Activation Of Disease Resistance Research Articles

A canonical protein complex controls immune homeostasis and multipathogen resistance.

The Ca2+ sensor, ROD1, is a master regulator of immunity in rice. By screening suppressors of rod1 mutants, we show that ROD1 governs immune homeostasis by surveilling the activation of a canonical immune pathway. Mutations in OsTIR (TIR-only protein), OsEDS1 (Enhanced Disease Susceptibility 1), OsPAD4 (Phytoalexin Deficient 4), and OsADR1 (Activated Disease Resistance 1) all abolish enhanced disease resistance of rod1 plants. OsTIR catalyzes the production of second messengers 2'-(5''-phosphoribosyl)-5'-adenosine monophosphate (pRib-AMP) and diphosphate (pRib-ADP), which trigger formation of an OsEDS1-OsPAD4-OsADR1 (EPA) immune complex. ROD1 interacts with OsTIR and inhibits its enzymatic activity while mutation of ROD1 leads to constitutive activation of the EPA complex. Thus, we unveil an immune network that fine-tunes immune homeostasis and multipathogen resistance in rice.

OsHLP1 is an endoplasmic-reticulum-phagy receptor in rice plants

The endoplasmic reticulum (ER) is the largest intracellular endomembrane system; it shows dynamic changes upon environmental stress. To maintain ER morphology and homeostasis under stress, the excessive ER membrane and the associated unwanted proteins can be removed via ER-phagy. Although a few ER-phagy receptors have been reported in mammals and yeast, their functional counterparts in plants remain largely unexplored. Here, we report that the HVA22 family protein OsHLP1 is an uncharacterized ER-phagy receptor in rice (Oryza sativa L.). OsHLP1 interacts with OsATG8b and recruits ER subdomains and the cargo protein OsNTL6, a negative immune regulator, to autophagosomes upon infection with the fungus Magnaporthe oryzae, which substantially activates disease resistance in rice. AtHVA22J, an Arabidopsis thaliana OsHLP1 ortholog, induced similar ER-phagy in plants. Altogether, we unraveled a conservative protein family that may act as ER-phagy receptors in higher plants, and in particular, we highlighted their roles in rice immune responses.

The NLR immune receptor ADR1 and lipase-like proteins EDS1 and PAD4 mediate stomatal immunity in Nicotiana benthamiana and Arabidopsis.

In the presence of pathogenic bacteria, plants close their stomata to prevent pathogen entry. Intracellular nucleotide-binding leucine-rich repeat (NLR) immune receptors recognize pathogenic effectors and activate effector-triggered immune responses. However, the regulatory and molecular mechanisms of stomatal immunity involving NLR immune receptors are unknown. Here, we show that the Nicotiana benthamiana RPW8-NLR central immune receptor ACTIVATED DISEASE RESISTANCE 1 (NbADR1), together with the key immune proteins ENHANCED DISEASE SUSCEPTIBILITY 1 (NbEDS1) and PHYTOALEXIN DEFICIENT 4 (NbPAD4), plays an essential role in bacterial pathogen- and flg22-induced stomatal immunity by regulating the expression of salicylic acid (SA) and abscisic acid (ABA) biosynthesis or response-related genes. NbADR1 recruits NbEDS1 and NbPAD4 in stomata to form a stomatal immune response complex. The transcription factor NbWRKY40e, in association with NbEDS1 and NbPAD4, modulates the expression of SA and ABA biosynthesis or response-related genes to influence stomatal immunity. NbADR1, NbEDS1, and NbPAD4 are required for the pathogen infection-enhanced binding of NbWRKY40e to the ISOCHORISMATE SYNTHASE 1 promoter. Moreover, the ADR1-EDS1-PAD4 module regulates stomatal immunity in Arabidopsis (Arabidopsis thaliana). Collectively, our findings show the pivotal role of the core intracellular immune receptor module ADR1-EDS1-PAD4 in stomatal immunity, which enables plants to limit pathogen entry.

