Receptor-like Kinase Research Articles

A large-scale screening identifies receptor-like kinases with common features in kinase domains that are potentially related to disease resistance in planta

IntroductionThe plant genome encodes a plethora of proteins with structural similarity to animal receptor protein kinases, collectively known as receptor-like protein kinases (RLKs), which predominantly localize to the plasma membrane where they activate their kinase domains to convey extracellular signals to the interior of the cell, playing crucial roles in various signaling pathways. Despite the large number of members within the RLK family, to date, only a few have been identified as pattern-recognition receptors (PRRs), leaving many potential RLKs that could play roles in plant immunity undiscovered.MethodsIn this study, a recombinant strategy was initially employed to screen the kinase domains of 133 RLKs in the Arabidopsis genome to determine their involvement in the pathogen-triggered immunity (PTI) pathway. Subsequently, 6 potential immune-related recombinant RLKs (rRLKs) were selected for the creation of transgenic materials and underwent functional characterization analysis. Finally, a sequence analysis was conducted on the kinase domains of these 133 RLKs as well as the known immune RLK receptor kinase domains from other species.ResultsIt was found that 24 rRLKs activated the PTI response in Arabidopsis fls2 mutant protoplasts following flg22 treatment. Consistently, when 6 of these rRLKs were individually expressed in fls2 background, they exhibited diverse PTI signal transduction capabilities via different pathways while all retained membrane localization. Intriguingly, sequence analysis revealed multiple conserved amino acid sites within kinase domains of these experimentally identified immune-related RLKs in Arabidopsis. Importantly, these patterns are also preserved in RLKs involved in PTI in other species.DiscussionThis study, on one hand, identifies common features that theoretically can enhance our understanding of immune-related RLKs and facilitate the discovery of novel immune-related RLKs in the future. On the other hand, it provides experimental evidence for the use of recombinant technique to develop diverse rRLKs for molecular breeding, thereby conferring high resistance to plants without compromising their normal growth and development.

The Multifaceted Ubiquitination of BIK1 During Plant Immunity in Arabidopsis thaliana

As sessile organisms, the plant immune system plays a vital role in protecting plants from the widespread pathogens in the environment. The Arabidopsis thaliana (Arabidopsis) receptor-like cytoplasmic kinase BOTRYTIS-INDUCED KINASE1 (BIK1) acts as a central regulator during plant immunity. As such, not only the BIK1 protein accumulation but also the attenuation is tightly regulated to ensure effective immune responses. Recent studies have highlighted the critical roles of ubiquitination in maintaining BIK1 homeostasis. Here, we review the latest advances in the ubiquitination of BIK1 in plant immunity, which is mediated by ubiquitin ligases PUB25/26, RHA3A/B, RGLG1/2, and PUB4. Additionally, we summarize and discuss the sites and types of BIK1 ubiquitination. Collectively, these analyses not only illustrate that the differential modifications on BIK1 by multiple ubiquitin ligases hold a crucial position in plant immunity but also provide a good example for future studies on ubiquitin-mediated modifications in plants.

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. Here we present the cryogenic electron microscopy structure of a ternary complex consisting of the extracellular leucine-rich repeat (LRR) of MIK2 (MIK2LRR), SCOOP12 and the extracellular LRR of the co-receptor BAK1 (BAK1LRR) at a resolution of 3.34 Å. The structure reveals that a DNHH motif in MIK2LRR plays a critical role in specifically recognizing the highly conserved SxS motif of SCOOP12. Furthermore, the structure demonstrates that N-glycans at MIK2LRRAsn410 directly interact with the N-terminal capping region of BAK1LRR. Mutation of the glycosylation site, MIK2LRRN410D, completely abolishes the SCOOP12-independent interaction between MIK2LRR and BAK1LRR and substantially impairs the assembly of the MIK2LRR-SCOOP12-BAK1LRR complex. Supporting the biological relevance of N410-glycosylation, MIK2N410D substantially compromises SCOOP12-triggered immune responses in plants. Collectively, these findings elucidate the mechanism underlying the loose specificity of SCOOP recognition by MIK2 and reveal an unprecedented mechanism by which N-glycosylation modification of LRR-RK promotes receptor activation.

