Receptor-like Protein Research Articles

The Deubiquitinating Enzyme AMSH1 Contributes to Plant Immunity Through Regulating the Stability of BDA1

Plants utilize plasma membrane localized receptors like kinases (RLKs) or receptor-like proteins (RLPs) to recognize pathogens and activate pattern-triggered immunity (PTI) responses. A gain-of-function mutation in the Arabidopsis RLP SNC2 (SUPPRESSOR OF NPR1-1, CONSTITUTIVE 2) leads to constitutive activation of defense responses in snc2-1D mutant plants. Transcription factors, SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1 (SARD1) and CALMODULIN-BINDING PROTEIN 60g (CBP60g), define two parallel pathways downstream of SNC2. The autoimmunity of snc2-1D was partially affected by single mutations in SARD1 or CBP60g but completely suppressed by the sard1 cbp60g double mutant. From a suppressor screen using sard1-1 snc2-1D, we identified a deubiquitinating enzyme ASSOCIATED MOLECULE WITH THE SH3 DOMAIN OF STAM 1 (AMSH1) as a key component in SNC2-mediated plant immunity. A loss-of-function mutation in AMSH1 can suppress the autoimmune responses of sard1-1 snc2-1D. In eukaryotes, selective protein degradation often occurs through the ubiquitination/deubiquitination system. The deubiquitinating enzymes that remove ubiquitin from target proteins play essential roles in controlling the level of target protein ubiquitination and degradation. As loss of AMSH1 results in decreased BDA1 abundance and BDA1 is a transmembrane protein required for SNC2-mediated immunity, AMSH1 likely contributes to immunity regulation through controlling BDA1 stability.

The Rac1 homolog CED-10 is a component of the MES-1/SRC-1 pathway for asymmetric division of the C. elegans EMS blastomere.

Asymmetric cell division is essential for the creation of cell types with different identities and functions. The EMS blastomere of the four-cell Caenorhabditis elegans embryo undergoes an asymmetric division in response to partially redundant signaling pathways. One pathway involves a Wnt signal from the neighboring P2 cell, while the other pathway is defined by the receptor-like MES-1 transmembrane protein localized at the EMS-P2 cell contact, and the cytoplasmic kinase SRC-1. In response to these signals, the EMS nuclear-centrosome complex rotates so that the spindle forms on the anterior-posterior axis; after division, the daughter cell contacting P2 becomes the endodermal precursor cell. Here we identify the Rac1 homolog CED-10 as a new component of the MES-1/SRC-1 pathway. Loss of CED-10 affects both spindle positioning and endoderm specification in the EMS cell. SRC-1 dependent phosphorylation at the EMS-P2 contact is reduced. However, the asymmetric division of the P2 cell, which is also MES-1 and SRC-1 dependent, appears normal in ced-10 mutants. These and other results suggest that CED-10 acts upstream of, or at the level of, SRC-1 activity in the EMS cell. In addition, we find that the branched actin regulator ARX-2 is enriched at the EMS-P2 cell contact site, in a CED-10 dependent manner. Loss of ARX-2 results in EMS spindle orientation defects, suggesting that CED-10 acts through branched actin to promote spindle orientation in the EMS cell.

RNAseq of peripheral blood mononucleated cells exposed to platelet-rich fibrin and enamel matrix derivatives

