Defense Pathways Research Articles

Curcumin: A Potential Detoxifier Against Chemical and Natural Toxicants.

The human body gets exposed to a variety of toxins intentionally or unintentionally on a regular basis from sources such as air, water, food, and soil. Certain toxins can be synthetic, while some are biological. The toxins affect the various parts of the body by activating numerous pro-inflammatory markers, like oxidative stresses, that tend to disturb the normal function of the organs ultimately. Nowadays, people use different types of herbal treatments, viz., herbal drinks that contain different spices for detoxification of their bodies. One such example is turmeric, the most commonly available spice in the kitchen and used across all kinds of households. Turmeric contains curcumin, which is a natural polyphenol. Curcumin is a medicinal compound with different biological activities, such as antioxidant, antineoplastic, anti-inflammatory, and antibacterial. Hence, this review gives a comprehensive insight into the promising potential of curcumin in the detoxification of heavy metals, carbon tetrachloride, drugs, alcohol, acrylamide, mycotoxins, nicotine, and plastics. The review encompasses diverse animal-based studies portraying curcumin's role in nullifying the different toxic effects in various organs of the body (especially the liver, kidney, testicles, and brain) by enhancing defensive signaling pathways, improving antioxidant enzyme levels, inhibiting pro-inflammatory markers activities and so on. Furthermore, this review also argues over curcumin's safety assessment for its utilization as a detoxifying agent.

Genome assembly and population analysis of tetraploid marama bean reveal two distinct genome types

Tylosema esculentum (marama bean), an underutilized orphan legume native to southern Africa, holds significant potential for domestication as a rescue crop to enhance local food security. Well-adapted to harsh desert environments, it offers valuable insights into plant resilience to extreme drought and high temperatures. In this study, k-mer analysis indicated marama as an ancient allotetraploid legume. Using 21.5 Gb of PacBio HiFi data, the genome was assembled with two assemblers, HiCanu and Hifiasm, followed by scaffolding with Omni-C data from Dovetail Genomics (Cantata Bio) using HiRise, resulting in a 558.78 Mb assembly with near chromosome-level continuity (N50 = 22.68 Mb, L50 = 8). Repeats accounted for 58.43% of the genome. Phylogenetic analysis indicated a close relationship with Bauhinia variegata and Cercis canadensis, diverging approximately 27.22 and 31.68 million years ago (Ma), respectively. Whole-genome duplication (WGD) analysis revealed an ancient duplication event in marama. Gene family analysis revealed expanded families enriched in pathways related to stress adaptation, energy metabolism, and environmental signaling, including the spliceosome, citrate cycle, and carbon fixation pathways. These findings highlight marama’s resilience to arid environments. In contrast, contracted gene families associated with secondary metabolite biosynthesis and defense pathways suggest a trade-off, potentially due to reduced pathogen pressure. Marama-specific genes were enriched in amino acid catabolism pathways, potentially playing roles in stress signaling and energy regulation. Core gene families shared with other legumes were enriched in conserved pathways, such as photosynthesis and hormone signaling, which are fundamental for plant growth and survival. Population analysis of geographically diverse samples revealed two distinct clusters, though phenotypic differences remain unclear. Overall, this study presents the first high-quality genome assembly of marama bean, offering a valuable genomic reference for understanding its unique biology and highlighting its potential for crop improvement in challenging environments.

Shallow-water mussels (Mytilus galloprovincialis) adapt to deep-sea environment through transcriptomic and metagenomic insights

Recent studies have unveiled the deep sea as a rich biosphere, populated by species descended from shallow-water ancestors post-mass extinctions. Research on genomic evolution and microbial symbiosis has shed light on how these species thrive in extreme deep-sea conditions. However, early adaptation stages, particularly the roles of conserved genes and symbiotic microbes, remain inadequately understood. This study examined transcriptomic and microbiome changes in shallow-water mussels Mytilus galloprovincialis exposed to deep-sea conditions at the Site-F cold seep in the South China Sea. Results reveal complex gene expression adjustments in stress response, immune defense, homeostasis, and energy metabolism pathways during adaptation. After 10 days of deep-sea exposure, shallow-water mussels and their microbial communities closely resembled those of native deep-sea mussels, demonstrating host and microbiome convergence in response to adaptive shifts. Notably, methanotrophic bacteria, key symbionts in native deep-sea mussels, emerged as a dominant group in the exposed mussels. Host genes involved in immune recognition and endocytosis correlated significantly with the abundance of these bacteria. Overall, our analyses provide insights into adaptive transcriptional regulation and microbiome dynamics of mussels in deep-sea environments, highlighting the roles of conserved genes and microbial community shifts in adapting to extreme environments.