The Arabidopsis receptor-like kinase WAKL4 limits cadmium uptake via phosphorylation and degradation of NRAMP1 transporter

Cadmium (Cd) is a detrimental heavy metal propagated from soil to the food chain via plants, posing a great risk to human health upon consumption. Despite the understanding of Cd tolerance mechanisms in plants, whether and how plants actively respond to Cd and in turn restrict its uptake and accumulation remain elusive. Here, we identify a cell wall-associated receptor-like kinase 4 (WAKL4) involved in specific tolerance to Cd stress. We show that Cd rapidly and exclusively induces WAKL4 accumulation by promoting WAKL4 transcription and blocking its vacuole-dependent proteolysis in roots. The accumulated WAKL4 next interacts with and phosphorylates the Cd transporter NRAMP1 at Tyr488, leading to the enhanced ubiquitination and vacuole-dependent degradation of NRAMP1, and consequently reducing Cd uptake. Our findings therefore uncover a mechanism conferred by the WAKL4-NRAMP1 module that enables plants to actively respond to Cd and limit its uptake, informing the future molecular breeding of low Cd accumulated crops or vegetables.

Recognition of a Fungal Effector Potentiates Pathogen-Associated Molecular Pattern-Triggered Immunity in Cotton.

Plants are equipped with multi-layered immune systems that recognize pathogen-derived elicitors to activate immunity. Verticillium dahliae is a soil-borne fungus that infects a broad range of plants and causes devastating wilt disease. The mechanisms underlying immune recognition between plants and V. dahliae remain elusive. Here, a V. dahliae secretory protein, elicitor of plant defense gene (VdEPD1), acts as an elicitor that triggers defense responses in both Nicotiana benthamiana and cotton plants is identified. Targeted gene deletion of VdEPD1 enhances V. dahliae virulence in plants. Expression of VdEPD1 triggers the accumulation of reactive oxygen species (ROS) and the activation of cell death in cotton plants. Gossypium barbadense EPD1-interacting receptor-like cytoplasmic kinase (GbEIR5A) and GbEIR5D interact with VdEPD1. Silencing of GbEIR5A/D significantly impairs VdEPD1-triggered cell death in cotton plants, indicating the contribution of GbEIR5A/D to VdEPD1-activated effector-triggered immunity (ETI). VdEPD1 stimulates the expression of GbEIR5A and GbEIR5D in cotton plants. Interestingly, cotton plants with silenced GbEIR5A/D genes exhibit compromised pathogen-associated molecular patterns (PAMPs)-triggered ROS accumulation, whereas overexpression of GbEIR5A or GbEIR5D enhances PAMP-induced ROS. These findings indicate that recognition of VdEPD1 potentiates GbEIRs to enhance cotton PAMP-triggered immunity (PTI), uncovering a cooperative interplay of PTI and ETI in cotton.

Upstairs, Downstairs - conserved and divergent CLAVATA signalling in shoot meristem development and root symbioses.

The CLV3/EMBRYO-SURROUNDING REGION (CLE) peptides control plant development and response to the environment. Key conserved roles include the regulation of shoot apical meristems and the long-distance control of root colonisation by nutrient-acquiring microbes, including the widespread symbioses with arbuscular mycorrhizal fungi and nodulation with nitrogen-fixing bacteria in legumes. At least some signalling elements appear to operate across both processes but clear gaps in our understanding remain. In legumes, although CLE peptide signalling has been examined in detail in symbioses, the role of this pathway in SAM development of legumes is poorly understood. In this Research in Context, we review the literature to clarify the conserved and divergent elements of the CLAVATA-CLE peptide signalling pathways that control SAM, mycorrhizal colonisation and nodulation. We used novel pea mutants to determine the role of CLE signalling in regulating SAM development of a model legume, including interaction with temperature. We found that in pea both genetic and environmental buffering of the CLE pathway influences SAM development. In pea, the CLAVATA2 (CLV2) CLE receptor-like protein and the unknown gene product encoded by the K301 gene are required to limit SAM size and floral organ production under cool temperatures. In contrast, the CLAVATA1 receptor-like kinase promotes SAM proliferation and appears to do so via a CLV2-independent pathway. In contrast, we found no role for the RDN1 enzyme, capable of arabinosylating CLE peptides, in SAM development. Future studies in other legumes are required to examine the role of other CLE peptide signalling elements in SAM control. Studies in non-vascular mycorrhizal hosts could explore if symbioses control is also an ancestral role for this signalling pathway.