Platelet-rich fibrin (PRF) and Enamel Matrix Derivatives (EMD) can support the local regenerative events in periodontal defects. There is reason to suggest that PRF and EMD exert part of their activity by targeting the blood-derived cells accumulating in the early wound healing blastema. However, the impact of PRF and EMD on blood cell response remains to be discovered. To this aim, we have exposed human peripheral blood mononucleated cells (PBMCs) to PRF lysates prepared by a swing-out rotor and EMD, followed by bulk RNA sequencing. A total of 111 and 8 genes are up- and down-regulated by PRF under the premise of an at least log2 two-fold change and a minus log10 significance level of two, respectively. Representative is a characteristic IFN response indicated by various human leukocyte antigens (HLA-DPA1, HLA-DPB1, HLA-DQA1, HLA-DQA2, HLA-DRA, HLA-DRB1, HLA-DRB5), gamma Fc receptors (FCGR1A, FCGR1B, FCGR3B), chemokines (CXCL9-11), and calprotectin (S100A8/9 and S100A12), complement (C1QA/B, C2) and interferon-induced guanylate-binding proteins (GBP1, GBP5). With EMD, 67 and 29 genes are up- and down-regulated, respectively. Characteristic of the upregulated genes are tensins (TNS1 and TNS3). Among the genes downregulated by EMD were epsilon Fc receptors (FCER1A; FCER2), Fc receptor-like proteins (FCRL1, FCRL3) and CX3CR1. Genes commonly upregulated by PRF and EMD were most noticeably NXPH4 and MN1, as well as FN1, MMP14, MERTK, and AXL. Our findings suggest that PRF provokes an inflammatory response, while EMD dampens IgE signaling in peripheral mononucleated blood cells.

Cryo-EM reveals cholesterol binding in the lysosomal GPCR-like protein LYCHOS.

Cholesterol plays a pivotal role in modulating the activity of mechanistic target of rapamycin complex 1 (mTOR1), thereby regulating cell growth and metabolic homeostasis. LYCHOS, a lysosome-localized G-protein-coupled receptor-like protein, emerges as a cholesterol sensor and is capable of transducing the cholesterol signal to affect the mTORC1 function. However, the precise mechanism by which LYCHOS recognizes cholesterol remains unknown. Here, using cryo-electron microscopy, we determined the three-dimensional structural architecture of LYCHOS in complex with cholesterol molecules, revealing a unique arrangement of two sequential structural domains. Through a comprehensive analysis of this structure, we elucidated the specific structural features of these two domains and their collaborative role in the process of cholesterol recognition by LYCHOS.

A Glutamate Receptor-Like Gene AtGLR25 With Its Unusual Splice Variant Has a Role in Mediating Glutamate-Elicited Changes in Arabidopsis Root Architecture.

The occurrence of external L-glutamate at the Arabidopsis root tip triggers major changes in root architecture, but the mechanism of -L-Glu sensing is unknown. Members of the family of GLUTAMATE RECEPTOR-LIKE (GLR) proteins are known to act as amino acid-gated Ca2+-permeable channels and to have signalling roles in diverse plant processes. To investigate the possible role of GLRs in the root architectural response to L-Glu, we screened a collection of mutants with T-DNA insertions in each of the 20 AtGLR genes. Reduced sensitivity of root growth to L-Glu was found in mutants of one gene, GLR2.5. Interestingly, GLR2.5 was found to apparently produce four transcript variants encoding hypothetical proteins of 169-720 amino acids. One of these transcripts, GLR2.5c, encodes a truncated GLR protein lacking both the conserved amino-terminal domain and part of the ligand-binding domain. When a glr2.5 mutant was transformed with a construct constitutively expressing GLR2.5c, both L-Glu sensitivity of root growth and L-Glu-elicited Ca2+ currents in root tip protoplasts were restored. These results, along with homology modelling of the truncated ligand-binding domain of GLR2.5c, suggest that GLR2.5c has a regulatory or scaffolding role in heteromeric GLR complex(es) that may involve triggering the root architectural response to L-Glu.

Damage activates EXG1 and RLP44 to suppress vascular differentiation during regeneration in Arabidopsis.

