Receptor-like Kinase Research Articles

The ZmWAKL-ZmWIK-ZmBLK1-ZmRBOH4 module provides quantitative resistance to gray leaf spot in maize.

Gray leaf spot (GLS), caused by the fungal pathogens Cercospora zeae-maydis and Cercospora zeina, is a major foliar disease of maize worldwide (Zea mays L.). Here we demonstrate that ZmWAKL encoding cell-wall-associated receptor kinase-like protein is the causative gene at the major quantitative disease resistance locus against GLS. The ZmWAKLY protein, encoded by the resistance allele, can self-associate and interact with a leucine-rich repeat immune-related kinase ZmWIK on the plasma membrane. The ZmWAKLY/ZmWIK receptor complex interacts with and phosphorylates the receptor-like cytoplasmic kinase (RLCK) ZmBLK1, which in turn phosphorylates its downstream NADPH oxidase ZmRBOH4. Upon pathogen infection, ZmWAKLY phosphorylation activity is transiently increased, initiating immune signaling from ZmWAKLY, ZmWIK, ZmBLK1 to ZmRBOH4, ultimately triggering a reactive oxygen species burst. Our study thus uncovers the role of the maize ZmWAKL-ZmWIK-ZmBLK1-ZmRBOH4 receptor/signaling/executor module in perceiving the pathogen invasion, transducing immune signals, activating defense responses and conferring increased resistance to GLS.

Phototropin2 3’UTR overlaps with the AT5G58150 gene encoding an inactive RLK kinase

BackgroundThis study examines the biological implications of an overlap between two sequences in the Arabidopsis genome, the 3’UTR of the PHOT2 gene and a putative AT5G58150 gene, encoded on the complementary strand. AT5G58150 is a probably inactive protein kinase that belongs to the transmembrane, leucine-rich repeat receptor-like kinase family. Phot2 is a membrane-bound UV/blue light photoreceptor kinase. Thus, both proteins share their cellular localization, on top of the proximity of their loci.ResultsThe extent of the overlap between 3’UTR regions of AT5G58150 and PHOT2 was found to be 66 bp, using RACE PCR. Both the at5g58150 T-DNA SALK_093781C (with insertion in the promoter region) and 35S::AT5G58150-GFP lines overexpress the AT5G58150 gene. A detailed analysis did not reveal any substantial impact of PHOT2 or AT5G58150 on their mutual expression levels in different light and osmotic stress conditions. AT5G58150 is a plasma membrane protein, with no apparent kinase activity, as tested on several potential substrates. It appears not to form homodimers and it does not interact with PHOT2. Lines that overexpress AT5G58150 exhibit a greater reduction in lateral root density due to salt and osmotic stress than wild-type plants, which suggests that AT5G58150 may participate in root elongation and formation of lateral roots. In line with this, mass spectrometry analysis identified proteins with ATPase activity, which are involved in proton transport and cell elongation, as putative interactors of AT5G58150. Membrane kinases, including other members of the LRR RLK family and BSK kinases (positive regulators of brassinosteroid signalling), can also act as partners for AT5G58150.ConclusionsAT5G58150 is a membrane protein that does not exhibit measurable kinase activity, but is involved in signalling through interactions with other proteins. Based on the interactome and root architecture analysis, AT5G58150 may be involved in plant response to salt and osmotic stress and the formation of roots in Arabidopsis.

Mutation of BAM2 rescues the sunn hypernodulation phenotype in Medicago truncatula, suggesting that a signaling pathway like CLV1/BAM in Arabidopsis affects nodule number.