A novel protein elicitor (Cs08297) from Ciboria shiraiana enhances plant disease resistance.

Ciboria shiraiana is a necrotrophic fungus that causes mulberry sclerotinia disease resulting in huge economic losses in agriculture. During infection, the fungus uses immunity elicitors to induce plant tissue necrosis that could facilitate its colonization on plants. However, the key elicitors and immune mechanisms remain unclear in C. shiraiana. Herein, a novel elicitor Cs08297 secreted by C. shiraiana was identified, and it was found to target the apoplast in plants to induce cell death. Cs08297 is a cysteine-rich protein unique to C. shiraiana, and cysteine residues in Cs08297 were crucial for its ability to induce cell death. Cs08297 induced a series of defence responses in Nicotiana benthamiana, including the burst of reactive oxygen species (ROS), callose deposition, and activation of defence-related genes. Cs08297 induced-cell death was mediated by leucine-rich repeat (LRR) receptor-like kinases BAK1 and SOBIR1. Purified His-tagged Cs08297-thioredoxin fusion protein triggered cell death in different plants and enhanced plant resistance to diseases. Cs08297 was necessary for sclerotial development, oxidative-stress adaptation, and cell wall integrity but negatively regulated virulence of C. shiraiana. In conclusion, our results revealed that Cs08297 is a novel fungal elicitor in fungi inducing plant immunity. Furthermore, its potential to enhance plant resistance provides a new target to control agricultural diseases biologically.

CDK6-mediated endothelial cell cycle acceleration drives arteriovenous malformations in hereditary hemorrhagic telangiectasia.

Increased endothelial cell proliferation is a hallmark of arteriovenous malformations (AVMs) in hereditary hemorrhagic telangiectasia (HHT). Here, we report a cyclin-dependent kinase 6 (CDK6)-driven mechanism of cell cycle deregulation involved in endothelial cell proliferation and HHT pathology. Specifically, endothelial cells from the livers of HHT mice bypassed the G1/S checkpoint and progressed through the cell cycle at an accelerated pace. Phosphorylated retinoblastoma (pRB1)-a marker of G1/S transition through the restriction point-accumulated in endothelial cells from retinal AVMs of HHT mice and endothelial cells from skin telangiectasia samples from HHT patients. Mechanistically, inhibition of activin receptor-like kinase 1 signaling increased key restriction point mediators, and treatment with the CDK4/6 inhibitors palbociclib or ribociclib blocked increases in pRB1 and retinal AVMs in HHT mice. Palbociclib also improved vascular pathology in the brain and liver, and slowed cell cycle progression in endothelial cells and endothelial cell proliferation. Endothelial cell-specific deletion of CDK6 was sufficient to protect HHT mice from AVM pathology. Thus, clinically approved CDK4/6 inhibitors might have the potential to be repurposed for HHT.

A peptide-receptor module links cell wall integrity sensing to pattern-triggered immunity.

Plants employ cell-surface receptors to perceive non- or altered-self, including the integrity of their cell wall. Here we identify a specific ligand-receptor module responsive to cell wall damage that potentiates immunity in Arabidopsis. Disruption of cell wall integrity by inhibition of cellulose biosynthesis promotes pattern-triggered immunity transcriptionally in a manner dependent on the receptor kinase MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2 (MIK2). Notably, while MIK2 can perceive peptides of the large SERINE RICH ENDOGENOUS PEPTIDE family, a single member of this family, SCOOP18, is transcriptionally induced upon cell wall damage and is required for subsequent responses such as lignification and immunity potentiation. Collectively, our results identify the SCOOP18-MIK2 ligand-receptor module as an important central hub, connecting plant cell wall integrity sensing with immunity.