Plants possess remarkable regenerative abilities to form de novo vasculature after damage and in response to pathogens that invade and withdraw nutrients. To look for common factors that affect vascular formation upon stress, we searched for Arabidopsis thaliana genes differentially expressed upon Agrobacterium infection, nematode infection and plant grafting. One such gene was cell wall related and highly induced by all three stresses and was named ENHANCED XYLEM AND GRAFTING1 (EXG1) since mutations in it promoted ectopic xylem formation in Vascular cell Induction culture System Using Arabidopsis Leaves (VISUAL) and enhanced graft formation. Further observations revealed that exg1 mutants inhibited cambium development and callus formation but enhanced tissue attachment, syncytium size, phloem reconnection and xylem formation. Given that brassinosteroids also promote xylem differentiation, we analyzed brassinosteroid-related genes and found that mutations in a receptor-like protein, RLP44, caused similar regeneration-related phenotypes as mutations in EXG1. Like EXG1, RLP44 expression was induced by grafting and wounding. Mutations in EXG1 and RLP44 affected the expression of many genes in common including those related to cell walls and genes important for vascular regeneration. We propose that EXG1 integrates information from wounding or pathogen stresses and functions with RLP44 to suppress vascular differentiation during regeneration and healing.

The 14-3-3 protein CaTFT7 interacts with transcription factor CaHDZ27 to positively regulate pepper immunity against Ralstonia solanacearum

Abstract Bacterial wilt, caused by Ralstonia solanacearum, is a devastating disease affecting plants in the Solanaceae family. In our previous study, CaHDZ27 was shown to act crucially in the pepper defense response to R. solanacearum. However, the molecular basis underlying CaHDZ27 function remains unexplored. In this study, we demonstrate that CaHDZ27 is post-translationally regulated by the 14-3-3 protein CaTFT7, which functions as a positive regulator in pepper immunity against R. solanacearum. RT-qPCR analysis revealed that CaTFT7 is transcriptionally induced by R. solanacearum infection. The data from virus-induced gene silencing revealed that CaTFT7 positively affects pepper immunity, which was further confirmed by the data of CaTFT7-overexpressing Nicotiana benthamiana. CaTFT7 interacted with CaHDZ27, thereby promoting the stability of CaHDZ27 and enhancing CaHDZ27 binding to the promoter of cysteine-rich receptor-like protein kinase 5 (CaCRK5), a gene that positively affects pepper defense against R. solanacearum. The above data indicated that CaTFT7 enhanced CaHDZ27 stability and promoted its ability to activate pepper immunity, shedding light on the mechanisms underlying pepper resistance to bacterial wilt.

Enhancing Fruit Resistance against Fungal Pathogens Using a Pathogen-Associated Molecular Pattern PdEIX.

Fruit is an essential part of the human diet, and postharvest fungal diseases are the major cause of fruit postharvest losses worldwide. Pathogen-associated molecular patterns (PAMPs) are important elicitors from microbes, and the recognition between microbial PAMPs and plant receptors leads to PAMP-triggered immunity. Here, we identified a PAMP, PdEIX, that is an important protein elicitor with plant immunity-inducing activity, from the citrus green mold pathogen Penicillium digitatum. PdEIX showed an apoplastic location similar to that of known PAMPs, and plant receptor-like protein NbEIX2, receptor-like kinase BAK1, and other signaling components of plant immunity were required for PdEIX-triggered plant cell death in the model plant Nicotiana benthamiana. Moreover, PdEIX triggered a series of immune responses in citrus fruit and enhanced the resistance of citrus and other fruit against fungal pathogens. Our results indicate that application of a microbial PAMP as the plant immunity inducer is an effective strategy for controlling postharvest fungal diseases of fruit.

Immune targets for schistosomiasis control identified by a genome-wide association study of African snail vectors.

Schistosomiasis, a neglected tropical disease, is transmitted by freshwater snails. Interruption of transmission will require novel vector-focused interventions. We performed a genome-wide association study of African snails, Biomphalaria sudanica , exposed to Schistosoma mansoni in an endemic area of high transmission in Kenya. Two snail genomic regions, SudRes1 and SudRes2, were significantly associated with snail immunity to schistosomes. SudRes1 includes receptor-like protein tyrosine phosphatases while SudRes2 includes a class of leucine-rich repeat-containing G-protein coupled receptors, both comprising diverse extracellular binding domains suggestive of host-pathogen interaction. Resistant and susceptible haplotypes show numerous coding differences including presence/absence of entire genes. No loci previously tied to schistosome resistance in neotropical snail species showed any association with compatibility suggesting that loci involved in the resistance of African vectors are distinct. Snail ancestry was also strongly correlated with parasite compatibility. These results will inform future efforts to predict and manipulate immunity of a major schistosome vector.