The unique evolutionary adaptation of legumes for nitrogen-fixing symbiosis leading to nodulation is tightly regulated by the host plant. The autoregulation of nodulation (AON) pathway negatively regulates the number of nodules formed in response to the carbon/nitrogen metabolic status of the shoot and root by long-distance signaling to and from the shoot and root. Central to AON signaling in the shoots of Medicago truncatula is SUNN, a leucine-rich repeat receptor-like kinase with high sequence similarity with CLAVATA1 (CLV1), part of a class of receptors in Arabidopsis involved in regulating stem cell populations in the root and shoot. This class of receptors in Arabidopsis includes the BARELY ANY MERISTEM family, which, like CLV1, binds to CLE peptides and interacts with CLV1 to regulate meristem development. M. truncatula contains five members of the BAM family, but only MtBAM1 and MtBAM2 are highly expressed in the nodules 48 hours after inoculation. Plants carry mutations in individual MtBAMs, and several double BAM mutant combinations all displayed wild-type nodule number phenotypes. However, Mtbam2 suppressed the sunn-5 hypernodulation phenotype and partially rescued the short root length phenotype of sunn-5 when present in a sunn-5 background. Grafting determined that bam2 suppresses supernodulation from the roots, regardless of the SUNN status of the root. Overexpression of MtBAM2 in wild-type plants increases nodule numbers, while overexpression of MtBAM2 in some sunn mutants rescues the hypernodulation phenotype, but not the hypernodulation phenotypes of AON mutant rdn1-2 or crn. Relative expression measurements of the nodule transcription factor MtWOX5 downstream of the putative bam2 sunn-5 complex revealed disruption of meristem signaling; while both bam2 and bam2 sunn-5 influence MtWOX5 expression, the expression changes are in different directions. We propose a genetic model wherein the specific root interactions of BAM2/SUNN are critical for signaling in nodule meristem cell homeostasis in M. truncatula.

The LRR receptor-like kinase ALR1 is a plant aluminum ion sensor

Plant survival requires an ability to adapt to differing concentrations of nutrient and toxic soil ions, yet ion sensors and associated signaling pathways are mostly unknown. Aluminum (Al) ions are highly phytotoxic, and cause severe crop yield loss and forest decline on acidic soils which represent ∼30% of land areas worldwide. Here we found an Arabidopsis mutant hypersensitive to Al. The gene encoding a leucine-rich-repeat receptor-like kinase, was named Al Resistance1 (ALR1). Al ions binding to ALR1 cytoplasmic domain recruits BAK1 co-receptor kinase and promotes ALR1-dependent phosphorylation of the NADPH oxidase RbohD, thereby enhancing reactive oxygen species (ROS) generation. ROS in turn oxidatively modify the RAE1 F-box protein to inhibit RAE1-dependent proteolysis of the central regulator STOP1, thus activating organic acid anion secretion to detoxify Al. These findings establish ALR1 as an Al ion receptor that confers resistance through an integrated Al-triggered signaling pathway, providing novel insights into ion-sensing mechanisms in living organisms, and enabling future molecular breeding of acid-soil-tolerant crops and trees, with huge potential for enhancing both global food security and forest restoration.

Rice receptor kinase FLR7 regulates rhizosphere oxygen levels and enriches the dominant Anaeromyxobacter that improves submergence tolerance in rice.

Oxygen is one of the determinants of root microbiome formation. However, whether plants regulate rhizosphere oxygen levels to affect microbiota composition and the underlying molecular mechanisms remain elusive. The receptor-like kinase (RLK) family member FERONIA modulates the growth-defense tradeoff in Arabidopsis. Here, we established that rice FERONIA-like RLK 7 (FLR7) controls rhizosphere oxygen levels by methylene blue staining, oxygen flux, and potential measurements. The formation of oxygen-transporting aerenchyma in roots is negatively regulated by FLR7. We further characterized the root microbiota of 11 FLR mutants including flr7 and wild-type Nipponbare (Nip) grown in the field by 16S ribosomal RNA gene profiling and demonstrated that the 11 FLRs are involved in regulating rice root microbiome formation. The most abundant anaerobic-dependent genus Anaeromyxobacter in the Nip root microbiota was less abundant in the root microbiota of all these mutants, and this contributed the most to the community differences between most mutants and Nip. Metagenomic sequencing revealed that flr7 increases aerobic respiration and decreases anaerobic respiration in the root microbiome. Finally, we showed that a representative Anaeromyxobacter strain improved submergence tolerance in rice via FLR7. Collectively, our findings indicate that FLR7 mediates changes in rhizosphere oxygen levels and enriches the beneficial dominant genus Anaeromyxobacter and may provide insights for developing plant flood prevention strategies via the use of environment-specific functional soil microorganisms.