A plasma membrane nucleotide-binding leucine-rich repeat receptor mediates the recognition of the Ralstonia pseudosolanacearum effector RipY in Nicotiana benthamiana

Bacterial wilt disease caused by several Ralstonia species is one of the most destructive diseases in Solanaceae crops. Only a few functional resistance genes against bacterial wilt have been cloned to date. Here, we show that the broadly conserved type III secreted effector RipY is recognized by the Nicotiana benthamiana immune system, leading to cell death induction, induction of defense-related gene expression, and restriction of bacterial pathogen growth. Using a multiplexed virus-induced gene-silencing-based N. benthamiana nucleotide-binding and leucine-rich repeat receptor (NbNLR) library, we identified a coiled-coil (CC) nucleotide-binding and leucine-rich repeat receptor (CNL) required for recognition of RipY, which we named RESISTANCE TO RALSTONIA SOLANACEARUM RIPY (RRS-Y). Genetic complementation assays in RRS-Y-silenced plants and stable rrs-y knockout mutants demonstrated that RRS-Y is sufficient to activate RipY-induced cell death and RipY-induced immunity to Ralstonia pseudosolanacearum. RRS-Y function is dependent on the phosphate-binding loop motif of the nucleotide-binding domain but independent of the characterized signaling components ENHANCED DISEASE SUSCEPTIBILITY 1, ACTIVATED DISEASE RESISTANCE 1, and N REQUIREMENT GENE 1 and the NLR helpers NB-LRR REQUIRED FOR HR-ASSOCIATED CELL DEATH-2, -3, and -4 in N. benthamiana. We further show that RRS-Y localization at the plasma membrane is mediated by two cysteine residues in the CC domain and is required for RipY recognition. RRS-Y also broadly recognizes RipY homologs across Ralstonia species. Lastly, we show that the C-terminal region of RipY is indispensable for RRS-Y activation. Together, our findings provide an additional effector/receptor pair system to deepen our understanding of CNL activation in plants.

Effector XopQ-induced stromule formation in Nicotiana benthamiana depends on ETI signaling components ADR1 and NRG1.

In Nicotiana benthamiana, the expression of the Xanthomonas effector XANTHOMONAS OUTER PROTEIN Q (XopQ) triggers RECOGNITION OF XOPQ1 (ROQ1)-dependent effector-triggered immunity (ETI) responses accompanied by the accumulation of plastids around the nucleus and the formation of stromules. Both plastid clustering and stromules were proposed to contribute to ETI-related hypersensitive cell death and thereby to plant immunity. Whether these reactions are directly connected to ETI signaling events has not been tested. Here, we utilized transient expression experiments to determine whether XopQ-triggered plastid reactions are a result of XopQ perception by the immune receptor ROQ1 or a consequence of XopQ virulence activity. We found that N. benthamiana mutants lacking ROQ1, ENHANCED DISEASE SUSCEPTIBILITY 1, or the helper NUCLEOTIDE-BINDING LEUCINE-RICH REPEAT IMMUNE RECEPTORS (NLRs) N-REQUIRED GENE 1 (NRG1) and ACTIVATED DISEASE RESISTANCE GENE 1 (ADR1), fail to elicit XopQ-dependent host cell death and stromule formation. Mutants lacking only NRG1 lost XopQ-dependent cell death but retained some stromule induction that was abolished in the nrg1_adr1 double mutant. This analysis aligns XopQ-triggered stromules with the ETI signaling cascade but not to host programmed cell death. Furthermore, data reveal that XopQ-triggered plastid clustering is not strictly linked to stromule formation during ETI. Our data suggest that stromule formation, in contrast to chloroplast perinuclear dynamics, is an integral part of the N. benthamiana ETI response and that both NRG1 and ADR1 hNLRs play a role in this ETI response.

