Yixiao formula (YXF), a traditional Chinese herbal medicine, has demonstrated clinical efficacy in alleviating symptoms of diabetic cardiomyopathy (DCM). The therapeutic mechanism underlying YXF's effects on DCM remains poorly understood. Myocardial fibrosis is a key pathogenic mechanism in DCM, and previous studies have indicated that miR-133a may be involved in its progression. Given that the TGF-β/Smads signaling pathway is a well-established mediator of myocardial fibrosis, investigating the mechanistic role of YXF through miR-133a and the TGF-β/Smads pathway warrants further exploration.

Quorum sensing (QS) is a critical communication system in bacteria that enables them to sense population density through auto-inducers, notably, N-acyl homoserine lactones (AHLs). This study focuses on the role of QS in Vibrio parahaemolyticus, a significant pathogen affecting vannamei shrimp, where it regulates virulence factors such as hemolysins and biofilm formation. We explored the potential of anti-QS agents derived from a Psychrobacter sp., which produces AHL lactonase capable of degrading AHLs and disrupting QS signaling pathways. The purification of AHL lactonase was achieved through chromatographic techniques, yielding a protein with a molecular weight of 28-30 kDa, consistent with previous findings. AHL degradation tests have demonstrated that AHL lactonase was significantly more effective than metabolites from Psychrobacter in breaking down AHLs. However, the metabolites exhibited superior biofilm inhibition activity, indicating distinct mechanisms in disrupting bacterial adherence and virulence. Gene expression analysis revealed that AHL lactonase effectively suppressed virulence-related genes, while the metabolites influenced gene regulation differently. This study highlights the dual mechanisms of action from a Psychrobacter sp. - direct AHL degradation and inhibition of AHL synthesis, offering a promising biocontrol strategy against V. parahaemolyticus infections in shrimp aquaculture. These findings suggest that integrating these approaches could enhance pathogen management, ultimately supporting sustainable aquaculture practices. Further research is warranted to elucidate the underlying molecular mechanisms and optimize the application of these biocontrol agents in disease management.

Glucagon-like peptide-2 (GLP-2) has been demonstrated to stimulate bone formation and increase bone mass. Conversely, aberrant expression of fibroblast growth factor 23 (FGF23), a crucial bone-derived hormone that regulates phosphate metabolism and mineralization, is implicated in the pathogenesis of osteoporosis. This study aimed to elucidate the mechanisms by which GLP-2 ameliorates postmenopausal osteoporosis, focusing on whether it exerts bone-protective effects through downregulation of FGF23 expression via the PI3K/AKT/FOXO1 signalling pathway.

CK2 is an antiapoptotic kinase overactive in various malignancies. Here we show that CK2 inhibition dramatically affects neuroblastoma growth both in vitro and in vivo. In particular, here we report on the identification of CK2-TN03, a CK2 inhibitor showing greater selectivity and cellular efficacy than silmitasertib, the only available clinical grade CK2 inhibitor with orphan status for cholangiocarcinoma and in clinical trials for medulloblastoma. CK2-TN03 acts by suppressing survivin, which is overexpressed in all high-risk neuroblastomas. Survivin function is affected by direct inhibition of its phosphorylation by CK2; its messenger RNA and protein levels are reduced through CK2 regulation of the MDM2/p53 balance via AKT1 and BRD4/MYCN. Accordingly, neuroblastoma cells persistently stall in mitosis before going to apoptosis. Finally, CK2-TN03 does not affect noncycling cells and significantly reduces tumor growth in mice xenografts without any apparent toxicity.

This study aimed to initially characterize the effects of GANT61, a Hedgehog (Hh) signaling pathway inhibitor, on the biological behaviors of ALK-positive anaplastic large cell lymphoma (ALK + ALCL) cell lines and explore its underlying mechanisms. Cell proliferation was determined by CCK-8 assays. Cell cycle distribution and apoptotic rates were assessed by flow cytometry. Differential gene analysis and pathway enrichment studies were conducted using datasets from the GEO database with R packages. Protein expression levels of apoptosis-related markers (Bcl-2, Bax, caspase-3, cleaved caspase-3) and signaling molecules (Gli1, PIK3IP1, Akt, phosphorylated Akt) were quantitatively examined by western blotting. Corresponding mRNA levels were quantified by qRT-PCR. GANT61 treatment inhibited proliferation in a dose- and time-dependent manner, induced cell cycle arrest, and promoted apoptosis in ALK + ALCL cell lines. Notably, PIK3IP1 expression was markedly reduced compared with normal lymphocyte controls, while GAS1 expression showed significant upregulation in ALK + ALCL cell lines. Gene Set Enrichment Analysis (GSEA) demonstrated significant enrichment of the PI3K/Akt and Hh signaling pathways. Mechanistically, GANT61 upregulated PIK3IP1 while downregulating both Gli1 protein level and Akt phosphorylation. The Gli-targeting agent GANT61 may inhibit ALK + ALCL cell growth, trigger cell cycle arrest and induce apoptosis through Gli1 inhibition, potentially leading to PIK3IP1 upregulation and subsequent attenuation of PI3K/Akt pathway activity. These findings indicate that the Hh-PIK3IP1-Akt signaling axis may participate in ALK + ALCL tumorigenesis, showing that conventional target drugs can be employed for ALK + ALCL treatment.