Phytosulfokine peptides, their receptors, and functions.

Phytosulfokines (PSKs) are a class of disulfated pentapeptides and are regarded as plant peptide hormones. PSK-α, -γ, -δ, and -ϵ are four bioactive PSKs that are reported to have roles in plant growth, development, and immunity. In this review, we summarize recent advances in PSK biosynthesis, signaling, and function. PSKs are encoded by precursor genes that are widespread in higher plants. PSKs maturation from these precursors requires a sulfation step, which is catalyzed by a tyrosylprotein sulfotransferase, as well as proteolytic cleavage by subtilisin serine proteases. PSK signaling is mediated by plasma membrane-localized receptors PSKRs that belong to the leucine-rich repeat receptor-like kinase family. Moreover, multiple biological functions can be attributed to PSKs, including promoting cell division and cell growth, regulating plant reproduction, inducing somatic embryogenesis, enhancing legume nodulation, and regulating plant resistance to biotic and abiotic stress. Finally, we propose several research directions in this field. This review provides important insights into PSKs that will facilitate biotechnological development and PSK application in agriculture.

Green leaf volatiles co-opt proteins involved in molecular pattern signalling in plant cells.

The green leaf volatiles (GLVs) Z-3-hexen-1-ol (Z3-HOL) and Z-3-hexenyl acetate (Z3-HAC) are airborne infochemicals released from damaged plant tissues that induce defenses and developmental responses in receiver plants, but little is known about their mechanism of action. We found that Z3-HOL and Z3-HAC induce similar but distinctive physiological and signaling responses in tomato seedlings and cell cultures. In seedlings, Z3-HAC showed a stronger root growth inhibition effect than Z3-HOL. In cell cultures, the two GLVs induced distinct changes in MAP kinase (MAPK) activity and proton fluxes as well as rapid and massive changes in the phosphorylation status of proteins within 5 min. Many of these phosphoproteins are involved in reprogramming the proteome from cellular homoeostasis to stress and include pattern recognition receptors, a receptor-like cytoplasmic kinase, MAPK cascade components, calcium signaling proteinsand transcriptional regulators. These are well-known components of damage-associated molecular pattern (DAMP) signaling pathways. These rapid changes in the phosphoproteome may underly the activation of defense and developmental responses to GLVs. Our data provide further evidence that GLVs function like DAMPs and indicate that GLVs coopt DAMP signaling pathways.

Small but mighty: Peptides regulating abiotic stress responses in plants.

Throughout evolution, plants have developed strategies to confront and alleviate the detrimental impacts of abiotic stresses on their growth and development. The combat strategies involve intricate molecular networks and a spectrum of early and late stress-responsive pathways. Plant peptides, consisting of fewer than 100 amino acid residues, are at the forefront of these responses, serving as pivotal signalling molecules. These peptides, with roles similar to phytohormones, intricately regulate plant growth, development and facilitate essential cell-to-cell communications. Numerous studies underscore the significant role of these small peptides in coordinating diverse signalling events triggered by environmental challenges. Originating from the proteolytic processing of larger protein precursors or directly translated from small open reading frames, includingmicroRNA (miRNA) encoded peptides from primary miRNA, these peptides exert their biological functions through binding with membrane-embedded receptor-like kinases. This interaction initiates downstream cellular signalling cascades, often involving major phytohormones or reactive oxygen species-mediated mechanisms. Despite these advances, the precise modes of action for numerous other small peptides remain to be fully elucidated. In this review, we delve into the dynamics of stress physiology, mainly focusing on the roles of major small signalling peptides, shedding light on their significance in the face of changing environmental conditions.

