Pesticide Biochemistry and Physiology最新文献

The abundance of monoterpenoids and phenolic compounds determines the medicinal quality and anti-insect properties of Agastache rugosa, which can be compromised by biotic stress such as herbivore attacks. The traditional use of chemical pesticides to mitigate herbivore interference is increasingly incompatible with sustainable agriculture. In response, nanotechnology-based biostimulants, which can activate metabolic processes to enhance plant growth and stress resistance, offer a more cost-effective and environmentally-friendly alternative. However, to date, it remains unknown how nano-biostimulants improve the therapeutic value and insect resistance of medicinal plants simultaneously. This study investigates the effect of 0–1000 mg/L of a nano-biostimulant salicylic acid functionalized chitosan nanocomposite (SCN) on the pharmacological and anti-herbivore properties of medicinal plant A. rugosa. Results showed that 100 mg/L SCN significantly inhibited Spodoptera litura growth by 62.9 %, and increased plant shoot and root biomass by 107.2 % and 77.6 %, respectively. Moreover, 100 mg/L SCN significantly upregulated the expression of the key genes (e.g., LS, L3OH, and CHS) involved in monoterpene and phenolic compounds biosynthesis by 1.4–10.1 folds, thus boosting the production of active compounds such as pulegone, β-myrcene, and chlorogenic acid by 1.5–24.4 folds. These enhancements were superior to salicylic acid or chitosan alone. Altogether, our findings promote the sustainable and eco-friendly application of nano-biostimulant in improving the quality of medicinal plants and green pest control in agroecosystems.

Gray mold caused by Botrytis spp. is a common disease on various hosts, including strawberries. In this study, we obtained 59 Botrytis isolates from strawberries from greenhouses in Zhejiang Province, China. Identification of the sampled isolates at species level was performed by a duplex PCR assay method, the result showed that, in Zhejiang, gray mold on strawberry fruits is caused by a complex of Botrytis groups including B. cinerea group N (47.5 %) and B. cinerea group S (52.5 %). The sensitivities of all Botrytis isolates to pyrimethanil were determined based on discriminatory dose method on L-asparagine-based agar medium plate. Our results showed that the isolates obtained from the greenhouses with continuous use of pyrimethanil developed severe resistance to pyrimethanil, and the resistance frequencies of B. cinerea group N and group S isolates were 89.3 % and 41.9 %, respectively. By sequencing, four different resistance-related point mutations were identified in 38 Botrytis isolates: Bcpos5^L412F (16 isolates, 42.1 %), Bcpos5^L412V (14 isolates, 36.8 %), Bcmdl1^E407K (2 isolates, 5.3 %), and Bcpos5^L412S⸱Bcmdl1^E407K (1 isolate, 2.6 %). The exogenous addition of methionine could not completely alter the resistance of Botrytis isolates to pyrimethanil. In this study, the pyrimethanil resistance in Botrytis isolates was steadily inherited, and compared to the pyrimethanil-sensitive isolates, the resistant mutants exhibited good fitness in sporulation capacity, spore germination rate, and virulence on strawberries. In conclusion, our results provided a description of the genetic structure of Botrytis groups complex on strawberry fruits and reminded growers to focus on the stable pyrimethanil resistance in Botrytis isolates, caused by point mutations in BcPos5 and BcMdl1.

Arsenic is a toxic element that can cause severe liver damage in humans and animals. Arsenic-based inorganic pesticides, such as lead arsenate, copper arsenate, and calcium arsenate, are widely used for insect control and can eventually affect human health through accumulation in the food chain. However, the relationship between arsenic trioxide (ATO)-induced hepatotoxicity and the cGAS-STING signaling pathway has not been reported. The aim of this study was to investigate the potential role of inflammatory response in ATO-induced hepatotoxicity in chickens. In this study, we found that ATO exposure resulted in mtDNA leakage into the cytoplasm of chicken hepatocytes, which activated the cGAS-STING pathway and significantly increased the cGAS, STING, TBK1, and IRF7 mRNA and protein expression levels. Moreover, type I interferon response was activated. Concurrently, STING triggered the activation of the traditional NF-κB signaling pathway and promoted the expression of pro-inflammatory cytokine genes, including TNF-α, IL-6, and IL-1β. Subsequently, we found that both mtDNA clearance with EtBr and inhibition of the cGAS-STING pathway with H-151 reversed the ATO-induced innate immune and inflammatory responses. In summary, the above findings indicate that chicken hepatocytes can induce innate immune responses and inflammatory responses via mtDNA-cGAS-STING under ATO-exposure conditions, which is of great significance for further studies on the toxicity mechanism of ATO.