SCOOP10 And SCOOP12 Peptides Act Through MIK2 Receptor-Like Kinase to Antagonistically Regulate Arabidopsis Leaf Senescence

Leaf senescence plays a critical role in a plant's overall reproductive success due to its involvement in nutrient remobilization and allocation. However, our current understanding of the molecular mechanisms controlling leaf senescence remains limited. In this study, we demonstrate that the receptor-like kinase MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2 (MIK2) functions as a negative regulator of leaf senescence. We report that the SERINE-RICH ENDOGENOUS PEPTIDE 12, previously known to physically interact with MIK2, competes with SCOOP10 to control MIK2-dependent senescence regulatory mechanisms. We observed that increased expression of SCOOP10 or the application of exogenous SCOOP10 peptides accelerated leaf senescence in a MIK2-dependent manner. Conversely, SCOOP12 acted as a suppressor of MIK2-dependent senescence regulation. We also found that SCOOP12 enhanced while SCOOP10 diminished MIK2 phosphorylation. Thus, the SCOOP12-MIK2 module might function antagonistically on SCOOP10-MIK2 signaling at late senescing stages, allowing for fine-tuned modulation of the leaf senescence process. Our research sheds light on the complex mechanisms underlying leaf senescence and provides valuable insights into the interplay between receptors, peptides, and the regulation of plant senescence.

Arabidopsis uses a molecular grounding mechanism and a biophysical circuit breaker to limit floral abscission signaling

Abscission is the programmed separation of plant organs. It is widespread in the plant kingdom with important functions in development and environmental response. In Arabidopsis, abscission of floral organs (sepals, petals, and stamens) is controlled by two receptor-like protein kinases HAESA (HAE) and HAESA LIKE-2 (HSL2), which orchestrate the programmed dissolution of the abscission zone connecting floral organs to the developing fruit. In this work, we use single-cell RNA sequencing to characterize the core HAE/HSL2 abscission gene expression program. We identify the MAP KINASE PHOSPHATASE-1/MKP1 gene as a negative regulator of this pathway. MKP1 acts prior to activation of HAE/HSL2 signaling to establish a signaling threshold required for the initiation of abscission. Furthermore, we use single-cell data to identify genes expressed in two subpopulations of abscission zone cells: those proximal and those distal to the plane of separation. We identify INFLORESCENCE DEFICIENT IN ABSCISSION/IDA family genes, encoding activating ligands of HAE/HSL2, as enriched in distal abscission zone cells at the base of the abscising organs. We show how this expression pattern forms a biophysical circuit breaker whereby, when the organ is shed, the source of the IDA peptides is removed, leading to cessation of HAE/HSL2 signaling. Overall, this work provides insight into the multiple control mechanisms acting on the abscission-signaling pathway.

A novel LRR receptor-like kinase BRAK reciprocally phosphorylates PSKR1 to enhance growth and defense in tomato.

Plants face constant threats from pathogens, leading to growth retardation and crop failure. Cell-surface leucine-rich repeat receptor-like kinases (LRR-RLKs) are crucial for plant growth and defense, but their specific functions, especially to necrotrophic fungal pathogens, are largely unknown. Here, we identified an LRR-RLK (Solyc06g069650) in tomato (Solanum lycopersicum) induced by the economically important necrotrophic pathogen Botrytis cinerea. Knocking out this LRR-RLK reduced plant growth and increased sensitivity to B. cinerea, while its overexpression led to enhanced growth, yield, and resistance. We named this LRR-RLK as BRAK (B. cinerea resistance-associated kinase). Yeast two-hybrid screen revealed BRAK interacted with phytosulfokine (PSK) receptor PSKR1. PSK-induced growth and defense responses were impaired in pskr1, brak single and double mutants, as well as in PSKR1-overexpressing plants with silenced BRAK. Moreover, BRAK and PSKR1 phosphorylated each other, promoting their interaction as detected by microscale thermophoresis. This reciprocal phosphorylation was crucial for growth and resistance. In summary, we identified BRAK as a novel regulator of seedling growth, fruit yield and defense, offering new possibilities for developing fungal disease-tolerant plants without compromising yield.