Rice transcription factor bHLH25 confers resistance to multiple diseases by sensing H2O2.

Hydrogen peroxide (H2O2) is a ubiquitous signal regulating many biological processes, including innate immunity, in all eukaryotes. However, it remains largely unknown that how transcription factors directly sense H2O2 in eukaryotes. Here, we report that rice basic/helix-loop-helix transcription factor bHLH25 directly senses H2O2 to confer resistance to multiple diseases caused by fungi or bacteria. Upon pathogen attack, rice plants increase the production of H2O2, which directly oxidizes bHLH25 at methionine 256 in the nucleus. Oxidized bHLH25 represses miR397b expression to activate lignin biosynthesis for plant cell wall reinforcement, preventing pathogens from penetrating plant cells. Lignin biosynthesis consumes H2O2 causing accumulation of non-oxidized bHLH25. Non-oxidized bHLH25 switches to promote the expression of Copalyl Diphosphate Synthase 2 (CPS2), which increases phytoalexin biosynthesis to inhibit expansion of pathogens that escape into plants. This oxidization/non-oxidation status change of bHLH25 allows plants to maintain H2O2, lignin and phytoalexin at optimized levels to effectively fight against pathogens and prevents these three molecules from over-accumulation that harms plants. Thus, our discovery reveals a novel mechanism by which a single protein promotes two independent defense pathways against pathogens. Importantly, the bHLH25 orthologues from available plant genomes all contain a conserved M256-like methionine suggesting the broad existence of this mechanism in the plant kingdom. Moreover, this Met-oxidation mechanism may also be employed by other eukaryotic transcription factors to sense H2O2 to change functions.

Escalation of genome defense capacity enables control of an expanding meiotic driver

From RNA interference to chromatin silencing, diverse genome defense pathways silence selfish genetic elements to safeguard genome integrity. Despite their diversity, different defense pathways share a modular organization, where numerous specificity factors identify diverse targets and common effectors silence them. In the PIWI-interacting RNA (piRNA) pathway, target RNAs are first identified by complementary base pairing with piRNAs and then silenced by PIWI-clade nucleases. Such a binary architecture allows the defense systems to be readily adaptable, where new targets can be captured via innovation of specificity factors. Thus, our current understanding of genome defense against lineage-specific selfish genes has been largely limited to specificity factor innovations, while it remains poorly understood whether other types of innovations are required. Here, we describe a new type of innovation, which escalates the genome defense capacity to control a recently expanded selfish gene in Drosophila melanogaster. Through a targeted RNAi screen for repressors of Stellate-a recently evolved meiotic driver-we identified a defense factor, Trailblazer. Trailblazer is a transcription factor that promotes the expression of two PIWI-clade nucleases, Aub and AGO3, to match Stellate in abundance. Recent innovation in the DNA-binding domain of Trailblazer enabled it to elevate Aub and AGO3 expression, thereby escalating the silencing capacity of piRNA pathway to tame expanded Stellate and safeguard fertility. As copy-number expansion is a recurrent feature of diverse selfish genes across the tree of life, we envision that augmenting the defense capacity to quantitatively match selfish genes is a repeatedly employed defense strategy in evolution.

The role of cGAS-STING signaling pathway in ferroptosis.