Responses of transcriptome and metabolome in peanut leaves to dibutyl phthalate during whole growth period.

The application of agricultural film mulching technology has significantly contributed to increasing crop yield and income, but the pollution caused by residual film has seriously affected agricultural production and the natural environment. Agricultural film is commonly employed to enhance the yield of peanuts; its use may lead to excessive dibutyl phthalate (DBP) residues in peanut kernels. But, limited investigations have been conducted on the regulatory mechanism of peanut leaves in response to DBP exposure throughout the entire growth period. To bridge this knowledge gap, we investigated the differences in transcriptome and metabolome of peanut leaves under DBP stress. According to visual observations, the results of morphological response showed that the growth of peanut plants was significantly inhibited from seedling to pod stage under DBP treatment. Transcriptomic analysis results showed that the genes AH19G05510 (LRR receptor-like serine threonine-protein kinase) and AH20G31870 (disease resistance), belonging to the FAR1 family and bZIP family respectively, may be key genes involved in the resistance to DBP stress throughout its growth stages. Metabolomic analysis results showed that during the initial stage of DBP stress, the key metabolites in peanut leaves response to stress were carboxylic acids and derivatives, as well as fatty acyls. As peanut growth progressed, flavonoids gradually became more prominent in the resistance to DBP stress. By integrating metabolomics and transcriptomics analysis, we have identified that purine metabolism during seedling and flowering stages, as well as the flavone and flavonol biosynthesis pathways during pod and maturity stages, played a crucial role in response to DBP stress. These findings not only provide valuable key gene and metabolic information for studying anti-plasticizer pollution throughout the entire growth period of peanuts, but also offer reference for enhancing crop resistance to plasticizer pollution through genetic modification and metabolic regulation.

Fine-mapping of a major locus for Fusarium wilt resistance in flax (Linum usitatissimum L.)

Key messageFine-mapping of a locus on chromosome 1 of flax identified an S-lectin receptor-like kinase (SRLK) as the most likely candidate for a major Fusarium wilt resistance gene.Fusarium wilt, caused by the soil-borne fungal pathogen Fusarium oxysporum f. sp. lini, is a devastating disease in flax. Genetic resistance can counteract this disease and limit its spread. To map major genes for Fusarium wilt resistance, a recombinant inbred line population of more than 700 individuals derived from a cross between resistant cultivar ‘Bison’ and susceptible cultivar ‘Novelty’ was phenotyped in Fusarium wilt nurseries at two sites for two and three years, respectively. The population was genotyped with 4487 single nucleotide polymorphism (SNP) markers. Twenty-four QTLs were identified with IciMapping, 18 quantitative trait nucleotides with 3VmrMLM and 108 linkage disequilibrium blocks with RTM-GWAS. All models identified a major QTL on chromosome 1 that explained 20–48% of the genetic variance for Fusarium wilt resistance. The locus was estimated to span ~ 867 Kb but included a ~ 400 Kb unresolved region. Whole-genome sequencing of ‘CDC Bethune’, ‘Bison’ and ‘Novelty’ produced ~ 450 Kb continuous sequences of the locus. Annotation revealed 110 genes, of which six were considered candidate genes. Fine-mapping with 12 SNPs and 15 Kompetitive allele-specific PCR (KASP) markers narrowed down the interval to ~ 69 Kb, which comprised the candidate genes Lus10025882 and Lus10025891. The latter, a G-type S-lectin receptor-like kinase (SRLK) is the most likely resistance gene because it is the only polymorphic one. In addition, Fusarium wilt resistance genes previously isolated in tomato and Arabidopsis belonged to the SRLK class. The robust KASP markers can be used in marker-assisted breeding to select for this major Fusarium wilt resistance locus.