Human Cripto-1 and Cripto-3 Protein Expression in Normal and Malignant Settings That Conflicts with Established Conventions

Background/Objectives: Cripto-1 (CR1) is a plurifunctional embryonic protein required for implantation and re-expressed in the adult during wound repair, inflammation, and tumorigenesis. CR1 and its predicted CR1 pseudogene product Cripto-3/CR3 are highly homologous proteins, and given this physical attribute, commercially available antibodies cannot discriminate between CR1 and CR3. Methods: A series of mouse monoclonal antibodies [MoAbs] were developed with a high-affinity binding that can differentiate human CR1/CR3 proteins and showed no measurable cross-reactivity. Results: Using these reagents, we confirm that CR3 is a bona fide translated protein found in human tumor tissue, cancer cell lysates, and in normal/cancer patient donor sera. We also reveal that CR1 and CR3 compete for binding to signal transduction protein Nodal, glucose-regulated protein 78Da (GRP78), and activin receptor-like kinase 4 (Alk4). Our discriminatory MoAbs provide new reagents to help clarify current CR1/CR3 protein expression vagaries in the Cripto field of study, challenging established CR1 conventions. In addition, our data validate CR3 involvement in human carcinogenesis and cell signaling pathways, with potential clinical relevance in determining cancer patient prognosis and disease severity.

Heat stress causes chromatin accessibility and related gene expression changes in crown tissues of barley (Hordeum vulgare).

Plant responses to stress caused by high temperatures involve changes occurring at the molecular, metabolic, and physiological levels. Understanding the mechanisms by which plants recognize signals to activate this response is a prerequisite for identifying key genes and signaling pathways and for obtaining heat-tolerant plants. We demonstrated the first implementation of an assay for transposase-accessible chromatin to identify open chromatin regions (OCRs) in crown tissues of barley using three genotypes carrying different allelic forms of the sdw1 gene encoding gibberellin 20-oxidase subjected to elevated temperatures. In parallel, we performed gene expression analysis, which allowed us to relate changes in chromatin state to changes in transcriptional activity. The obtained data revealed that the hypersensitive chromatin regions within the genes were more repeatable than those outside the gene intervals. We observed that prolonged exposure to high temperatures increased chromatin accessibility. Genes with OCRs in their regulatory regions were involved in stress signaling and tolerance, including calcium-dependent protein kinase, mitogen-activated protein kinase (MAPK3), receptor-like cytoplasmic kinase (RLK), TIFY domain-containing transcriptional regulator, bZIP transcription factor, and regulatory protein NPR1. The effect of genotype on gene expression was not as pronounced as that of temperature. By combining results from the differential analysis of chromatin accessibility and expression profiles, we identified genes with high temperature-induced changes in chromatin accessibility associated with expression alterations. Importantly, our data revealed a relationship between the loss of chromatin accessibility in response to heat and the downregulation of genes related to gibberellin signaling.

Osmotic signaling releases PP2C-mediated inhibition of Arabidopsis SnRK2s via the receptor-like cytoplasmic kinase BIK1.

Osmotic stress and abscisic acid (ABA) signaling are important for plant growth and abiotic stress resistance. Activation of osmotic and ABA signaling downstream of the PYL-type ABA receptors requires the release of SnRK2 protein kinases from the inhibition imposed by PP2Cs. PP2Cs are core negative regulators that constantly interact with and inhibit SnRK2s, but how osmotic signaling breaks the PP2C inhibition of SnRK2s remains unclear. Here, we report that an Arabidopsis receptor-like cytoplasmic kinase, BIK1, releases PP2C-mediated inhibition of SnRK2.6 via phosphorylation regulation. The dominant abi1-1 ABA-signaling mutation (G180D) disrupts PYL-PP2C interactions and disables PYL-initiated release of SnRK2s; in contrast, BIK1 releases abi1-1-mediated inhibition of SnRK2.6. BIK1 interacts with and phosphorylates SnRK2.6 at two tyrosine residues, which are critical for SnRK2.6 activation and function. Phosphorylation of the two tyrosine residues may affect the docking of the tryptophan "lock" of PP2C into SnRK2.6. Moreover, the bik1 mutant is defective in SnRK2 activation, stress-responsive gene expression, ABA accumulation, growth maintenance, and water loss under osmotic stress. Our findings uncover the critical role of BIK1 in releasing PP2C-mediated inhibition of SnRK2s under osmotic stress.