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway has been identified as a crucial mechanism in antiviral defense and innate immunity pathway. Ferroptosis, characterized by iron dependence and lipid peroxidation, represents a specialized form of cell death. A burgeoning collection of studies has demonstrated that the cGAS-STING signaling pathway participates in the homeostatic regulation of the organism by modulating ferroptosis-associated enzyme activity or gene expression. Consequently, elucidating the specific roles of the STING signaling pathway and ferroptosis in vivo is vital for targeted disease intervention. This review systematically examines the interactions between the cGAS-STING signaling pathway and ferroptosis, highlighting their influence on disease progression in the contexts of inflammation, injury, and cancerous cell dynamics. Understanding these interactions may provide novel therapeutic strategies. The STING pathway has been implicated in the regulation of various cell death mechanisms, including apoptosis, pyroptosis, necroptosis, autophagy, and ferroptosis. Our focus primarily addresses the role and mechanism of the cGAS-STING signaling pathway and ferroptosis in diseases, limiting discussion of other cell death modalities and precluding a comprehensive overview of the pathway's additional functions.

Insight into Rice Resistance to the Brown Planthopper: Gene Cloning, Functional Analysis, and Breeding Applications.

This review provides a comprehensive overview of the current understanding of rice resistance to the brown planthopper (BPH), a major pest that poses significant threats to rice production through direct feeding damage and by transmitting viruses such as Rice grassy stunt virus (RGSV) and Rice ragged stunt virus (RRSV). We highlight the emergence of various BPH biotypes that have overcome specific resistance genes in rice. Advances in genetic mapping and cloning have identified 17 BPH resistance genes, classified into typical R genes encoding nucleotide-binding leucine-rich repeat (NLR) proteins and atypical R genes such as lectin receptor kinases and proteins affecting cell wall composition. The molecular mechanisms of these genes involve the activation of plant defense pathways mediated by phytohormones like jasmonic acid (JA), salicylic acid (SA), and ethylene, as well as the production of defensive metabolites. We also examine the complex interactions between BPH salivary proteins and rice defense responses, noting how salivary effectors can both suppress and trigger plant immunity. The development and improvement of BPH-resistant rice varieties through conventional breeding and molecular marker-assisted selection are discussed, including strategies like gene pyramiding to enhance resistance durability. Finally, we outline the challenges and future directions in breeding for durable BPH resistance, emphasizing the need for continued research on resistance mechanisms and the development of rice varieties with broad-spectrum and long-lasting resistance.

Enhancing salicylic acid levels by its exogenous pretreatment to mitigate Fusarium oxysporum-induced biotic stress in Vigna mungo: defense pathways insights.

Fusarium oxysporum disrupts redox homeostasis in Vigna mungo, likely by interfering with salicylic acid signaling, which can be ameliorated by boosting PAL and its related pathways via salicylic acid pretreatment. Fusarium oxysporum, a widespread soil-borne fungus, significantly threatens global crops. This study centers on elucidating the infection strategies employed by F. oxysporum against a new and underexplored host Vigna mungo, a leguminous crop of high agronomic value, and the defense mechanisms that can be activated against the infection, aiming to uncover how these responses can be leveraged to develop potential countermeasures. Building on prior work demonstrating the in vitro antifungal efficacy of phytohormones, including salicylic acid (SA), this study further investigates SA pretreatment at 100µM, which previously reduced reactive oxygen species (ROS) and improved germination under Fusarium stress. Through a comprehensive analysis of V. mungo plants pretreated with SA and subjected to F. oxysporum infection, we observed that fungal exposure reduced growth, chlorophyll content, and levels of proteins, phenolics and flavonoids, while increasing stress markers and antioxidant activity. SA pretreatment mitigated these effects by boosting antioxidant molecules and activating the phenylalanine ammonia-lyase (PAL) pathway, thereby enhancing endogenous SA and ROS scavenging. Furthermore, qRT-PCR analysis confirmed SA-mediated upregulation of antioxidant (catalase and peroxidase), fungal stress response genes ((pathogenesis-related gene 4 (PR4) and defensin (DEF)) and SA synthesis and regulator genes (PAL and WRKY70) involved in plant systemic resistance, while LC-MS data revealed an altered metabolic profile with increased phytoalexins and antioxidants synthesis. Overall, SA pretreatment confers resistance against F. oxysporum in V. mungo by modulating endogenous SA and metabolic profile to activate key defense pathways and redox homeostasis, highlighting its potential in plant defense strategies and reinforcing our proposed model of SA action.