Lrg1 silencing attenuates ischemia-reperfusion renal injury by regulating autophagy and apoptosis through the TGFβ1- Smad1/5 signaling pathway

BackgroundDysfunction in the processes of autophagy and apoptosis within renal tubular epithelial cells (RTEc) contributes to renal ischemia-reperfusion injury (IRI). However, the factors influencing this dysfunction remain unclear. Leucine-rich alpha-2-glycoprotein 1 (Lrg1) plays a role in the progression of diabetic nephropathy and kidney fibrosis by modulating the activin receptor-like kinase 1 (ALK1)-Smad1/5/8 and TGF-β1/Smad3 pathways, respectively. Therefore, we aimed to investigate whether Lrg1 is involved in the pathological mechanisms of renal IRI and whether its effects are related to the dysregulation of autophagy and apoptosis in RTEc. MethodsWe conducted in vitro and in vivo experiments using CoCl2-induced hypoxic human kidney-2 (HK-2) cells and mice with renal IRI, respectively. Lrg1 was silenced using siRNA and lentiviral vectors in HK-2 cells and mouse kidneys. Rapamycin (Rapa) and methyladenine were applied to regulate autophagy in renal IRI models. ResultsIncreased Lrg1 expression was observed in hypoxic HK-2 cells and in the kidneys of mice with renal IRI. Silencing of Lrg1 through siRNA and lentiviral approaches restored autophagy and suppressed apoptosis in CoCl2-induced hypoxic HK-2 cells and renal IRI models. Additionally, reduced Lrg1 expression alleviated kidney damage caused by renal IRI. The downregulation of Lrg1 expression restrained the TGFβ-Smad1/5 signaling pathway in hypoxic-induced HK-2 cells and renal IRI by reducing ALK1 expression. Lastly, the enhancement of autophagy, achieved through Rapa treatment, provided protection against renal IRI in mice. ConclusionsOur findings suggest that Lrg1 silencing can be applied as a potential therapeutic target to inhibit the TGFβ1-Smad1/5 pathway, thereby enhancing autophagy and decreasing apoptosis in patients with acute kidney injury.

Increased Collagen I/Collagen III Ratio Is Associated with Hemorrhage in Brain Arteriovenous Malformations in Human and Mouse.

Background: The increase in the collagen I (COL I)/COL III ratio enhances vessel wall stiffness and renders vessels less resistant to blood flow and pressure changes. Activated microglia enhance inflammation-induced fibrosis. Hypotheses: The COL I/COL III ratio in human and mouse brain arteriovenous malformations (bAVMs) is associated with bAVM hemorrhage, and the depletion of microglia decreases the COL I/COL III ratio and hemorrhage. Method: COL I, COL III, and hemorrhages were analyzed in 12 human bAVMs and 6 control brains, and mouse bAVMs induced in three mouse lines with activin receptor-like kinase 1 (n = 7) or endoglin (n = 7) deleted in the endothelial cells or brain focally (n = 5). The controls for the mouse study were no-gene-deleted litter mates. Mouse bAVMs were used to test the relationships between the Col I/Col III ratio and hemorrhage and whether the transient depletion of microglia reduces the Col I/Col III ratio and hemorrhage. Results: The COL I/COL III ratio was higher in the human and mouse bAVMs than in controls. The microhemorrhage in mouse bAVMs was positively correlated with the Col I/Col III ratio. Transient depletion of microglia reduced the Col I/Col III ratio and microhemorrhage. Conclusions: The COL I/COL III ratio in the bAVMs was associated with bAVM hemorrhage. The depletion of microglia reduced the bAVM Col I/Col III ratio and hemorrhage.

Pathogenic Variant Frequencies in Hereditary Haemorrhagic Telangiectasia Support Clinical Evidence of Protection from Myocardial Infarction.