Time-Course Transcriptomics Analysis Reveals Molecular Mechanisms of Salt-Tolerant and Salt-Sensitive Cotton Cultivars in Response to Salt Stress.

Salt stress is an environmental factor that limits plant seed germination, growth, and survival. We performed a comparative RNA sequencing transcriptome analysis during germination of the seeds from two cultivars with contrasting salt tolerance responses. A transcriptomic comparison between salt-tolerant cotton cv Jin-mian 25 and salt-sensitive cotton cv Su-mian 3 revealed both similar and differential expression patterns between the two genotypes during salt stress. The expression of genes related to aquaporins, kinases, reactive oxygen species (ROS) scavenging, trehalose biosynthesis, and phytohormone biosynthesis and signaling that include ethylene (ET), gibberellin (GA), abscisic acid (ABA), jasmonic acid (JA), and brassinosteroid (BR) were systematically investigated between the cultivars. Despite the involvement of these genes in cotton's response to salt stress in positive or negative ways, their expression levels were mostly similar in both genotypes. Interestingly, a PXC2 gene (Ghir_D08G025150) was identified, which encodes a leucine-rich repeat receptor-like protein kinase (LRR-RLK). This gene showed an induced expression pattern after salt stress treatment in salt-tolerant cv Jin-mian 25 but not salt-sensitive cv Su-mian 3. Our multifaceted transcriptome approach illustrated a differential response to salt stress between salt-tolerant and salt-sensitive cotton.

Cotton RLP6 Interacts With NDR1/HIN6 to Enhance Verticillium Wilt Resistance via Altering ROS and SA.

Cotton Verticillium wilt (VW) is often a destructive disease that results in significant fibre yield and quality losses in Gossypium hirsutum. Transferring the resistance trait of Gossypium barbadense to G. hirsutum is optional but challenging in traditional breeding due to limited molecular dissections of resistance genes. Here, we discovered a species-diversified structural variation (SV) in the promoter of receptor-like protein 6 (RLP6) that caused distinctly higher expression level of RLP6 in G. barbadense with the SV than G. hirsutum without the SV. Functional experiments showed that RLP6 is an important regulator in mediating VW resistance. Overexpressing RLP6 significantly enhanced resistance and root growth, whereas the opposite phenotype appeared in RLP6-silenced cotton. A series of experiments indicated that RLP6 regulated reactive oxygen species (ROS) and salicylic acid (SA) signalling, which induced diversified defence-related gene expression with pathogenesis-related (PR) proteins and cell wall proteins enrichments for resistance improvement. These findings could be valuable for the transfer of the G. barbadense SV locus to improve G. hirsutum VW resistance in future crop disease resistance breeding.

Proteome-wide analysis reveals G protein-coupled receptor-like proteins in rice (Oryza sativa)

ABSTRACT G protein-coupled receptors (GPCRs) constitute the largest family of transmembrane proteins in metazoans that mediate the regulation of various physiological responses to discrete ligands through heterotrimeric G protein subunits. The existence of GPCRs in plant is contentious, but their comparable crucial role in various signaling pathways necessitates the identification of novel remote GPCR-like proteins that essentially interact with the plant G protein α subunit and facilitate the transduction of various stimuli. In this study, we identified three putative GPCR-like proteins (OsGPCRLPs) (LOC_Os06g09930.1, LOC_Os04g36630.1, and LOC_Os01g54784.1) in the rice proteome using a stringent bioinformatics workflow. The identified OsGPCRLPs exhibited a canonical GPCR ‘type I’ 7TM topology, patterns, and biologically significant sites for membrane anchorage and desensitization. Cluster-based interactome mapping revealed that the identified proteins interact with the G protein α subunit which is a characteristic feature of GPCRs. Computational results showing the interaction of identified GPCR-like proteins with G protein α subunit and its further validation by the membrane yeast-two-hybrid assay strongly suggest the presence of GPCR-like 7TM proteins in the rice proteome. The absence of a regulator of G protein signaling (RGS) box in the C- terminal domain, and the presence of signature motifs of canonical GPCR in the identified OsGPCRLPs strongly suggest that the rice proteome contains GPCR-like proteins that might be involved in signal transduction.

