mechanisms underlying SCOOP recognition and activation of MIK2 remain poorly understood.

DGK5 phosphorylation finetunes PA homeostasis in plant immunity.

Phosphatidic acid (PA) as a universal second messenger is transiently and rapidly produced upon immune activation in plants. A recent study by Kong et al. elucidated a mechanism for maintaining PA homeostasis via two uncoupled phosphorylation events of DIACYLGLYCEROL KINASE 5 (DGK5) at different phosphorylation sites by two distinct kinases.

WRR4B contributes to a broad-spectrum disease resistance against powdery mildew in Arabidopsis.

Oidium heveae HN1106, a powdery mildew (PM) that infects rubber trees, has been found to trigger disease resistance in Arabidopsis thaliana through ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1)-, PHYTOALEXIN DEFICIENT 4 (PAD4)- and salicylic acid (SA)-mediated signalling pathways. In this study, a typical TOLL-INTERLEUKIN 1 RECEPTOR, NUCLEOTIDE-BINDING, LEUCINE-RICH REPEAT (TIR-NB-LRR)-encoding gene, WHITE RUST RESISTANCE 4 (WRR4B), was identified to be required for the resistance against O. heveae in Arabidopsis.

Small holes, big impact: Stomata in plant-pathogen-climate epic trifecta.

The regulation of stomatal aperture opening and closure represents an evolutionary battle between plants and pathogens, characterized by adaptive strategies that influence both plant resistance and pathogen virulence. The ongoing climate change introduces further complexity, affecting pathogen invasion and host immunity. This review delves into recent advances on our understanding of the mechanisms governing immunity-related stomatal movement and patterning with an emphasis on the regulation of stomatal opening and closure dynamics by pathogen patterns and host phytocytokines.

Detection of Ligand-Induced Receptor Kinase and Signaling Component Phosphorylation with Mn-Phos-Tag SDS-PAGE.

Plasma membrane-resident receptor kinases (RKs) are crucial for plants to sense endogenous and exogenous signals in regulating growth, development, and stress response. Upon perception of ligands by the extracellular domain, RKs are usually activated by auto- and/or trans-phosphorylation of the cytoplasmic kinase domain, which in turn phosphorylates downstream substrates to relay the signaling. Therefore, monitoring ligand-induced in vivo phosphorylation dynamics of RKs and their associated proteins provides mechanistic insight into RK activation and downstream signal transduction.

Kinase fusion proteins: intracellular R-proteins in plant immunity.

Resistance (R) genes in the Triticeae tribe include not only genes encoding the canonical intracellular nucleotide-binding leucine-rich-repeat proteins (NLRs) but also genes encoding kinase fusion proteins (KFPs). Exploring these unconventional KFPs may expand the scope of effector-triggered immunity (ETI) and will have significant implications for crop improvement.

Bacteria manipulate host cells with channel-forming effectors.

Bacterial pathogens deliver effectors into host cells mostly to manipulate signaling and metabolic molecules, thereby subverting host immunity. A recent study by Nomura et al. demonstrates that certain effectors create membrane channels in host cells, enabling bacteria to access water and solutes for multiplication.

Maize MITOGEN-ACTIVATED PROTEIN KINASE 20 mediates high-temperature-regulated stomatal movement.

High temperature induces stomatal opening; however, uncontrolled stomatal opening is dangerous for plants in response to high temperature. We identified a high-temperature sensitive (hts) mutant from the ethyl methane sulfonate (EMS)-induced maize (Zea mays) mutant library that is linked to a single base change in MITOGEN-ACTIVATED PROTEIN KINASE 20 (ZmMPK20). Our data demonstrated that hts mutants exhibit substantially increased stomatal opening and water loss rate, as well as decreased thermotolerance, compared to wild-type plants under high temperature.

THESEUS1 activation by stress: isomerization and peptide perception?

Plant cell-wall perturbation upon environmental stress triggers adaptive cellular responses mediated by plasma membrane-resident sensors. We discuss a recent study by Bacete et al. showing that THESEUS1 (THE1) regulates plant cell adaptive responses to cell-wall disruption and update the working model for THE1 activation.

Phytocytokine signalling reopens stomata in plant immunity and water loss.

Stomata exert considerable effects on global carbon and water cycles by mediating gas exchange and water vapour. Stomatal closure prevents water loss in response to dehydration and limits pathogen entry. However, prolonged stomatal closure reduces photosynthesis and transpiration and creates aqueous apoplasts that promote colonization by pathogens.

Plant elicitor peptide 1 fortifies root cell walls and triggers a systemic root-to-shoot immune signaling in .

Plant immunity is initiated by cell surface-localized receptors upon perception of pathogen-derived microbe or pathogen-associated molecular patterns (MAMPs/PAMPs), damage/danger-associated molecular patterns (DAMPs), and phytocytokines. Different patterns activate highly overlapping immune signaling at the early stage but divergent physiological responses at the late stage. Here, we indicate that plant elicitor peptide 1 (Pep1), a well-known DAMP, induces lignin and callose depositions, two types of late immune responses for strengthening the plant cell wall.

Phytocytokines function as immunological modulators of plant immunity.

Plant plasma membrane-resident immune receptors regulate plant immunity by recognizing microbe-associated molecular patterns (MAMPs), damage-associated molecular patterns (DAMPs), and phytocytokines. Phytocytokines are plant endogenous peptides, which are usually produced in the cytosol and released into the apoplast when plant encounters pathogen infections. Phytocytokines regulate plant immunity through activating an overlapping signaling pathway with MAMPs/DAMPs with some unique features.

Stress-induced activation of receptor signaling by protease-mediated cleavage.