Hereditary haemorrhagic telangiectasia (HHT) is a vascular dysplasia inherited as an autosomal dominant trait, due to a single heterozygous loss-of-function variant, usually in ACVRL1 (encoding activin receptor-like kinase 1 [ALK1]), ENG (encoding endoglin [CD105]), or SMAD4. In a consecutive single-centre series of 37 positive clinical genetic tests performed in 2021-2023, a skewed distribution pattern was noted, with 30 of 32 variants reported only once, but ACVRL1 c.1231C>T (p.Arg411Trp) identified as the disease-causal gene in five different HHT families. In the same centre's non-overlapping 1992-2020 series where 110/134 (82.1%) HHT-causal variants were reported only once, ACVRL1 c.1231C>T (p.Arg411Trp) was identified in nine further families. In a 14-country, four-continent HHT Mutation Database where 181/250 (72.4%) HHT-causal variants were reported only once, ACVRL1 c.1231C>T (p.Arg411Trp) was reported by 12 different laboratories, the adjacent ACVRL1 c.1232G>A (p.Arg411Gln) by 14, and ACVRL1 c.1120C>T (p.Arg374Trp) by 18. Unlike the majority of HHT-causal ACVRL1 variants, these encode ALK1 protein that reaches the endothelial cell surface but fails to signal. Six variants of this type were present in the three series and were reported 6.8-25.5 (mean 8.9) times more frequently than the other ACVRL1 missense variants (all p-values < 0.0039). Noting lower rates of myocardial infarction reported in HHT, we explore potential mechanisms, including a selective paradigm relevant to ALK1's role in the initiating event of atherosclerosis, where a plausible dominant negative effect of these specific variants can be proposed. In conclusion, there is an ~9-fold excess of kinase-inactive, cell surface-expressed ACVRL1/ALK1 pathogenic missense variants in HHT. The findings support further examination of differential clinical and cellular phenotypes by HHT causal gene molecular subtypes.

Structural and biochemical basis of FLS2-mediated signal activation and transduction in rice

The receptor-like kinase FLAGELLIN-SENSITIVE 2 (FLS2) functions as a bacterial flagellin receptor localized on the cell membrane of plants. In Arabidopsis, the co-receptor BRI1-ASSOCIATED RECEPTOR KINASE 1 (BAK1) cooperates with FLS2 to detect the flagellin epitope flg22, resulting in formation of a signaling complex that triggers plant defense responses. However, the co-receptor responsible for recognizing and signaling the flg22 epitope in rice remains to be determined, and the precise structural mechanism underlying FLS2-mediated signal activation and transduction has not been clarified. This study presents the structural characterization of a kinase-dead mutant of the intracellular kinase domain of OsFLS2 (OsFLS2-KDD1013A) in complex with ATP or ADP, resolved at resolutions of 1.98 Å and 2.09 Å, respectively. Structural analysis revealed that OsFLS2 can adopt an active conformation in the absence of phosphorylation, although it exhibits only weak basal catalytic activity for autophosphorylation. Subsequent investigations demonstrated that OsSERK2 effectively phosphorylates OsFLS2, which reciprocally phosphorylates OsSERK2, leading to complete activation of OsSERK2 and rapid phosphorylation of the downstream substrate receptor-like cytoplasmic kinases OsRLCK176 and OsRLCK185. Through mass spectrometry experiments, we successfully identified critical autophosphorylation sites on OsSERK2, as well as sites transphosphorylated by OsFLS2. Furthermore, we demonstrated the interaction between OsSERK2 and OsFLS2, which is enhanced in the presence of flg22. Genetic evidence suggests that OsRLCK176 and OsRLCK185 may function downstream of the OsFLS2-mediated signaling pathway. Our study reveals the molecular mechanism by which OsFLS2 mediates signal transduction pathways in rice and provides a valuable example for understanding RLK-mediated signaling pathways in plants.

Transcriptome analysis of tomato plants following salicylic acid-induced immunity against Clavibacter michiganensis ssp. michiganensis.