Exosomal PVRL4 Promotes Lung Adenocarcinoma Progression by Enhancing the Generation of Myeloid-Derived Suppressor Cell-Secreted TGF-β1.

The cancer cell marker poliovirus receptor-like protein 4 (PVRL4) has been shown to be highly expressed in many cancers, including lung cancer. Myeloid-derived suppressor cells (MDSCs) are a population of immature myeloid cells with immunosuppressive roles that can attenuate the anticancer response. Here, the precise functions and the relationship between PVRL4 and MDSCs in lung adenocarcinoma (LUAD) progression were investigated. Detection of levels of mRNAs and proteins was conducted using qRT-PCR and western blotting. The CCK-8, colony formation, transwell, wound healing assays, and flow cytometry were used to explore cell growth, invasion, migration, and apoptosis, respectively. ELISA analysis detected TGF-β1 contents. LUAD mouse models were established for invivo assay. Exosomes were isolated by ultracentrifugation. MDSCs were induced from peripheral blood mononuclear cells (PBMCs) by cytokine or co-culture with cancer cells. LUAD tissues and cells showed high PVRL4 expression, and PVRL4 deficiency suppressed LUAD cell proliferation, invasion, migration, and induced cell apoptosis invitro, and impeded LUAD growth invivo. Thereafter, we found that PVRL4 was packaged into exosomes in LUAD cells, and could be transferred into PBMCs to promote MDSC induction and the expression of MDSC-secreted TGF-β1. Functionally, the silencing of exosomal PVRL4 impaired LUAD cell proliferation, invasion, migration, and evoked cell apoptosis, which could be reversed by the incubation of TGF-β1-overexpressed MDSCs. Exosomal PVRL4 promoted LUAD progression by inducing the secretion of TGF-β1 in MDSCs, indicating a novel direction for LUAD immunotherapy.

SgR1, Encoding a Leucine-Rich Repeat Containing Receptor-like Protein, Is a Major Aphid (Schizaphis graminum) Resistance Gene in Sorghum.

Greenbug, Schizaphis graminum, is one of the important cereal aphid pests of sorghum in the United States and other parts of the world. Sorghum bicolor variety PI 607900 carries the Schizaphis graminum resistance (SgR1) gene that underlies plant resistance to greenbug biotype I (GBI). Now, the SgR1 has been determined as the major gene conferring greenbug resistance based on the strong association of its presence with the resistance phenotype in sorghum. In this study, we have successfully isolated the SgR1 gene using a map-based cloning approach, and subsequent molecular characterization revealed it encodes a leucine-rich repeat containing receptor-like protein (LRR-RLP). According to DNA sequence analysis, the SgR1 gene are conserved among GBI-resistance sorghum accessions but are variable within susceptible lines. Furthermore, an InDel (-965 nt) at its promoter region and a single-nucleotide polymorphism (SNP, 592 nt) in the CDS of the SgR1 were detected and they are well conserved within resistant genotypes. When the SgR1 gene was cloned and transferred into Arabidopsis plants, the SgR1 was activated in the transgenic Arabidopsis plants in response to attack by green peach aphids according to the results of the histochemical assay, and GUS activity was detected in situ in spots around the vasculature of the leaf where the phloem is located, suggesting its biological function in those transgenic Arabidopsis plants. Overall, this study confirms that the SgR1 gene coding for an LRR-RLP is the major resistance gene to greenbug, a destructive pest in sorghum and wheat. This represents the first greenbug resistance gene cloned so far and indicates that the simple-inherited GBI resistance gene can be used for sorghum improvement with genetic resistance to GBI via molecular breeding or cross-based conventional breeding technologies.

A Leucine-Rich Receptor Like Kinase LRK2 Is Involved in the Regulation of Cold Tolerance and Yield in Rice.