EDS1 modules as two-tiered receptor complexes for TIR-catalyzed signaling molecules to activate plant immunity

Plant intracellular nucleotide-binding leucine-rich repeat (NLR) receptors with an N-terminal Toll/Interleukin-1 receptor (TIR) domain detect pathogen effectors to produce TIR-catalyzed signaling molecules for activation of plant immunity. Plant immune signaling by TIR-containing NLR (TNL) proteins converges on Enhanced Disease Susceptibility 1 (EDS1) and its direct partners Phytoalexin Deficient 4 (PAD4) or Senescence-Associated Gene 101 (SAG101). TNL signaling also require helper NLRs N requirement gene 1 (NRG1) and activated disease resistance 1 (ADR1). In two recent remarkable papers published in Science, the authors show that the TIR-containing proteins catalyze and produce two types of signaling molecules, ADPr-ATP/diADPR and pRib-AMP/ADP. Importantly, they demonstrate that EDS1-SAG101 and EDS1-PAD4 modules are the receptor complexes for ADPr-ATP/diADPRp and Rib-AMP/ADP, respectively, which allosterically promote EDS1-SAG101 interaction with NRG1 and EDS1-PAD4 interaction with ADR1. Thus, two different small molecules catalyzed by TIR-containing proteins selectively activate the downstream two distinct branches of EDS1-mediated immune signalings. These breakthrough studies significantly advance our understanding of TNL downstream signaling pathway.

Identification and receptor mechanism of TIR-catalyzed small molecules in plant immunity.

Plant nucleotide-binding leucine-rich repeat-containing (NLR) receptors with an N-terminal Toll/interleukin-1 receptor (TIR) domain sense pathogen effectors to enable TIR-encoded nicotinamide adenine dinucleotide hydrolase (NADase) activity for immune signaling. TIR-NLR signaling requires the helper NLRs N requirement gene 1 (NRG1), Activated Disease Resistance 1 (ADR1), and Enhanced Disease Susceptibility 1 (EDS1), which forms a heterodimer with each of its paralogs Phytoalexin Deficient 4 (PAD4) and Senescence-Associated Gene 101 (SAG101). Here, we show that TIR-containing proteins catalyze the production of 2'-(5''-phosphoribosyl)-5'-adenosine monophosphate (pRib-AMP) and diphosphate (pRib-ADP) in vitro and in planta. Biochemical and structural data demonstrate that EDS1-PAD4 is a receptor complex for pRib-AMP and pRib-ADP, which allosterically promote EDS1-PAD4 interaction with ADR1-L1 but not NRG1A. Our study identifies TIR-catalyzed pRib-AMP and pRib-ADP as a missing link in TIR signaling through EDS1-PAD4 and as likely second messengers for plant immunity.

Research on ADR1s helps understanding the plant immune network

Plant innate immunity begins with the recognition of pathogens by plasma membrane localized pattern-recognition receptors (PRRs) and intracellular nucleotide-binding domain leucine-rich repeat containing receptors (NLRs), which lead to pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), respectively. For a long time, PTI and ETI have been regarded as two independent processes although they share multiple components and signal outputs. Increasing evidence shows an intimate link between PTI and ETI. PTI and ETI mutually potentiate each other, and this is essential for robust disease resistance during pathogen infection. An ancient class of NLRs called RNLs, so named because they carry a Resistance to Powdery Mildew 8 (RPW8)-like coiled-coil (CC) domain in the N terminus, has emerged as a key node connecting PTI and ETI. RNLs not only act as helper NLRs that signal downstream of sensor NLRs, they also directly mediate PTI signaling by associating with PRR complexes. Here, we focus on Activated Disease Resistance 1 (ADR1), a subclass of RNLs, and discuss its role and mechanism in plant immunity.

Cytokine profile in serum and gingival crevicular fluid of children with inflammatory bowel disease: A case-control study.

To evaluate the cytokine profile in gingival crevicular fluid (GCF) and serum of pediatric inflammatory bowel disease (IBD) patients and determine the cluster patterns of cytokines. Fifty IBD patients and 21 systemically healthy children were enrolled in the study. The GCF samples were collected from the participants during periodontal examination and periodontal indices were recorded. Based on activity indexes and response to conventional treatment, patients with IBD were further categorized into subgroups as: remission, active disease, and treatment-resistant. Serum samples were obtained from IBD patients to determine serum levels of cytokines. The levels of pro- (interleukin (IL)-1β, IL-12, IL-21, IL-22, IL-23, IL-17A, IL-17F) and anti-inflammatory (IL-4, IL-10) cytokines in serum and GCF were measured using Enzyme-linked Immunosorbent Assay (ELISA) kits. Among 50 IBD patients, 58% were in remission, 20% had active disease, and 22% were defined as treatment-resistant. The severity of gingival inflammation measured by the criteria of Löe had increasing trends in IBD patients with active disease and treatment resistance. GCF IL-1β level was lower and GCF IL-4 and GCF IL-23 levels were higher in IBD patients compared to healthy controls. In the active disease group, more cytokine clusters occurred compared to the control group and other IBD subgroups, as explained by increased cytokine-cytokine interactions. Considering the increased complexity of cytokine interactions and the increased severity of gingival inflammation in patients with active disease, it can be concluded that disease activity might have an impact on gingival inflammation in pediatric patients with IBD.