The leucine-rich repeat receptor kinase QSK1 regulates PRR-RBOHD complexes targeted by the bacterial effector HopF2Pto.

Plants detect pathogens using cell-surface pattern recognition receptors (PRRs) such as ELONGATION Factor-TU (EF-TU) RECEPTOR (EFR) and FLAGELLIN SENSING 2 (FLS2), which recognize bacterial EF-Tu and flagellin, respectively. These PRRs belong to the leucine-rich repeat receptor kinase (LRR-RK) family and activate the production of reactive oxygen species via the NADPH oxidase RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD). The PRR-RBOHD complex is tightly regulated to prevent unwarranted or exaggerated immune responses. However, certain pathogen effectors can subvert these regulatory mechanisms, thereby suppressing plant immunity. To elucidate the intricate dynamics of the PRR-RBOHD complex, we conducted a comparative coimmunoprecipitation analysis using EFR, FLS2, and RBOHD in Arabidopsis thaliana. We identified QIAN SHOU KINASE 1 (QSK1), an LRR-RK, as a PRR-RBOHD complex-associated protein. QSK1 downregulated FLS2 and EFR abundance, functioning as a negative regulator of PRR-triggered immunity (PTI). QSK1 was targeted by the bacterial effector HopF2Pto, a mono-ADP ribosyltransferase, reducing FLS2 and EFR levels through both transcriptional and transcription-independent pathways, thereby inhibiting PTI. Furthermore, HopF2Pto transcriptionally downregulated PROSCOOP genes encoding important stress-regulated phytocytokines and their receptor MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2. Importantly, HopF2Pto requires QSK1 for its accumulation and virulence functions within plants. In summary, our results provide insights into the mechanism by which HopF2Pto employs QSK1 to desensitize plants to pathogen attack.

Arterial-Lymphatic-Like Endothelial Cells Appear in Hereditary Hemorrhagic Telangiectasia 2 and Contribute to Vascular Leakage and Arteriovenous Malformations.

Arteriovenous malformations (AVMs) are characteristic of hereditary hemorrhagic telangiectasia. Loss-of-function mutations in the activin receptor-like kinase 1 (Alk1) are linked to hemorrhagic telangiectasia type 2. Endothelial-specific deletion of Alk1, endothelial lineage tracing, transcriptomics of single-cell analysis, and electron microscopy were performed to examine the vascular phenotype and characteristics of ALK1-deficient endothelial cells (ECs) after EC-specific Alk1 deletion. Ischemia assays were used to examine the cell capacity for vascular malformation. Connectivity Map with transcriptomic analysis was applied to identify chemical compounds. Specific methods for arteriovenous malformations, such as micro-computed tomography, with other molecular and cell biological tools were also performed. We performed endothelial-specific deletion of Alk1 in mice and found severe arteriovenous malformations and vascular leakage. The transcriptomics of single-cell analysis revealed a new distinctive cell cluster formed after Alk1 deletion where the cells coexpressed arterial and lymphatic endothelial markers. The analysis projected that these cells potentially originated from arterial ECs after Alk1 deletion. This new population was referred to as arterial-lymphatic-like ECs according to its cellular markers, and its appearance was validated in the pulmonary small arteries after Alk1 deletion. Transplantation of these cells caused vascular malformations. Endothelial lineage tracing confirmed that these new arterial-lymphatic-like ECs were derived from ALK1 depleted ECs, potentially arterial ECs. We discovered that SOX17 (SRY-box transcription factor 17) induction was responsible for the derivation of these arterial-lymphatic-like ECs. We showed that direct binding of MDM2 (mouse double minute 2) was required for Sox17 to execute this activity. Inhibition of MDM2 reduced the arteriovenous malformations in the mouse model. Together, our studies revealed the mechanistic underpinnings of ALK1 signaling in regulating the endothelial phenotype and provided possibilities for new therapeutic strategies in hemorrhagic telangiectasia type 2.