Mechanism of action of the toxic proline mimic azetidine 2-carboxylic acid in plants.

Plants have an amazing capacity to outcompete neighboring organisms for space and resources. Toxic metabolites are major players in these interactions, which can have a broad range of effectiveness by targeting conserved molecular mechanisms, such as protein biosynthesis. However, lack of knowledge about defensive metabolite pathways, their mechanisms of action, and resistance mechanisms limits our ability to manipulate these pathways for enhanced crop resilience. Nonproteogenic amino acids (NPAAs) are a structurally diverse class of metabolites with a variety of functions but are typically not incorporated during protein biosynthesis. Here, we investigate the mechanism of action of the NPAA azetidine-2-carboxylic acid (Aze), an analog of the amino acid proline (Pro). Using a combination of plate-based assays, metabolite feeding, metabolomics, and proteomics, we show that Aze inhibits the root growth of Arabidopsis and other plants. Aze-induced growth reduction was restored by supplementing L-, but not D-Pro, and nontargeted proteomics confirm that Aze is misincorporated for Pro during protein biosynthesis, specifically on cytosolically translated proteins. Gene expression analysis, free amino acid profiling, and proteomics show that the unfolded protein response is upregulated during Aze treatment implicating that Aze misincorporation results in accumulation of misfolded proteins triggering a global stress response. This study demonstrates the mechanism of action of Aze in plants and provides a foundation for understanding the biological functions of proteotoxic metabolites.

Defensive responses of most antioxidant genes in the freshwater dinoflagellate Palatinus apiculatus to cadmium stress and their implications

Photosynthetic dinoflagellates are one of the major microalgal taxa, playing essential roles in biogeochemical cycles and food webs in aquatic environments. Some freshwater dinoflagellates are known to be sensitive to environmental conditions, like water quality and contaminants; however, their molecular toxicological responses are insufficiently discovered. In the present study, we evaluated the physiological and transcriptomic responses of the freshwater dinoflagellate Palatinus apiculatus exposed to cadmium (Cd), focusing on stress-responsive genes. The cell number of P. apiculatus decreased significantly at Cd concentrations above 0.25 mg/L after 72 h, with an estimated EC50 value of 1.35 mg/L. In addition, we constructed 87,207 transcriptomic contigs from the P. apiculatus cells exposed to the Cd. Differential expression gene analysis showed that 21.0 % of total contigs were statistically significant, including 8647 up-regulated and 4195 down-regulated genes. Gene Ontology enrichment results revealed that genes responsive to stress and external stimuli were highly expressed in Cd-treated cells. Moreover, Cd significantly induced reactive oxygen species (ROS) production in P. apiculatus cells, and their patterns were similar to the expressions of certain antioxidant genes. Among the selected genes, GR expression levels were down-regulated, which may lead to the failure of cell defense against heavy metals. These results showed molecular defense pathways of the freshwater dinoflagellate P. apiculatus against the heavy metal that could be served as potential sensitive biomarkers for evaluating molecular toxicity in freshwater ecosystems.

The Potential Protective Mechanisms of Exercise-Responsive Molecules in Chronic Kidney Disease

PURPOSE: Chronic kidney disease (CKD) is a major global health issue characterized by a gradual and irreversible decline in renal function. Despite its increasing prevalence, effective therapeutic options remain limited, highlighting the need for novel treatment approaches. This review highlights the importance of exercise as a nonpharmacological intervention by exploring the role of exerciseinduced bioactive molecules in CKD management.METHODS: An extensive literature review was conducted using PubMed, Scopus, Web of Science, and Google Scholar. The search terms included “myokine,” “exerkine,” “chronic kidney disease,” “nephropathy,” “renal function,” “podocyte,” “mesangial cell,” “exercise,” “physical activity,” and other related terms.RESULTS: Exercise-induced molecules, particularly myokines and exerkines, can slow the progression of CKD through protective mechanisms. These molecules reduce oxidative stress via antioxidant defense pathways, regulate immune responses to limit inflammation, and inhibit fibrotic signaling by interacting with TGF-β and other pro-fibrotic factors. Furthermore, they preserve renal function by maintaining podocyte and mesangial cell integrity and modulating autophagy, thereby preventing kidney damage.CONCLUSIONS: This review consolidates the current knowledge on the therapeutic potential and diverse functions of exercise-induced molecules in CKD, offering insights into their ability to slow disease progression and improve patient outcomes through nonpharmacological strategies.