The truncated TNL receptor TN2-mediated immune responses require ADR1 function.

The loss of function of exocyst subunit EXO70B1 leads to autoimmunity, which is dependent on TIR-NBS2 (TN2), a truncated intracellular nucleotide-binding and leucine-rich repeat receptor (NLR). However, how TN2 triggers plant immunity and whether typical NLRs are required in TN2-activated resistance remain unclear. Through the CRISPR/Cas9 gene editing system and knockout analysis, we found that the spontaneous cell death and enhanced resistance in exo70B1-3 were independent of the full-length NLR SOC3 and its closest homolog SOC3-LIKE 1 (SOC3-L1). Additionally, knocking out SOC3-L1 or TN2 did not suppress the chilling sensitivity conferred by chilling sensitive 1-2 (chs1-2). The ACTIVATED DISEASE RESISTANCE 1 (ADR1) family and the N REQUIREMENT GENE 1 (NRG1) family have evolved as helper NLRs for many typical NLRs. Through CRISPR/Cas9 gene editing methods, we discovered that the autoimmunity of exo70B1-3 fully relied on ADR1s, but not NRG1s, and ADR1s contributed to the upregulation of TN2 transcript levels in exo70B1-3. Furthermore, overexpression of TN2 also led to ADR1-dependent autoimmune responses. Taken together, our genetic analysis highlights that the truncated TNL protein TN2-triggered immune responses require ADR1s as helper NLRs to activate downstream signaling, revealing the importance and complexity of ADR1s in plant immunity regulation.

ZAR1 resistosome and helper NLRs: Bringing in calcium and inducing cell death

ZAR1 resistosome and helper NLRs: Bringing in calcium and inducing cell death

Plant "helper" immune receptors are Ca2+-permeable nonselective cation channels.

Plant nucleotide-binding leucine-rich repeat receptors (NLRs) regulate immunity and cell death. In Arabidopsis, a subfamily of "helper" NLRs is required by many "sensor" NLRs. Active NRG1.1 oligomerized, was enriched in plasma membrane puncta, and conferred cytoplasmic calcium ion (Ca2+) influx in plant and human cells. NRG1.1-dependent Ca2+ influx and cell death were sensitive to Ca2+ channel blockers and were suppressed by mutations affecting oligomerization or plasma membrane enrichment. Ca2+ influx and cell death mediated by NRG1.1 and ACTIVATED DISEASE RESISTANCE 1 (ADR1), another helper NLR, required conserved negatively charged N-terminal residues. Whole-cell voltage-clamp recordings demonstrated that Arabidopsis helper NLRs form Ca2+-permeable cation channels to directly regulate cytoplasmic Ca2+ levels and consequent cell death. Thus, helper NLRs transduce cell death signals directly.

Effect of necrotrophic fungus and PGPR on the comparative histochemistry of Vigna radiata by using multiple microscopic techniques.

Rapid advances in the field of pathogen detection have opened new opportunities and better understanding for their management approaches. Aim of this study was to elucidate histopathological observations of different tissues affected by Macrophomina phaseolina and to observe the defense responses of plant growth promoting rhizobacteria (PGPR) in mungbean plants. Sections of the stem and root were prepared and stained with ferric chloride, Lugol's iodine and Wiesner's reagent and were then observed under multiple microscopic techniques. Results revealed that both pathogen and PGPR produce responses on the plant that include colonization of xylem vessels by hyphae and sclerotia, hypertrophy and hyperplasia of the cells, destruction of xylem fibers and amyloplasts in parenchymatous cells; and production of gels by the plant were observed. There was a significant increase in lignin and phenolic compounds deposition in stem and root sections of PGPR treated and non-treated mungbean plants. Whereas the soil amended with PGPR showed very less to no starch production. Moreover, production of gels and gums were also observed in both stem and root sections. Compared to light microscopy, scanning electron microscope provided greater depth of focus and resolution of the pathogen attack on plant tissues, associated bacteria. As a whole, the data demonstrated that inoculation of PGPR can be an effective strategy to stimulate plant growth and they could significantly activate disease resistance against M. phaseolina.