Intricate intracellular kinase network regulates the Spodoptera lituta-derived elicitor response signaling in Arabidopsis.

Plants defend themselves against herbivores by recognizing herbivore-derived elicitors and activating intracellular signaling. In Arabidopsis, the receptor-like kinase HAK1 recognizes the poly-saccharide elicitor (FrA) from Spodoptera litura larvae, leading to the expression of defense-related genes such as PDF1.2. During this process, the cytoplasmic kinase CRK2 phosphorylates PBL27, triggers the ERF13 expression via ethylene signaling and subsequently leads to PDF1.2 expression. Herein, we investigated four cytoplasmic kinases from the same receptor-like cytoplasmic kinase (RLCK) VII family as PBL27 that interacts with CRK2. Among them, PBL11, like PBL27, is phosphorylated by CRK2 and induces PDF1.2 expression but does not affect ERF13 expression. The weight gain of S. litura larvae on PBL11-deficient mutant plants was only slightly higher than that of wild-type plants, suggesting that PBL11 may function as a minor RLCK that supports the defense response.

The pathogen-induced peptide CEP14 is perceived by the receptor-like kinase CEPR2 to promote systemic disease resistance in Arabidopsis.

Secreted plant peptides that trigger cellular signaling are crucial for plant growth, development, and adaptive responses to environmental stresses. In Arabidopsis (Arabidopsis thaliana), the C-TERMINALLY ENCODED PEPTIDE (CEP) family is a class of secreted signaling peptides that is phylogenetically divided into two groups: group I (CEP1-CEP12) and group II (CEP13-CEP15). Several group I CEP peptides regulate root architecture and nitrogen starvation responses, whereas the biological activity and roles of group II CEPs remain unknown. Here, we report that a group II CEP peptide, CEP14, functions as a pathogen-induced elicitor of Arabidopsis immunity. In response to infection by the bacterial pathogen Pseudomonas syringae, CEP14 expression was highly induced via the salicylic acid pathway in Arabidopsis leaves and roots. In the absence of pathogen attack, treatment of Arabidopsis plants with synthetic CEP14 peptides was sufficient to trigger immune responses. Genetic and biochemical analyses demonstrated that the receptor-like kinase CEP RECEPTOR 2 (CEPR2) perceives CEP14 to trigger plant immunity. The SOMATIC EMBRYOGENESIS RECEPTOR KINASES (SERKs) BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE 1 (BAK1) and SERK4 also participated in CEP14 perception by forming CEP14-induced complexes with CEPR2. Overexpression of CEP14 largely enhanced Arabidopsis resistance to P. syringae, while CEP14 or CEPR2 mutation significantly attenuated Arabidopsis systemic resistance to P. syringae. Taken together, our data reveal that the pathogen-induced CEP14 peptide, which is perceived by the CEPR2-BAK1/SERK4 receptor complexes, acts as an endogenous elicitor to promote systemic disease resistance in Arabidopsis.

Regulated cleavage and translocation of FERONIA control immunity in Arabidopsis roots.

Plant roots exhibit localized immunity (LI) mainly in the transition zone (TZ) and elongation zone (EZ). Plasma membrane-localized receptor-like kinases (RLKs) can mediate the plant's response to rhizosphere bacteria. However, how RLKs are involved in triggering LI in roots remains unclear. Here we identified dual actions for the RLK FERONIA (FER) in the LI response of Arabidopsis (Arabidopsis thaliana). The FER cytoplasmic domain is cleaved and translocated to the nucleus (FERN) to activate LI in the TZ and EZ in response to colonization by beneficial and pathogenic bacteria. In the absence or cessation of bacterial infection, full-length FER is plasma membrane-localized to maintain growth. Upon colonization and invasion by a high titre of bacteria, mature RAPID ALKALINIZATION FACTOR23 peptide accumulates and activates the matrix metalloproteinase At2-MMP, which triggers FER cytoplasmic domain cleavage specifically in the TZ and EZ to activate LI. This work demonstrates that two molecular forms of a single RLK balance growth and immunity via LI activation in Arabidopsis roots.