Alternative NADH dehydrogenase: A complex I backup, a drug target, and a tool for mitochondrial gene therapy

Alternative NADH dehydrogenase, also known as type II NADH dehydrogenase (NDH-2), catalyzes the same redox reaction as mitochondrial respiratory chain complex I. Specifically, it oxidizes reduced nicotinamide adenine dinucleotide (NADH) while simultaneously reducing ubiquinone to ubiquinol. However, unlike complex I, this enzyme is non-proton pumping, comprises of a single subunit, and is resistant to rotenone. Initially identified in bacteria, fungi and plants, NDH-2 was subsequently discovered in protists and certain animal taxa including sea squirts. The gene coding for NDH-2 is also present in the genomes of some annelids, tardigrades, and crustaceans. For over two decades, NDH-2 has been investigated as a potential substitute for defective complex I. In model organisms, NDH-2 has been shown to ameliorate a broad spectrum of conditions associated with complex I malfunction, including symptoms of Parkinson's disease. Recently, lifespan extension has been observed in animals expressing NDH-2 in a heterologous manner. A variety of mechanisms have been put forward by which NDH-2 may extend lifespan. Such mechanisms include the activation of pro-longevity pathways through modulation of the NAD+/NADH ratio, decreasing production of reactive oxygen species (ROS) in mitochondria, or then through moderate increases in ROS production followed by activation of defense pathways (mitohormesis). This review gives an overview of the latest research on NDH-2, including the structural peculiarities of NDH-2, its inhibitors, its role in the pathogenicity of mycobacteria and apicomplexan parasites, and its function in bacteria, fungi, and animals.

Molecular Interactions Between Plants and Aphids: Recent Advances and Future Perspectives.

Aphids are small, notorious insect pests that negatively impact plant health and agricultural productivity through direct damage, such as sap-sucking, and indirectly as vectors of plant viruses. Plants respond to aphid feeding with a variety of molecular mechanisms to mitigate damage. These responses are diverse and highly dynamic, functioning either independently or in combination. Understanding plant-aphid interactions is crucial for revealing the full range of plant defenses against aphids. When aphids infest, plants detect the damage via specific receptor proteins, initiating a signaling cascade that activates defense mechanisms. These defenses include a complex interaction of phytohormones that trigger defense pathways, secondary metabolites that deter aphid feeding and reproduction, lectins and protease inhibitors that disrupt aphid physiology, and elicitors that activate further defense responses. Meanwhile, aphids counteract plant defenses with salivary effectors and proteins that suppress plant defenses, aiding in their successful colonization. This review offers a detailed overview of the molecular mechanisms involved in plant-aphid interactions, emphasizing both established and emerging plant defense strategies. Its uniqueness lies in synthesizing the recent progress made in plant defense responses to aphids, along with aphids' countermeasures to evade such defenses. By consolidating current knowledge, this review provides key insights for developing sustainable strategies to achieve crop protection and minimize dependence on chemical pesticides.

Caenorhabditis elegans inositol hexaphosphate pathways couple to RNA interference and pathogen defense