The role of androgen deprivation therapy on the clinical course of COVID-19 infection in men with prostate cancer.

41 Background: TMPRSS2, a cell surface protease which is commonly upregulated in prostate cancer (PC) and regulated by androgens, is a necessary component for SARS-CoV2 cellular entry into respiratory epithelial cells. PC patients receiving ADT were reported to have a lower risk of SARS-CoV-2 infection. However, whether ADT may have an impact on the severity of COVID-19 illness in this population is poorly understood. Methods: In this study performed across 7 US medical centers, we retrospectively evaluated patients with active PC and SARS-COV-2 viral detection by PCR between 03/01/20 and 05/31/20. We collected information on demographics; medical comorbidities; medications; PC Gleason score at initial diagnosis; presence of active disease, metastases, and castration resistance; ADT use as defined by GnRH analog or antagonist within 3 months or castration levels of testosterone < 50 ng/dL within 6 months of COVID-19 diagnosis, or history of bilateral orchiectomy; active non-ADT systemic therapies including, but not limited to, androgen-receptor-targeted therapies and chemotherapy; and COVID-19-related outcomes including hospitalization, supplemental oxygen use, mechanical ventilation requirement, WHO COVID-19 ordinal scale for clinical improvement, follow-up duration, and vital status. Multivariable mixed-effect logistic regression was performed to evaluate any difference in COVID-19 clinical outcomes between patients on and not on ADT. Survival analysis was done using adjusted Cox proportion-hazards regression model. All tests were two-sided at 0.05 significance level. Results: We identified 465 evaluable patients with median age of 71 (61-81) years. Median duration of follow-up was 60 (12-114.2) days. In this follow up period, there were 195 (41.9%) hospitalizations and 111 (23.9%) deaths. When adjusted for age, BMI, and PC clinical disease state, overall survival (HR 1.28 [95%CI 0.79-2.08], P = 0.32), hospitalization status (HR 1.07 [0.61-1.87], P = 0.82), supplemental oxygen use (HR 1.29 [0.77-2.17], P = 0.34), and use of mechanical ventilation (HR 1.07 [0.51-2.23], P = 0.87) were not statistically different between ADT and non-ADT cohorts. Similarly, in subgroup analysis, no statistical difference in overall survival was found between ADT and non-ADT cohorts for hospitalized patients (HR 1.42 [0.82-2.47], P = 0.21) and those receiving supplemental oxygen (HR 1.10 [0.65-1.85], P = 0.73). Conclusions: In this retrospective cohort of PC patients, use of ADT prior to COVID-19 diagnosis does not protect against severe COVID-19 illness as defined by hospitalization, supplemental oxygen use, or death. Further preclinical work in understanding TMPRSS2 expression and androgen regulation in respiratory epithelial cells is needed. As well, longer clinical follow-up and additional clinical studies inclusive of prospective data are warranted to fully address this question.

Two unequally redundant "helper" immune receptor families mediate Arabidopsis thaliana intracellular "sensor"immune receptor functions.