Plants encode a large number of proteases in activating intracellular signaling through proteolytic cleavages of various protein substrates. One type of the substrates is proligands, including peptide hormones, which are perceived by cell surface-resident receptors. The peptide hormones are usually first synthesized as propeptides, and then cleaved by specific proteases for activation.

The LRR-RLK Protein HSL3 Regulates Stomatal Closure and the Drought Stress Response by Modulating Hydrogen Peroxide Homeostasis.

Guard cells shrink in response to drought stress and abscisic acid (ABA) signaling, thereby reducing stomatal aperture. Hydrogen peroxide (HO) is an important signaling molecule acting to induce stomatal closure. As yet, the molecular basis of control over the level of HO in the guard cells remains largely unknown.

PAMP-induced peptide 1 cooperates with salicylic acid to regulate stomatal immunity in .

Various pathogenic species are capable of penetrating plant leaves through stomata on the leaf surface for propagation by absorbing nutrients in plant interiors. Plants have evolved abilities to close stomata to restrict pathogen infections. The model plant () closes stomata when FLAGELLIN SENSING2 (FLS2), a receptor protein localized in the plasma membrane (PM) of stomatal guard cells, detects flagellin, a pathogen-associated molecular pattern (PAMP) derived from the bacterial pathogen .

Cleave and Unleash: Metacaspases Prepare Peps for Work.

Plant elicitor peptide 1 (Pep1) is a versatile immune modulator that is involved in plant defense against herbivores and pathogens. A recent study (Hander et al., Science, 2019) has uncovered that Arabidopsis thaliana Pep1 is released from the C-terminus of the tonoplast-resident precursor protein, PROPEP1, by Ca-activated metacaspases upon cell membrane rupture in damaged tissues.

Damage-Associated Molecular Pattern-Triggered Immunity in Plants.

As a universal process in multicellular organisms, including animals and plants, cells usually emit danger signals when suffering from attacks of microbes and herbivores, or physical damage. These signals, termed as damage-associated molecular patterns (DAMPs), mainly include cell wall or extracellular protein fragments, peptides, nucleotides, and amino acids. Once exposed on cell surfaces, DAMPs are detected by plasma membrane-localized receptors of surrounding cells to regulate immune responses against the invading organisms and promote damage repair.

The cloak, dagger, and shield: proteases in plant-pathogen interactions.

Plants sense the presence of pathogens or pests through the recognition of evolutionarily conserved microbe- or herbivore-associated molecular patterns or specific pathogen effectors, as well as plant endogenous danger-associated molecular patterns. This sensory capacity is largely mediated through plasma membrane and cytosol-localized receptors which trigger complex downstream immune signaling cascades. As immune signaling outputs are often associated with a high fitness cost, precise regulation of this signaling is critical.

IDL6-HAE/HSL2 impacts pectin degradation and resistance to Pseudomonas syringae pv tomato DC3000 in Arabidopsis leaves.

Plant cell walls undergo dynamic structural and chemical changes during plant development and growth. Floral organ abscission and lateral root emergence are both accompanied by cell-wall remodeling, which involves the INFLORESCENCE DEFICIENT IN ABSCISSION (IDA)-derived peptide and its receptors, HAESA (HAE) and HAESA-LIKE2 (HSL2). Plant cell walls also act as barriers against pathogenic invaders.

Characterization of the interaction between Oidium heveae and Arabidopsis thaliana.

Oidium heveae, an obligate biotrophic pathogen of rubber trees (Hevea brasiliensis), causes significant yield losses of rubber worldwide. However, the molecular mechanisms underlying the interplay between O. heveae and rubber trees remain largely unknown.

The secreted peptide PIP1 amplifies immunity through receptor-like kinase 7.

In plants, innate immune responses are initiated by plasma membrane-located pattern recognition receptors (PRRs) upon recognition of elicitors, including exogenous pathogen-associated molecular patterns (PAMPs) and endogenous damage-associated molecular patterns (DAMPs). Arabidopsis thaliana produces more than 1000 secreted peptide candidates, but it has yet to be established whether any of these act as elicitors. Here we identified an A.

One-step expression and tyrosine O-sulfonation of Ax21 in Escherichia coli.

Ax21 (activator of Xa21-mediated immunity), a pathogen-associated molecular pattern secreted by Xanthomonas oryzae pv. oryzae, can be perceived by a membrane-located pattern recognition receptor Xa21 and triggered immune responses in rice. An Ax21-derived peptide (17-amino acid) containing a sulfated tyrosine-22 (axY(S)22) is sufficient for Ax21 activity.

Pseudomonas syringae pv. phaseolicola effector HopF1 inhibits pathogen-associated molecular pattern-triggered immunity in a RIN4-independent manner in common bean (Phaseolus vulgaris).

Plant pathogens usually promote pathogenesis by secreting effector proteins into host plant cells. One of the secreted effectors of Pseudomonas syringae pv. phaseolicola, the causative agent of halo-blight disease in common bean (Phaseolus vulgaris), HopF1, activates effector-triggered immunity (ETI) in a bean cultivar containing R1 resistance gene, but displays virulence function in a bean cultivar without the R1 gene.

Plant immunity: evolutionary insights from PBS1, Pto, and RIN4.

Two layers of plant immune systems are used by plants to defend against phytopathogens. The first layer is pathogen-associate molecular patterns (PAMPs)-triggered immunity (PTI), which is activated by plant cell-surface pattern recognition receptors (PRRs) upon perception of microbe general elicitors. The second layer is effector-triggered immunity (ETI), which is initiated by specific recognition of pathogen type III secreted effectors (T3SEs) with plant intracellular resistance (R) proteins.