RNA interference (RNAi) is an evolutionarily conserved pathway that defends against viral infections in diverse organisms. Caenorhabditis elegans mutations that enhance RNAi have revealed pathways that may regulate antiviral defense. A genetic screen for C. elegans mutations that fail to up-regulate a defense response reporter transgene detected mutations that enhance RNAi to silence this reporter gene in the inositol polyphosphate multikinase impk-1, the synMuv B gene lin-15B, and the pathogen defense response gene pals-22. Using other assays for enhanced RNAi, we found that the impk-1 alleles and an ippk-1 gene inactivation of a later step in inositol hexaphosphate (IP6) synthesis, and the lin-15B and pals-22 alleles enhance RNAi. IP6 has been known for decades to bind and stabilize human adenosine deaminase that acts on RNA (ADAR) as well as the paralog tRNA editing ADAT. We show that the C. elegans IP6 pathway is also required for mRNA and tRNA editing. Thus, a deficiency in two axes of RNA editing enhances the already potent C. elegans RNAi antiviral defense, suggesting adenosine to inosine RNA editing may normally moderate this siRNA antiviral defense pathway. The C. elegans IP6-deficient mutants are synthetic lethal with a set of enhanced RNAi mutants that act in the polyploid hypodermis to regulate collagen secretion and signaling from that tissue, implicating IP6 signaling especially in this tissue. This enhanced antiviral RNAi response uses the C. elegans RIG-I-like receptor DRH-1 to activate the unfolded protein response (UPR). The production of primary siRNAs, rather than secondary siRNAs, contributes to this activation of the UPR through XBP-1 signaling. The gon-14 and pal-17 mutants that also emerged from this screen act in the mitochondrial defense pathway rather than by enhancing RNAi.

Foisc1 regulates growth, conidiation, sensitivity to salicylic acid, and pathogenicity of Fusarium oxysporum f. sp. cubense tropical race 4

The secreted isochorismatases derived from certain filamentous pathogens play vital roles in the infection of host plants by lowering salicylic acid (SA) levels and suppressing SA-mediated defense pathway. However, it remains unclear whether the fungus Fusarium oxysporum f. sp. cubense tropical race 4 (FocTR4), which causes vascular wilt in bananas, utilizes isochorismatases to modulate SA levels in the host and subvert the banana defense system for successful infection. In the current study, we selected and functionally characterized the foisc1 gene, one of 10 putative isochorismatase-encoding genes in FocTR4 that showed significant upregulation during early stages of infection. Deletion of foisc1 resulted in enhanced vegetative growth and conidiation, increased sensitivity to SA, reduced colonization within host plants, as well as impaired pathogenicity. Conversely, complementation restored phenotypes similar to those observed in the wild-type strain. Furthermore, deletion of foisc1 led to a notable rise in activities of defense-related enzymes such as catalase, peroxidase, and phenylalnine ammonialyase; along with an upregulated expression of several defense-related genes including PR genes and NPR1 genes within hosts' tissues. The non-secretory nature of Foisc1 protein was confirmed and its absence did not affect SA levels within host plants. Transcriptome analysis revealed that deletion of foisc1 resulted in decreased expression levels for numerous genes associated with pathogenicity including those involved in fusaric acid biosynthesis and effector genes as well as a catechol 1,2-dioxygenase gene essential for SA degradation; while increasing expression levels for numerous genes associated with hyphal growth and conidiation were observed instead. Therefore, our findings suggest that Foisc1 may influence hyphal growth, conidiation, sensitivity to SA, and pathogenicity of FocTR4 through modulation of various genes implicated in these processes. These findings provide valuable insights into the pathogenesis of FocTR4, and create a groundwork for the future development of innovative control strategies targeting vascular wilt disease of banana.

The heat of longevity: sex differences in lifespan and body temperature.

Dietary restriction (DR) has long been recognized as a powerful intervention for extending lifespan and improving metabolic health across species. In laboratory animals, DR-typically a 30%-40% reduction in caloric intake-delays aging and enhances mitochondrial function, oxidative defense, and anti-inflammatory pathways. In humans, findings from the CALERIE™ trial confirm DR's potential benefits, with a 25% caloric reduction over 2years resulting in reduced visceral fat, improved cardiometabolic health, and favorable gene expression changes linked to proteostasis, DNA repair, and inflammation. However, recent research in genetically diverse mouse populations reveals that the impact of DR on lifespan is substantially modulated by genetic background, underscoring the importance of individual variability. Additionally, emerging evidence challenges previous assumptions that lower body temperature universally benefits lifespan extension, with data indicating complex relationships between thermoregulation, sex, and longevity. These findings underscore the need for nuanced approaches to DR in both research and potential therapeutic applications, with considerations for genetic and sex-specific factors to maximize healthspan and lifespan outcomes.