Salicylic acid (SA) is known to be involved in the immunity against Clavibacter michiganensis ssp. michiganensis (Cmm) that causes bacterial canker in tomato. To identify the candidate genes associated with SA-inducible Cmm resistance, transcriptome analysis was conducted via RNA sequencing in tomato plants treated with SA. SA treatment upregulated various defense-associated genes, such as PR and GST genes, in tomato cotyledons. A comparison of SA- and Cmm-responsive genes revealed that both SA treatment and Cmm infection commonly upregulated a large number of genes. Gene Ontology (GO) analysis indicated that the GO terms associated with plant immunity were over-represented in both SA- and Cmm-induced genes. The genes commonly downregulated by both SA treatment and Cmm infection were associated with the cell cycle and may be involved in growth and immunity trade-off through cell division. After SA treatment, several proteins that were predicted to play a role in immune signaling, such as resistance gene analogs, Ca2+ sensors, and WRKY transcription factors, were transcriptionally upregulated. The W-box element, which was targeted by WRKYs, was over-represented in the promoter regions of genes upregulated by both SA treatment and Cmm infection, supporting the speculation that WRKYs are important for the SA-mediated immunity against Cmm. Prediction of protein-protein interactions suggested that genes encoding receptor-like kinases and EF-hand proteins play an important role in immune signaling. Thus, various candidate genes involved in SA-inducible Cmm resistance were identified.

The OsBSK1-2-MAPK module regulates blast resistance in rice

Receptor-like cytoplasmic kinase OsBSK1-2 was reported to play an important role in regulation of response to rice blast, but the signaling pathway remained unknown. In this study, we identified OsMAPKKK18 and previously uncharacterized MAPKKKs OsMAPKKK16 and OsMAPKKK19 that interact with OsBSK1-2. Expression of all three MAPKKKs was induced by Magnaporthe oryzae infection, and all three induced cell death when transiently expressed in Nicotiana benthamiana leaves. Knockout of OsMAPKKK16 and OsMAPKKK18 compromised blast resistance and overexpression of OsMAPKKK19 increased blast resistance, indicating that all three MAPKKKs are involved in regulation of rice blast response. Furthermore, both OsMAPKKK16 and OsMAPKKK19 interacted with and phosphorylated OsMKK4 and OsMKK5, and chitin-induced MAPK activation was suppressed in osmapkkk16 and osbsk1-2 mutants. OsMAPKKK18 was earlier reported to interact with and phosphorylate OsMKK4 and affect chitin-induced MAPK activation, suggesting that OsBSK1-2 is involved in regulation of immunity through multiple MAPK signaling pathways. Unlike BSK1 in Arabidopsis, OsBSK1-2 was not involved in response to avirulent M. oryzae strains. Taken together, our results revealed important roles of OsMAPKKK16/18/19 and a OsBSK1-2-OsMAPKKK16/18/19-OsMKK4/5 module in regulating response to rice blast.

Trancriptome data mining in combination with co-expression network analysis identifies the functional modules and critical regulators in Hordeum vulgare L. in response to cold stress

Cold stress, as an abiotic stress, is one of the most limiting factors which pose a great threat to the plant's productivity. To understand the transcriptional regulation and connectivity pattern of genes involved in barley cold stress responses, co-expression network analysis was performed based on the global transcriptome profiling. The microarray datasets related to cold stress treatments were retrieved from the Gene Expression Omnibus (GEO) and Array express databases. Four microarray datasets related to cold stress-responsive transcriptome in barley were included in our study. Gene co-expression analysis was constructed using WGCNA method. Module-Trait Relationships (MTR) analysis and hub genes determination and validation were carried out. Finally, transcription factor and kinase regulatory networks were Inferred using machine learning algorithm. The co-expression modules were determined using beta index = 10. In total 13 co-expressed modules were identified with an average size of 153 genes. Functional enrichment based on gene ontology (GO) showed that each of the stress related significant modules were enriched in different biological processes. Annotation of significant modules identifies some TFs and Kinases such as ethylene-responsive transcription factor 1-like, transcription factor PCL1-like, transcription factor MYC2, WRKY, serine/threonine-protein kinase PBL7, and receptor-like protein kinase At2g42960 were contributed in barley cold stress response. Our analysis highlighted the functional importance of ABA signaling pathway, ROS signaling, defensive and protective proteins, degrading protein, Ca2+ related signaling, ribosome-mediated translation and etc. in responding of barley to cold stress condition. The current findings add substantially to our understanding of the cold responsive underlying mechanism of barley which can serve in future studies and breeding programs.