Low temperature affects rice growth and yield. Receptor-like protein kinases play an important role in plant growth and development. In order to reveal the role of a leucine-rich receptor like kinase LRK2 in low temperature stress and growth and development of rice. In this study, we used the obtained LRK2 overexpressing plants for experiments and the results show that the cold tolerance and yield of LRK2 overexpressing plants were higher than that of wild type. LRK2 has high homology with the phytosulfokine receptors (PSKRs) gene of different species, and LRK2 gene is responsive to phytosulfokine (PSK). In addition, we observed that the proline content of LRK2 overexpressing plants was significantly higher than that of the wild-type at low temperature, while the malondialdehyde content was significantly lower than that of the wild-type. Yeast two-hybrid screening and bimolecular fluorescence complementary analysis showed that LRK2 interacts with rice growth hormone response factor 24 (OsARF24) in vitro. These results suggest that LRK2 gene may be involved in the regulation of cold stress response and yield in rice. These findings will help us understand PSKR signaling in other grasses and support improvements in rice genetics.

Synthetic T-Cell Receptor-like Protein Behaves as a Janus Particle in Solution.

Protein engineering enables the creation of tailor-made proteins for a variety of applications. ImmTACs stand out as promising therapeutics for cancer and other treatments while also presenting unique challenges for stability, formulation, and delivery. We have shown that ImmTACs behave as Janus particles in solution, leading to self-association at low concentrations, even when the average protein-protein interactions suggest that the molecule should be stable. The formation of small but stable oligomers was confirmed by static and dynamic light scattering and analytical ultracentrifugation. Modeling of the structure using AlphaFold leads to a rational explanation for this behavior, consistent with the Janus particle assembly observed for inverse patchy particles.

Comprehensive Genome-Wide Analysis of the Receptor-like Protein Gene Family and Functional Analysis of PeRLP8 Associated with Crown Rot Resistance in Passiflora edulis.

Passion fruit (Passiflora edulis Sims) is a Passifloraceae plant with high economic value. Crown rot caused by Rhizoctonia solani is a major fungal disease, which can seriously reduce the yield and quality of passion fruit. Receptor-like proteins (RLPs), which act as pathogen recognition receptors, are widely involved in plant immune responses and developmental processes. However, the role of RLP family members of passion fruit in resistance to crown rot remains unclear. In this study, evolutionary dynamics analysis and comprehensive genomic characterization of the RLP genes family were performed on passion fruit. A total of 141 PeRLPs in the genome of the 'Zixiang' cultivar and 79 PesRLPs in the genome of the 'Tainong' cultivar were identified, respectively. Evolutionary analysis showed that proximal and dispersed duplication events were the primary drivers of RLP family expansion. RNA-seq data and RT-qPCR analysis showed that PeRLPs were constitutively expressed in different tissues and induced by low temperature, JA, MeJA, and SA treatments. The PeRLP8 gene was identified as the hub gene by RNA-seq analysis of passion fruit seedlings infected by Rhizoctonia solani. The expression levels of PeRLP8 of the resistant variety Passiflora maliformis (LG) were significantly higher than those of the sensitive variety Passiflora edulis f. flavicarpa (HG). Transient overexpression of PeRLP8 tobacco and passion fruit leaves enhanced the resistance to Rhizoctonia solani, resulting in reduced lesion areas by 52.06% and 54.17%, respectively. In addition, it can increase reactive oxygen species levels and upregulated expression of genes related to active oxygen biosynthesis and JA metabolism in passion fruit leaves. Our research provides new insights into the molecular mechanism and breeding strategy of passion fruit resistance to crown rot.

Transcriptome analysis under pecan scab infection reveals the molecular mechanisms of the defense response in pecans.