Immunity and reproduction are vital functions for the survival and population maintenance of female insects. However, owing to limited resources, these two functions cannot be fulfilled simultaneously, resulting in an energy tradeoff between them. Notably, the mechanisms underlying this immune-reproductive trade-off, in which energy competition likely plays a central role, remain poorly understood. Fatty acid synthase (FAS), a key gene involved in lipid synthesis and insect energy metabolism, was investigated in this study using Locusta migratoria as the research subject. Bacterial infection and RNA interference (RNAi) technology were used to examine changes in the immunity, fecundity, and energy metabolism patterns of locusts under different treatments. The findings of this study demonstrate that infection with Micrococcus luteus triggers an immune response in locusts, significantly upregulates the expression of defensin 3 (DEF3) and Attacin, and enhances pHenoloxidase (PO) activity. Upon FAS2 silencing, bacterial attack upregulated DEF3 and Attacin expression to a lesser extent, leading to increased lysozyme activity instead of PO. Furthermore, bacterial infection results in a decrease in glycogen and glucose content in the fat body, accompanied by a significant increase in triacylglycerol (TAG) content. However, after FAS2 knockdown, both the lipid and carbohydrate contents were significantly reduced in the fat body. Compared with bacterial infection alone, low FAS2 expression further exacerbated fecundity impairment in locusts. The expression levels of vitellogenin A (VgA) and vitellogenin B (VgB) were significantly low, with severe ovarian atrophy observed. Notably, the ovarian weight was only 21 % compared to that of the control group. Moreover, females exhibited minimal egg-laying behavior. In summary, our findings suggest that following FAS2 gene silencing, there is a greater inclination toward immune stimulation energy activation in locusts, whereas reproductive investment is reduced. The outcomes of this study will contribute to the further exploration of the molecular mechanisms underlying the trade-off between immune and reproductive energy in locusts.

Abamectin (ABN) is an agricultural insecticide that is reported to damage various body organs including the heart. Velutin (VLN) is a plant-derived flavonoid that exhibits a wide range of medicinal properties. This study was planned to investigate the medicinal value of VLN against ABN induced cardiotoxicity in rats. Thirty-two male albino rats (Rattus norvegicus) were divided into four equal groups including the control, ABN (10 mg/kg), ABN (10 mg/kg) + VLN (20 mg/kg), and VLN (20 mg/kg) alone administrated group. The doses were administrated for 6 weeks orally. The results demonstrated that ABN intoxication promoted the gene expression of Nrf-2 and its associated antioxidant genes including glutathione reductase (GSR), heme‑oxygenase-1 (HO-1), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) while reducing the gene expression of Keap-1 as well as levels of ROS and MDA. Moreover, ABN exposure enhanced the gene expression of Janus kinase-1 (JAK1), Signal transducer and activator of transcription-3 (STAT3), NF-κB, TNF-α, C-reactive proteins, Interferon-gamma-induced protein 10 (IP-10), IL-1β, Monocyte chemoattractant protein-1 (MCP-1), IL-6 and COX-2. The concentrations of CK-MB, Brain natriuretic peptide (BNP), CPK, troponin-I, N-terminal pro b-type natriuretic peptide (NT-proBNP) and LDH were elevated after ABN administration. ABN intoxication abruptly upregulated the levels of Caspase-3, Caspase-9 and Bax while reducing the levels of Bcl-2 in cardiac tissues. Additionally, ABN exposure prompted various histopathological damages. Nevertheless, VLN treatment remarkably protected the cardiac tissues via regulating aforementioned disruptions. Lastly, molecular docking analysis was performed to determine the potential affinity of VLN and targeted protein i.e., Bax, NF-kB, Nrf-2/Keap1, JAK1 and STAT3. Our in-silico evaluation showed a strong binding affinitybetween VLN and the targeted proteins which further confirms its effectiveness as a cardioprotective agent.