Plant nucleotide-binding (NB) leucine-rich repeat (LRR) receptor (NLR) proteins function as intracellular immune receptors that perceive the presence of pathogen-derived virulence proteins (effectors) to induce immune responses. The 2 major types of plant NLRs that "sense" pathogen effectors differ in their N-terminal domains: these are Toll/interleukin-1 receptor resistance (TIR) domain-containing NLRs (TNLs) and coiled-coil (CC) domain-containing NLRs (CNLs). In many angiosperms, the RESISTANCE TO POWDERY MILDEW 8 (RPW8)-CC domain containing NLR (RNL) subclass of CNLs is encoded by 2 gene families, ACTIVATED DISEASE RESISTANCE 1 (ADR1) and N REQUIREMENT GENE 1 (NRG1), that act as "helper" NLRs during multiple sensor NLR-mediated immune responses. Despite their important role in sensor NLR-mediated immunity, knowledge of the specific, redundant, and synergistic functions of helper RNLs is limited. We demonstrate that the ADR1 and NRG1 families act in an unequally redundant manner in basal resistance, effector-triggered immunity (ETI) and regulation of defense gene expression. We define RNL redundancy in ETI conferred by some TNLs and in basal resistance against virulent pathogens. We demonstrate that, in Arabidopsis thaliana, the 2 RNL families contribute specific functions in ETI initiated by specific CNLs and TNLs. Time-resolved whole genome expression profiling revealed that RNLs and "classical" CNLs trigger similar transcriptome changes, suggesting that RNLs act like other CNLs to mediate ETI downstream of sensor NLR activation. Together, our genetic data confirm that RNLs contribute to basal resistance, are fully required for TNL signaling, and can also support defense activation during CNL-mediated ETI.

New Findings on the Resistance Mechanism of an Elite Diploid Wild Potato Species JAM1-4 in Response to a Super Race Strain of Phytophthora infestans.

Late blight is a devastating potato disease worldwide, caused by Phytophthora infestans. The P. infestans strain 2013-18-306 from Yunnan is a "supervirulent race" that overcomes all 11 known late blight resistance genes (R1 to R11) from Solanum demissum. In a previous study, we identified a diploid wild-type potato JAM1-4 (S. jamesii) with high resistance to 2013-18-306. dRenSeq analysis indicated the presence of novel R genes in JAM1-4. RNA-Seq was used to analyze the late blight resistance response genes and defense regulatory mechanisms of JAM1-4 against 2013-18-306. Gene ontology enrichment and KEGG pathway analysis showed that many disease-resistant pathways were significantly enriched. Analysis of differentially expressed genes (DEGs) revealed an active disease resistance mechanism of JAM1-4, and the essential role of multiple signal transduction pathways and secondary metabolic pathways comprised of SA-JA-ET in plant immunity. We also found that photosynthesis in JAM1-4 was inhibited to promote the immune response. Our study reveals the pattern of resistance-related gene expression in response to a super race strain of potato late blight and provides a theoretical basis for further exploration of potato disease resistance mechanisms, discovery of new late blight resistance genes, and disease resistance breeding.

Inferring RPW8-NLRs's evolution patterns in seed plants: case study in Vitis vinifera.

Genomic and transcriptomic studies in plants and, more in deep, in grapevine reveal that the disease-resistance RNL gene family is highly variable. RNLs (RPW8-NLRs) are a phylogenetically distinct class of nucleotide oligomerization domain (NOD)-like receptors (NLRs) identified in plants. Two RNLs, namely, the NRG1 (N Requirement Gene 1) and the ADR1 (Activated Disease Resistance 1), have been characterized; however, little is known about the RNL evolutionary history in higher plants. To trace the diversification of RNL gene subfamily, we scanned the NLR proteins of 73 plant genomes belonging to 29 taxa, revealing a noticeable diversification across species and within the same genus or botanic family together with a conspicuous expansion in important crop species. To explore the RNL variability in Vitis vinifera and gain information with respect to their structure, evolutionary diversification of five grape genomes ('Aglianico', 'Falanghina', 'Sultanina', 'Tannat', and 'Nebbiolo') has been compared to the reference genome ('Pinot Noir'). The number of RNLs ranged from 6 ('Sultanina') to 14 ('Nebbiolo'), in contrast to the 10 'Pinot Noir' RNLs. The phylogenetic study on grapevine RNLs revealed that all collapsed into NRG1-clade, rather than four. To investigate more in depth the means of intraspecific variability of grape RNL copies, a transcriptomic profiling in response to powdery mildew (PM) infection was carried out through qRT-PCRs and public databases interrogation. The RNL expression variability identified in transcriptome data sets supports the hypothesis of a functional expansion/contraction in grapevine varieties. Although no direct correlations between grapevine PM-resistance and RNL expression was identified, our work can provide good candidates for functional studies able to elucidate the putative "helper" role of RNLs in grape immune signalling.