Understanding the mechanisms of long noncoding RNAs in response to bacterial blight in rice

Plants are naturally subjected to biotic and abiotic stress conditions, which can lead to severe yield loss. Long noncoding RNAs (lncRNAs), a class of RNAs known as key gene regulators, are crucial in regulating signaling and defense pathways during biotic and abiotic stresses. The knowledge of lncRNA-mediated regulation of coding genes involved in pathways conferring resistance against bacterial blight remains limited. This study aims to decipher the lncRNAs in Oryza sativa triggered by Xanthomonas oryzae pv. oryzae (Xoo) infection. Through transcriptome assembly and lncRNA identification, 1,130 rice long noncoding RNAs were identified. Differential expression (DE) analysis revealed the upregulation of 39 lncRNAs and 1,649 protein-coding genes. Similarly, 54 lncRNAs and 1,892 protein-coding genes were downregulated during bacterial blight infection. Nine DElncRNAs were found to interact with 66 DE protein-coding genes. Through detailed transcriptome analysis, this research identified lncRNAs and their interactions with protein-coding genes involved in major defense pathways, including arginine and proline metabolism as well as linolenic acid metabolism. Furthermore, this study validated the expression levels and negative correlation between identified lncRNAs and their interacting mRNAs using the Xoo-resistant Indian rice cultivar ADT55. The downregulation of lncRNAs leads to the upregulation of genes essential for plant defense, including those encoding arginase, agmatine deiminase, and linoleate 13-s-lipoxygenase. These genes contribute to the biosynthesis of polyamines and jasmonic acid, which are key molecules in plant stress responses and wound healing. The findings of the present study provide a foundational understanding of the molecular interactions between lncRNAs and mRNAs in rice defense mechanisms. The identified lncRNAs can serve as epigenetic markers for identifying bacterial blight stress-tolerant plants, thereby facilitating the development of high-yielding, stress-tolerant rice varieties through breeding programs.

Root-Knot Nematode Early Infection Suppresses Immune Response and Elicits the Antioxidant System in Tomato.

The immune response in plants is regulated by several phytohormones and involves the overexpression of defense genes, including the pathogenesis-related (PR-) genes. The data reported in this paper indicate that nematodes can suppress the immune response by inhibiting the expression of defense genes. Transcripts from nine defense genes were detected by qRT-PCR in the roots of tomato plants at three and seven days post-inoculation (dpi) with living juveniles (J2s) of Meloidogyne incognita (root-knot nematodes, RKNs). All the salicylic acid (SA)-responsive genes tested (PR-1, PR-2, PR-4b, PR-5) were down-regulated in response to nematode infection. On the contrary, the expression of jasmonic acid (JA)-responsive genes, including ACO (encoding the enzyme 1-aminocyclopropane-1-carboxylic acid oxidase, which catalyzes the last step of ethylene (ET) biosynthesis) and JERF3 (Jasmonate Ethylene Response Factor 3), was unaffected by the infection. Conversely, the effect of nematode attack on the activities of the defense enzymes endoglucanase and endochitinase, encoded by PR-2 and PR-3, respectively, changed depending on the tested dpi. At 5 dpi, both enzymes were inhibited in inoculated plants compared to healthy controls. The genes encoding glutathione peroxidase (GPX) and catalase (CAT), both part of the antioxidant plant system, were highly overexpressed. Additionally, the activity of the antioxidant enzymes superoxide dismutase (SOD), CAT, and ascorbate peroxidase (APX) was enhanced in infected roots. Isoelectrofocusing of root extracts revealed novel SOD isoforms in samples from inoculated plants. Furthermore, plants were pre-treated with an array of key compounds, including hormone generators, inhibitors of SA or JA-mediated defense pathways, reactive oxygen species (ROS) scavengers and generators, inhibitors of ROS generation, and compounds that interfere with calcium-mediated metabolism. After treatments, plants were inoculated with RKNs, and nematodes were allowed to complete their life cycle. Factors of plant growth and infection level in treated plants were compared with those from untreated inoculated plants. Generally, compounds that decreased SA and/or ROS levels increased infection severity, while those that reduced JA/ET levels did not affect infection rates. ROS generators induced resistance against the pests. Compounds that silence calcium signaling by preventing its intake augmented infection symptoms. The data shown in this paper indicate that SA-mediated plant immune responses are consistently suppressed during the early stages of nematode infection, and this restriction is associated with the activation of the antioxidant ROS-scavenging system.