The BRD and extra-terminal domain (BET) family of proteins was inhibited using I-BET762, a small molecule inhibitor, which mimics interaction with acetylated lysin residue in BET protein. We explored the roles of the bromodomain (BRD) of chromatin adapators in regulating synovial inflammation in rheumatoid arthritis (RA). The expression levels of bromodomain proteins, c-Myc, and the components of the MAPK and NF-κB signaling pathways were detected by western blot. The BRD3, BRD4, and c-Myc expression were suppressed by I-BET762-treated RA-FLS. I-BET762 inhibited the phosphorylation of p38 MAPK and NF-κB signaling pathways. Moreover, secretion levels of pro-inflammatory mediators (IL-6 and IL-8), chemokine (CXCL-10), and MMP-1 and -3 significantly decreased after I-BET762 treatment. Cell migration and invasion were also reduced in response to I-BET762 treatment. I-BET762 treatment concurrently inhibited p38 MAPK and NF-κB, thereby suppressing the inflammatory properties of RA-FLS. In osteoclastogenesis, TRAP-positive multi-nucleated cells were reduced by I-BET762 in a dose-dependent manner. The actin ring formation of RANKL-induced osteoclast was inhibited in the presence of I-BET762. I-BET762 down-regulated pro-inflammatory, matrix-degrading, chemo-attractive properties in RA-FLS and, bone resorption in osteoclast. These data suggest that I-BET762 inhibit synovial inflammation and bone resorption in RA. In vivo animal experiment may be needed for confirmation.

Drought tolerance in highland barley (qingke) is modulated by distinct responses to ultraviolet-B radiation (UVB) and abscisic acid (ABA). Plants were exposed to two drought levels (moderate: 50 % soil water content and severe: 30 % soil water content), alongside two UVB intensities (low: 5-6 kJ m-2 d-1 and high: 14-15 kJ m-2 d-1), and two ABA concentrations (low: 70 μM and high: 150 μM). Physiological analyses revealed that UVB exposure significantly reduced the photosynthetic rate by 46.5 % under severe drought conditions. In contrast, ABA treatment helped to maintain the rate and improved water use efficiency by 15 % compared to UVB treatment. ABA primarily affected the starch and sucrose biosynthesis. ABA upregulated genes involved in sucrose synthase and starch synthase, promoting enhanced starch and sugar accumulation. UVB, in contrast, showed weaker effects on these pathways, with only slight upregulation of genes involved in starch biosynthesis. The phenylpropanoid metabolism and flavonoid biosynthesis were notably upregulated under UVB, with significant enrichment in phenylalanine metabolism. On the other hand, ABA treatment enriched alpha-linolenic acid metabolism and amino acid biosynthesis. Hormonal analysis revealed significant shifts in ABA, jasmonic acid (JA), and salicylic acid (SA) signaling. Under ABA treatment, genes related to ABA signaling were upregulated, while UVB exposure suppressed ABA-related transcripts. JA and SA signaling were also affected, with the majority of JA-related genes being upregulated under ABA but downregulated under UVB conditions. UVB exposure also increased the content of flavonoids and fatty acids, while ABA treatment enhanced the accumulation of starch and sucrose. The findings established the distinct yet corresponding roles of UVB radiation and ABA in improving drought tolerance, with UVB inducing secondary metabolic responses and ABA regulating primary metabolic processes. Together, they contribute to the understanding of the molecular mechanisms underlying drought resistance in highland barley.