Dextran as an elicitor of phenylpropanoid and flavonoid biosynthesis in tomato fruit against gray mold infection

Alpha-1,3-glucan is often synthesized on the surface of pathogenic filamentous fungi cell walls to block pathogen-associated molecular patterns (PAMPs) generation by host plant enzymes and the subsequent immune system response of the plant. Here, Botrytis cinerea susceptibility was assessed in tomato fruit to determine whether the fruit could recognize this camouflage and mount an immune response to it. The results showed that local mechanical wounds treated with dextran and laminarin, except amylopectin, could locally and then systemically activate disease resistance against B. cinerea infection in tomato fruit. Dextran treatment effectively elicited fruit callose deposition and phenylpropanoid and flavonoid biosynthesis to a greater extent than α-glucanase activity relative to the mock group surface wounds. Enzymatic hydrolysis of this polysaccharide provided some help in improving host disease resistance. Taken together, these results demonstrate that tomato fruit can perceive α-1,3-glucan as a kind of PAMPs but have limited ability to degrade it.

Volatile organic compounds (VOCs) from Bacillus subtilis CF-3 reduce anthracnose and elicit active defense responses in harvested litchi fruits

In this study, we investigated the effects of volatile organic compounds (VOCs) produced by Bacillus subtilis CF-3 on the growth and development of Colletotrichum gloeosporioides and evaluated the elicitation of active defense responses in harvested litchi fruits. In vitro experiments were conducted to explore the bacteriostatic effect of VOCs in inhibiting pathogenic fungi by means of plate enthalpy test, scanning electron microscopy, transmission electron microscopy, and gas chromatography–mass spectrometry (GC–MS). The results showed that 2,4-di-tert-butylphenol and CF-3 24-h fermentation broth (24hFB) can significantly inhibit the germination of fungal spores, disrupt hyphal and cell morphology, and decrease cell membrane fluidity and integrity, resulting in the changes of indexes. In addition, the bacteriostasis of VOCs in the defensive ability of litchi fruits to C. gloeosporioides was studied, and it was shown that 2,4-di-tert-butylphenol and CF-3 24hFB can inhibit the activity of the pathogenic enzymes (pectinase and cellulase) secreted by C. gloeosporioides to reduce the decomposition of plant tissues, activate antioxidant enzymes (peroxidase, polyphenol oxidase, catalase, and superoxide dismutase) in the fruit to eliminate excessive reactive oxygen species in fruits in order to reduce plant cell damage and activate disease resistance enzymes (phenylalanineammonialyase, chitinases, β-1,3-glucanase) to enhance the resistance of litchi fruits to C. gloeosporioides and inhibit its growth. This study investigated the bacteriostasis of VOCs in inhibiting C. gloeosporioides and inducing the resistance of litchi fruits, providing a theoretical basis for future applications.

Cold stress activates disease resistance in Arabidopsis thaliana through a salicylic acid dependent pathway.

Exposure to short-term cold stress influences disease resistance by mechanisms that remain poorly characterized. The molecular basis of cold-activated immunity was therefore investigated in Arabidopsis thaliana inoculated with the bacterial pathogen Pst DC3000, using a transcriptomic analysis. Exposure to cold stress for 10hr was sufficient to activate immunity, as well as H2 O2 accumulation and callose deposition. Transcriptome changes induced by the 10-hr cold treatment were similar to those caused by pathogen infection, including increased expression of the salicylic acid (SA) pathway marker genes, PR2 and PR5, and genes playing positive roles in defence against (hemi)-biotrophs. In contrast, transcripts encoding jasmonic acid (JA) pathway markers such as PR4 and MYC2 and transcripts with positive roles in defence against necrotrophs were less abundant following the 10-hr cold treatment. Cold-activated immunity was dependent on SA, being partially dependent on NPR1 and ICS1/SID2. In addition, transcripts encoding SA biosynthesis enzymes such as ICS2, PAL1, PAL2, and PAL4 (but not ICS1/SID2) and MES9 were more abundant, whereas GH3.5/WES1 and SOT12 transcripts that encode components involved in SA modification were less abundant following cold stress treatment. These findings show that cold stress cross-activates innate immune responses via a SA-dependent pathway.