The chromosome-scale genome and the genetic resistance machinery against insect herbivores of the Mexican toloache, Datura stramonium.

Plant resistance refers to the heritable ability of plants to reduce damage caused by natural enemies, such as herbivores and pathogens, either through constitutive or induced traits like chemical compounds or trichomes. However, the genetic architecture-the number and genome location of genes that affect plant defense and the magnitude of their effects-of plant resistance to arthropod herbivores in natural populations remains poorly understood. In this study, we aimed to unveil the genetic architecture of plant resistance to insect herbivores in the annual herb Datura stramonium (Solanaceae) through quantitative trait loci mapping. We achieved this by assembling the species' genome and constructing a linkage map using an F2 progeny transplanted into natural habitats. Furthermore, we conducted differential gene expression analysis between undamaged and damaged plants caused by the primary folivore, Lema daturaphila larvae. Our genome assembly resulted in 6,109 scaffolds distributed across 12 haploid chromosomes. A single quantitative trait loci region on chromosome 3 was associated with plant resistance, spanning 0 to 5.17 cM. The explained variance by the quantitative trait loci was 8.44%. Our findings imply that the resistance mechanisms of D. stramonium are shaped by the complex interplay of multiple genes with minor effects. Protein-protein interaction networks involving genes within the quantitative trait loci region and overexpressed genes uncovered the key role of receptor-like cytoplasmic kinases in signaling and regulating tropane alkaloids and terpenoids, which serve as powerful chemical defenses against D. stramonium herbivores. The data generated in our study constitute important resources for delving into the evolution and ecology of secondary compounds mediating plant-insect interactions.

Unlocking a ‘lock–key’ mechanism governing pollen–pistil interactions

Pollen–pistil interactions ensure genetic diversity and shape the reproductive success of plants. Lan et al. recently revealed that the interaction among various receptor-like kinases, cell-wall proteins, and stigmatic RALF peptides (sRALFs) or pollen RALF peptides (pRALFs) on the stigma surface govern the penetration of pollen tubes in members of the Brassicaceae.

Comparative Analysis of Transcriptomics and Metabolomics Reveals Defense Mechanisms in Melon Cultivars against Pseudoperonospora cubensis Infection.

Melon (Cucumis melo L.) represents an agriculturally significant horticultural crop that is widely grown for its flavorful fruits. Downy mildew (DM), a pervasive foliar disease, poses a significant threat to global melon production. Although several quantitative trait loci related to DM resistance have been identified, the comprehensive genetic underpinnings of this resistance remain largely uncharted. In this study, we utilized integrative transcriptomics and metabolomics approaches to identify potential resistance-associated genes and delineate the strategies involved in the defense against DM in two melon cultivars: the resistant 'PI442177' ('K10-1') and the susceptible 'Huangdanzi' ('K10-9'), post-P. cubensis infection. Even in the absence of the pathogen, there were distinctive differentially expressed genes (DEGs) between 'K10-1' and 'K10-9'. When P. cubensis was infected, certain genes, including flavin-containing monooxygenase (FMO), receptor-like protein kinase FERONIA (FER), and the HD-ZIP transcription factor member, AtHB7, displayed pronounced expression differences between the cultivars. Notably, our data suggest that following P. cubensis infection, both cultivars suppressed flavonoid biosynthesis via the down-regulation of associated genes whilst concurrently promoting lignin production. The complex interplay of transcriptomic and metabolic responses elucidated by this study provides foundational insights into melon's defense mechanisms against DM. The robust resilience of 'K10-1' to DM is attributed to the synergistic interaction of its inherent transcriptomic and metabolic reactions.