Chemotherapy resistance remains a critical barrier in cancer treatment, partly driven by polyploid cells that survive therapy and contribute to tumor recurrence. Here, we investigated epigenomic and transcriptional changes associated with cisplatin-surviving polyploid cells compared to parental cancer cells in prostate cancer (PC3) and triple-negative breast cancer (MDA-MB-231) cell lines. We observed persistent dysregulation of chromatin compaction and altered nuclear structure in polyploid cells following cisplatin treatment. Genome-wide chromatin accessibility profiling via ATAC-seq revealed significant remodeling, notably decreased promoter accessibility at proliferation-associated loci and increased accessibility of distal regulatory elements linked to inflammation and stress response. RNA-seq analyses demonstrated a coordinated transcriptional shift away from proliferative signatures toward inflammatory and survival pathways, including activation of NFκB, interferon response, and integrated stress response pathways. Importantly, we identified subsets of genes showing concordant changes in promoter accessibility and transcriptional activity, directly linking chromatin remodeling to transcriptional reprogramming. These integrated findings highlight the role of chromatin dynamics and epigenetic plasticity in chemotherapy resistance, demonstrating that widespread chromatin accessibility changes facilitate the transition to a stress-adapted, polyploid cell state. This study provides new insights into the molecular mechanisms supporting cancer cell persistence after chemotherapy.

Matrix metalloproteinases (MMPs) play crucial roles in both physiological and pathological conditions by degrading the extracellular matrix; however, the roles and regulatory mechanisms of MMPs in brain development remain insufficiently understood. In this study, using the lepidopteran insect Helicoverpa armigera, the cotton bollworm, a serious agricultural pest, as an experimental model, we revealed that MMP2 is an important factor in insect brain development during metamorphosis under steroid hormone 20-hydroxyecdysone (20E) regulation. MMP2 is highly expressed in the brain during metamorphosis. MMP2 is localized in some surface and internal cells in the brain during metamorphosis. The knockdown of Mmp2 by RNA interference in larvae repressed brain development, accompanied by an increase in autophagy and a decrease in cell proliferation. In addition, the nutrient levels of glucose and glutamate decreased in the brain, and the expression of glucose transporters and glutamate transporters decreased after Mmp2 was knocked down. The transcription of Mmp2 was upregulated by 20E via the transcription factor forkhead box O (FOXO) in a time- and concentration-dependent manner. These data suggest that MMP2 facilitates neural cell proliferation and nutrient supply, and ultimately regulates brain development during insect metamorphosis.

Cadmium (Cd) pollution threatens agricultural productivity and food safety. O-acetylserine(thiol)lyase (OASTL) genes have been tied to plant responses to heavy metal stress, yet their roles in heterologous systems, particularly in Cd accumulation and tolerance, remain unclear. Here, we isolated a novel OASTL gene, BnaOASTL, from the high-Cd-accumulating oilseed rape cultivar Brassica napus "Nanyou 868" and expressed it in tobacco (Nicotiana benthamiana). Transgenic lines were exposed to Cd stress, and Cd content, glutathione (GSH) level, and BnaOASTL expression were evaluated. The full-length BnaOASTL cDNA (969 bp) encoded a cytoplasmic/nuclear protein of 322 amino acids. Under Cd stress, Bn-OASTL expression was significantly upregulated in transgenic plants, particularly in roots. However, compared with wild-type, transgenic lines showed no improvement in Cd tolerance or accumulation and no significant changes in GSH levels. The findings suggest that although BnaOASTL is transcriptionally responsive to Cd stress, its overexpression alone does not confer altered Cd tolerance or accumulation in tobacco. The study highlights the complexity of Cd response mechanisms and suggests that BnaOASTL functions within a broader, species-specific regulatory network.

Coriandrum sativum L. (coriander) is a medicinal herb with diverse pharmacological properties, but its molecular mechanism in clear cell renal cell carcinoma (ccRCC) remains unclear. This study aimed to systematically investigate the underlying mechanisms of coriander in ccRCC by multi-omics analysis. Active compounds were screened using Traditional Chinese Medicine Systems Pharmacology (TCMSP) and predicted targets identified via SwissTargetPrediction (STP) and Similarity ensemble approach (SEA). Transcriptomic data from GSE53757 were analysed with WGCNA and intersected with coriander targets. Key genes were selected using LASSO, SVM, and random forest models. NEK6 was further analysed for clinical relevance, methylation, immune association, single-cell expression, molecular docking and molecular dynamics simulation. Fourteen coriander compounds were identified, yielding 22 potential ccRCC-related targets. NEK6 and PYGL were consistently selected by all machine learning algorithms. NEK6 was overexpressed in ccRCC and associated with better prognosis, promoter hypomethylation, and lower mutation rates. NEK6 expression correlated with immune infiltration, particularly macrophages, and was enriched in tumour and myeloid cells at the single-cell level. Molecular docking and molecular dynamics simulation revealed strong and stable binding of luteolin, quercetin, and chryseriol to NEK6. NEK6 may function as a prognostic and immune-regulatory biomarker in ccRCC. Coriander flavonoids could target NEK6 to modulate the immune microenvironment, providing new insight into plant-based therapeutic strategies for ccRCC.