Pecan scab, caused by the fungal pathogen Venturia effusa, is the most devastating disease of pecan (Carya illinoinensis) in the southeastern United States. Resistance to this pathogen is determined by a complex interaction between host genetics and disease pathotype with even field-susceptible cultivars being resistant to most scab isolates. To understand the underlying molecular mechanisms of scab resistance in pecan, we performed a transcriptome analysis of the pecan cultivar, 'Desirable', in response to inoculation with a pathogenic and a non-pathogenic scab isolate at three different time points (24, 48, and 96 hrs. post-inoculation). Differential gene expression and gene ontology enrichment analyses showed contrasting gene expression patterns and pathway enrichment in response to the contrasting isolates with varying pathogenicity. The weighted gene co-expression network analysis of differentially expressed genes detected 11 gene modules. Among them, two modules had significant enrichment of genes involved with defense responses. These genes were particularly upregulated in the resistant reaction at the early stage of fungal infection (24 h) compared to the susceptible reaction. Hub genes in these modules were predominantly related to receptor-like protein kinase activity, signal reception, signal transduction, biosynthesis and transport of plant secondary metabolites, and oxidoreductase activity. Results of this study suggest that the early response of pathogen-related signal transduction and development of cellular barriers against the invading fungus are likely defense mechanisms employed by pecan cultivars against non-virulent scab isolates. The transcriptomic data generated here provide the foundation for identifying candidate resistance genes in pecan against V. effusa and for exploring the molecular mechanisms of disease resistance.

Critical radicle length window governing loss of dehydration tolerance in germinated Perilla seeds: insights from physiological and transcriptomic analyses

BackgroundPerilla (Perilla frutescens L. Britt.) is an important oilseed and medicinal crop that frequently faces seasonal drought stress during seed germination, leading to a loss of dehydration tolerance (DT), which affects seed emergence and significantly reduces yield. DT has been successfully re-established for many species seeds. However, the physiological mechanisms and gene networks that regulate Perilla’s response to DT loss remain unclear.ResultsPhenotypic analysis determined that the window for DT in Perilla seeds occurs at radicle lengths of 0–4 mm. Integrating physiological and transcriptomic analyses revealed that the loss of DT promotes the production of reactive oxygen species (ROS) and regulates oxidase activity and gene expression. This implies that DT may influence seed germination by modulating ROS activity. Four radicle length (i.e., 0, 1, 3, and 4 mm) stages were analyzed, and 262 differentially expressed genes (DEGs) were identified that responded to DT. The majority of these genes were associated with epigenetics, cell function, and transport mechanisms. Analysis of expression data shows that desiccation inhibits the signaling network of genes encoding small secreted peptides (SSPs) and receptor-like protein kinases (RLKs). Finally, a relevant network diagram of DT response was proposed. Based on this information, we have revealed the metabolism regulation maps of the four main pathways involving these DEGs (i.e., metabolic pathways, cell cycle, plant hormone signal transduction, and motor proteins).ConclusionsIn conclusion, these findings deepen our understanding of gene network responses to DT during Perilla seed germination and provide potential target genes for the genetic improvement of drought resistance in this crop.

Dual activation of soybean resistance against Phytophthora sojae by pectin lyase and degraded pectin oligosaccharides.

Phytophthora pathogens secrete numerous apoplastic effectors to manipulate host immunity. Herein, we identified a polysaccharide lyase 1 protein, PsPL1, which acts as an essential virulence factor of P. sojae infection in soybean. However, the overexpression of PsPL1 in P. sojae reduced infection and triggered enhanced immune responses in soybean. PsPL1 exhibited pectin lyase activity and degraded plant pectin to generate pectin oligosaccharides (POSs) with a polymerization degree of 3-14, exhibiting different levels of acetylation and methylation modifications. PsPL1 and the degraded pectin products triggered immune responses in soybean and different Solanaceous plants. The PsPL1-triggered immune responses required RSPL1, a membrane-localized leucine-rich repeat receptor-like protein, which is essential for Phytophthora resistance. Conversely, the PsPL1-degraded product-triggered immune responses depended on the membrane-localized lysin motif receptor-like kinase CERK1. This study reveals that the pectin lyase exhibits a dual immunogenic role during P. sojae infection, which activates plant resistance through different immune receptors and provides novel insights into the function of pectin lyase in host-pathogen interactions.