RNA-seq analysis reveals genes associated with Macrophomina phaseolina-induced host senescence in soybean

BackgroundCharcoal rot of soybean is caused by the hemibiotrophic fungus Macrophomina phaseolina, a global crop destroyer and an important pathogen in the midwestern USA. The quantitative nature of host resistance and the complexity of the soybean-M. phaseolina interaction at the molecular level have hampered resistance breeding. A previous study showed that L-ascorbic acid (LAA) pre-treatment before M. phaseolina inoculation reduced charcoal rot lesion length in excised soybean stems. This study aimed to elucidate the genetic underpinnings of M. phaseolina-induced senescence and the mitigating effects of ascorbic acid on this physiological process within the same pathosystem.ResultsRNA was sequenced from M. phaseolina-resistant and -susceptible soybean genotypes following M. phaseolina inoculation, LAA, and hydrogen peroxide (H2O2)—an oxidative stress inducer—application followed by inoculation. More genes were down-regulated in the resistant and susceptible genotypes than up-regulated when the M. phaseolina-inoculated treatments were compared to mock-inoculated control treatments. Gene ontology (GO) term and KEGG pathways analysis detected M. phaseolina-induced up-regulation of receptor-like kinase genes. In contrast, many genes related to antioxidants, defense, and hormonal pathways were down-regulated in both genotypes. LAA pre-treatment induced genes related to photosynthesis and reactive oxygen species responses in both genotypes. H2O2 pre-treatment following inoculation up-regulated many stress-response genes, while hormone signal transduction and photosynthesis-related genes were down-regulated in both genotypes.ConclusionsResults revealed transcriptional variation and genes associated with M. phaseolina-induced senescence in soybean. Ascorbic acid induced many photosynthetic genes, suggesting a complex regulation of defense and immunity in the plant against the hemibiotroph. Soybean plants also exhibited enhanced stress responsiveness when treated with H2O2 followed by inoculation with M. phaseolina. This study will broaden more research avenues related to transcriptional regulation during the M. phaseolina-soybean interaction and the potential role of receptor-like kinases, oxidative stress-responsive genes, ethylene-mediated signaling and enhanced photosynthetic gene expression when mounting host resistance to this important soybean pathogen.

Microbial consortia inoculants differently shape ecophysiological and systemic defence responses of field-grown grapevine cuttings

Despite microbe-based products for grapevine protection and growth improvement are available, only a few of them contain microbes directly isolated from vine tissues. Here, a collection of endophytic bacterial isolates obtained from grapevine woody tissues was used for producing an ad-hoc inoculum. Bacterial isolates were tested in biocontrol assays against some of the main grapevine pathogens and the seven most performing as biological control agents were selected for a consortium development (SynCom). Before putting them in field, a group of cuttings was inoculated with the developed SynCom, whereas a second one was inoculated with a commercial consortium formed by a mixed inoculum of arbuscular mycorrhizal fungi (AMF) and a rhizosphere Bacillus coagulans bacterial strain (B). After the transplanting in field, eco-physiological parameters were monitored, and samples for biochemical and molecular analyses were collected at the end of the experiment. Integration of physiological data with metabolite and transcriptome profiles have been performed. Results showed that the SynCom slowed down photosynthesis, suggesting a reallocation of energy towards defence pathways. Conversely, the AMF+B treatment led to more balanced physiological performances. Metabarcoding analysis revealed that SynCom-treated plants had a significantly lower abundance of wood-decay pathogens than control or AMF+B plants. Collectively, our findings provide information useful for enabling microbial inoculation exploitation with a refined awareness.