Antimicrobial resistance is a momentous global threat, demanding innovative approaches to combat drug-resistant pathogens. As a prevalent fungal pathogen, Candida albicans exhibits increasing resistance to conventional antifungals, especially the azoles. This study explores a novel approach combining sophorolipids (SLs), a glycolipid biosurfactant, with clinical azoles, including fluconazole (FLZ), itraconazole (ITZ), and ketoconazole (KCZ), against C. albicans biofilms. SLs from the yeast Starmerella riodocensis exhibited promising metabolic reduction and antibiofilm activity against Candida biofilms, with a biofilm inhibitory concentration (BIC50) of 512 mg/L. Among the tested azoles, ITZ exhibited the highest antibiofilm efficacy, prompting further investigation of SLs combinations. The ITZ-SLs combination markedly enhanced antibiofilm activity against preformed biofilms, with ITZ and SLs concentrations reduced by 16-fold and 4-fold, respectively, compared with their individual treatments (achieving a BIC₅₀ of 1 mg/L ITZ and 128 mg/L SLs). Quantitative real-time polymerase chain reaction analysis revealed significant downregulation of essential biofilm-associated genes such as BCR1, EFG1, and CDC28, demonstrating SLs's ability to inhibit various stages of biofilm development and stability. Thus, the synergy observed with azole drugs, particularly ITZ and SLs, was highly effective in biofilm removal, highlighting the compatibility of anti-biofilm biosurfactant SLs with some antifungal agents.

Ambient air pollution may accelerate biological aging, but the extent of its impact remains uncertain. Epigenetic clocks capture aging by comparing biological to chronological age, highlighting whether an individual is aging biologically faster (accelerating) or slower (decelerating) than expected. This systematic review and meta-analysis aimed to evaluate the association between long-term outdoor air pollution exposure [particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), or black carbon (BC)] and epigenetic clocks. We systematically searched the databases of PubMed, Scopus, and Google Scholar until April 2025. Random-effects models were used to estimate beta coefficients for the association between air pollutants and epigenetic age acceleration (EAA). The study protocol was registered on the International Prospective Register of Systematic Reviews (PROSPERO: CRD42024628148). Our meta-analysis included 18 studies with a combined sample size of 363,381 participants. Using the Horvath EAA, no significant associations were found for all pollutants [per 5 μg/m3 PM2.5: 0.523 y (95 %CI: -0.136, 1.182, p = 0.12); 5 μg/m3 PM10: 0.043 y (95 %CI: -0.281, 0.366, p = 0.80); 10 μg/m3 NO2: -0.078 y (95 %CI: -0.201, 0.044, p = 0.21); 0.5 μg/m3 BC: 0.268 y (95 %CI: -0.165, 0.701, p = 0.23)]. In a sensitivity analysis, when only including adult populations, the effect for a 5 µg/m3 increase in PM2.5 was more pronounced [0.740 y (95 %CI: -0.050, 1.529, p = 0.066)]. For PhenoAge EAA, inconsistent associations between pollutants and epigenetic aging were observed, which were driven by a single study. Finally, for GrimAge EAA, no associations with pollutant exposures were identified. In conclusion, this meta-analysis suggests a potential weak association between ambient particulate air pollution exposure and Horvath epigenetic age acceleration in adults; however, this currently lacks statistical significance. Other epigenetic clocks showed inconsistent or no associations. Additional high-quality longitudinal studies are needed to clarify the nature and strength of the potential link between air pollution exposure and epigenetic aging.

Chemoresistance is a reason for treatment failure in prostate cancer. Receptor-interacting protein kinase 2 (RIPK2) has been shown to play a role in drug resistance in various cancers; however, its role and the underlying mechanism of chemoresistance in prostate cancer are unclear. We analyzed data from The Cancer Genome Atlas for RIPK2 expression in prostate cancer and its association with clinicopathological features. We also elucidated the role and mechanism of action of RIPK2 in prostate cancer cell resistance to docetaxel (DTX). The results showed that RIPK2 expression was upregulated in prostate cancer tissues and was associated with poor pathological grading. RIPK2 was also upregulated in 22RV1/DTX, C4-2/DTX, PC-3/DTX, and DU145/DTX cell lines and involved in DTX resistance. Mechanistic experiments revealed that RIPK2 was involved in DTX resistance by upregulating P-glycoprotein (P-gp) expression through the activation of the NF-κB signaling pathway. Xenograft tumor experiments confirmed that inhibition of RIPK2 or P-gp enhanced the efficacy of DTX in suppressing PC-3/DTX growth. Taken together, these results suggest that RIPK2 mediates DTX resistance in prostate cancer cells through the NF-κB/P-gp signaling pathway. RIPK2 and its downstream signaling molecules are potential targets for the treatment of chemoresistant prostate cancer.

Pre-harvest sprouting (PHS) significantly reduces the yield and quality of Chenopodium quinoa (quinoa). A key determinant of PHS resistance is the balance between seed dormancy and germination, a process primarily regulated by phytohormones.

With unprecedented climate change, coastal overtopping is projected to increase up to 50-fold by 2100. Unlike complete flooding, overtopping imposes a salt-submergence stress for plants by combining oxygen (O2) deficiency with elemental toxicity. To address this, we investigated whether S-nitrosoglutathione (GSNO), a stable nitric oxide (NO) donor, could mitigate these dual stresses-submergence (Sub) and salt-mixed Sub (Salt + Sub)-in two Korean japonica rice varieties, Ilmi and Samgwang. Under Sub stress, both varieties relied on internode elongation and aerenchyma formation as escape strategies; however, these responses were significantly impaired under Salt + Sub. GSNO pretreatment effectively counteracted this impairment, not only by restoring the growth defects, but also improving overall biomass under both stresses. This response was mediated by ethylene, gibberellic acid (GA), and abscisic acid (ABA). Specifically, GSNO pretreatment reduced the level of ABA but increased the intermediates of GA and the relative expression of ethylene-related genes, ACO5 and EIN3, under both stress conditions. These changes led to downstream expression of marker genes associated with cell wall expansion, energy conservation, and ethylene signaling, particularly in Samgwang under Salt + Sub conditions. GSNO-treated Samgwang plants consistently outperformed Ilmi in terms of survival, largely due to improved detoxification of reactive oxygen species (ROS). Additionally, GSNO upregulated expression of Na+ transporter genes (SOS1, SOS2, HKT1, and NHX1), indicating improved Na+ extrusion and sequestration, thereby maintaining ion homeostasis during combined stress. Overall, GSNO conferred multifaceted protection against Sub and Salt + Sub stresses by improving hormonal balance, ROS-detoxification, and ion transport. These findings highlight GSNO's potential in conferring rice resilience to climate change-driven coastal challenges.

Neisseria gonorrhoeae (Gc) is the gram-negative bacterium that causes gonorrhea, a prevalent sexually transmitted infection that can have life-threatening clinical sequelae. Gc requires iron for human infection and uses the iron-responsive, iron-binding transcriptional repressor Fur to maintain iron homeostasis. Gc infects mucosal sites, where the neuroendocrine hormone norepinephrine (NE) is produced by the autonomic nervous system and various epithelial and immune cell types. Here, we show that NE derepresses the Fur regulon to alter bacterial iron homeostasis and increase Gc survival. By RNA-seq, we determined that NE rewires gonococcal gene expression to increase capacity for iron uptake while enabling increased intracellular iron availability. Of the 30 genes that were differentially expressed in NE-treated compared to untreated bacteria, 27 have Fur box-containing promoters. A possible mechanism for how NE derepresses the Fur regulon is through direct demetalation of Fur, as NE directly decreased binding of Fur in vitro to a DNA amplicon containing the Fur-binding sequence from Gc tbpB. NE increased the labile intracellular iron pool in Gc, evidenced by increased streptonigrin sensitivity, without significantly increasing the total bacterial iron content, suggesting that NE leads to the redistribution of cellular iron. The work presented here provides a novel mechanism for how Gc survives iron limitation within its obligate human host.IMPORTANCENeisseria gonorrhoeae (Gc) is the bacterial pathogen that causes gonorrhea, a sexually transmitted infection with an estimated global annual incidence of 87 million individuals. During infection, Gc must overcome iron limitation imposed by nutritional immunity. Here, we show that the host neuroendocrine hormone norepinephrine, which is present at the mucosal surfaces Gc infects, promotes the survival of iron-limited Gc. Our results support a novel mechanism by which norepinephrine works through the ferric uptake regulator, Fur, to enhance the capacity of Gc to take up iron and make it bioavailable. Our findings show that Gc responds to host-derived cues that enable it to resist iron limitation.

This study investigates how brassinosteroids (BRs) enhance stress tolerance in soybean under combined salt and drought stress by examining growth, chlorophyll content, photosynthesis, and reactive oxygen species (ROS) homeostasis. Salt and drought stress significantly reduced soybean growth and photosynthetic performance, as reflected by lower SPAD chlorophyll values and decreased photosystem II (PSII) efficiency. In contrast, BR (24-epibrassinolide, EBL) significantly improved growth parameters and spectral indices, indicating a healthier pigment status and improved canopy function. EBL-treated plants also exhibited enhanced PSII performance, as indicated by increased Fv/Fm and a higher performance index (PI). Furthermore, BRs modulated ROS levels and promoted cellular homeostasis by elevating the activities of antioxidant enzymes such as APX, CAT, and POX, thereby mitigating oxidative damage. Consistently, expression of key stress-responsive genes (GmCAT, GmSOD, and GmP5CS) was strongly induced under combined salt, drought, and EBL treatment, highlighting the synergistic role of EBL in transcriptional activation under combined stress. EBL treatment increased the proline content and the activities of ProDH and P5CS, supporting proline-mediated osmoprotection, while BR-treated plants exhibited reduced malondialdehyde (MDA) accumulation and electrolyte leakage (EL), indicating lower lipid peroxidation and better membrane integrity under stress. Overall, this study demonstrates that EBL enhances soybean resilience to combined salt and drought stress by improving growth, photosynthetic efficiency, antioxidant defense, osmotic adjustment, and membrane stability.

The application of biostimulants represents a sustainable strategy to enhance crop productivity and resilience. This study investigated the efficacy of Delonix regia pollen aqueous extract as a biostimulant on coriander (Coriandrum sativum). Seeds were primed with different concentrations of the extract (0%, 0.5%, 1%, and 1.5%) for 24-48 h. The 1% extract applied for 48 h was the most effective treatment, significantly increasing shoot fresh and dry weight, shoot length, and the content of total protein, phenolics, flavonoids, and terpenes. This treatment also led to a significant upregulation of the key biosynthetic genes Chalcone synthase (CHS) and geranylgeranyl pyrophosphate synthase (GGPS) by 1.4-fold and 2.1-fold, respectively. Principal component analysis confirmed a positive correlation among shoot fresh weight, total protein, terpene content, and GGPS expression. These findings demonstrate that D. regia pollen extract is a potent biostimulant that enhances coriander growth and the production of valuable bioactive compounds through the modulation of key metabolic pathways.

Cis-natural antisense transcript ELENA19 attenuates PAMP-triggered immunity by modulating ABA- and PAMP-inducible UGT71B6 expression, resulting in increased ABA levels and reduced ET-dependent flg22-induced callose deposition in Arabidopsis. Long noncoding RNAs (lncRNAs) have emerged as crucial regulators of various biological processes. However, the roles of lncRNAs in pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) remain largely unexplored in plants. Based on our previous custom lncRNA array analysis of Arabidopsis seedlings treated with PAMPs (elf18 and flg22), we identified a novel ELF18-INDUCED LONG NONCODING RNA, ELENA19. In this study, we characterized the function of ELENA19 as a natural antisense transcript of UDP-glycosyltransferase 71B6 (UGT71B6), which is responsible for the glycosylation of abscisic acid (ABA). ELENA19 expression was rapidly upregulated upon treatment with ABA or PAMPs (flg22 and elf18). Among the genes neighboring ELENA19, only UGT71B6 was responsive to both ABA and PAMP treatments. UGT71B6 expression was significantly attenuated in ELENA19-overexpressing (OX) plants compared to wild-type (WT) plants after PAMP or ABA treatment. ELENA19 OX plants were hypersensitive to ABA during germination and had higher endogenous ABA levels than WT plants, suggesting that ELENA19 down-regulates UGT71B6 expression and enhances endogenous ABA levels. Flg22-triggered callose deposition was reduced, and the expression of ethylene (ET)-dependent Flg22-induced genes was significantly down-regulated in ELENA19 OX plants compared to WT plants, confirming the antagonistic interaction between ABA and ET signaling in the flg22-mediated immune response. These results demonstrate that ELENA19 attenuates PAMP-triggered immunity by modulating UGT71B6 expression.