Insect cuticle acts as a first line of defense and a physical protective barrier against entomopathogens. Chitin biosynthesis pathway plays a crucial role in chitin formation in the cuticle of insects. Glucosamine-6-phosphate N-acetyltransferase (GNA) is a key enzyme in insect chitin biosynthesis that regulate the chitin formation. However, how GNA-mediated cuticle metabolism influences virulence of entomopathogenic fungi is still unknown. In this study, CmGNA gene was cloned and characterized from the rice leaffolder Cnaphalocrocis medinalis. The CmGNA contains an open read frame (ORF) 600 nucleotides, encoding 199 amino acids with an isoelectric point of 8.65 and a molecular weight of 22.30 kDa. The expression profile showed that CmGNA was highly expressed in 4th instar larvae and in the cuticle. Here, we also reported the impact of CmGNA gene and entomopathogenic fungi, Metarhizium anisopliae and Beauveria bassiana, on expression pattern of chitin biosynthesis genes, feeding behavior, survival rate and average body weight of infected larvae, phenotypic deformities, rate of pupation, and adult emergence. Our results showed that knockdown of CmGNA and application of M. anisopliae and B. bassiana three days after RNA interference (RNAi) significantly decreased the expression of CmGNA and other associated genes, reduced feeding efficiency and survival rate, and caused loss of average body weight, less rate of pupation and adult emergence of infected larvae. Knockdown of CmGNA gene also increased the lethality of larvae caused by M. anisopliae and B. bassiana and resulted in significantly phenotypic deformities of infected larvae. Our findings illustrated that RNAi-mediated CmGNA knockdown disturbed the chitin synthesis genes that led to enhancing the virulence of M. anisopliae and B. bassiana, which can provide us new insights to develop novel biocontrol strategies against C. medinalis.

Etofenprox is a pyrethroid insecticide that acts on the nervous system of insects. Due to its low toxicity to aquatic animals, it is permitted for use in controlling insect pests in rice fields. The brown planthopper (BPH), Nilaparvata lugens, a significant piercing-sucking pest feeding on rice exclusively, secretes various salivary components when feeding. Salivary proteins are essential for BPH feeding, but their response to etofenprox is not well understood. The application of etofenprox down-regulated the expression of 21 salivary protein genes, among which 9 genes (NlShpa, Salivap 3, CA, NlSEF1, Nl12, NlHSC70–3, NlSP1, NlG14, and NlDNAJB9) showed significant differences. Most differentially expressed genes are found important for BPH physiological processes, except Nl12. Here we found that silencing Nl12 impeded ovary development, thereby inhibiting oocyte formation. The potential explanation was that Nl12 was highly expressed in both salivary gland and ovary, and the ovary development abnormality may be due to the direct effect from expression reduction in ovary and/or indirect influence from expression reduction in salivary gland. Altogether, our findings provide a new insight into the mechanism of action of etofenprox on insect pests and explain part of the reason why etofenprox does not stimulate reproduction in BPH.

The application of Bacillus thuringiensis (Bt) has brought environmental benefits and delayed resistance development of pests. Most studies focus on the Bt insecticidal activity against pests, however, the molecular mechanism of Bt on impairing the growth and development of Spodoptera exigua remains unknown. Here, we show that juvenile hormone (JH) inhibits the lipogenesis mediated by fatty acid synthases (Fas) of S. exigua in response to Bt infection. The weight and lipid accumulation of S. exigua larvae post Bt infection were less than those of larvae without Bt infection. We further demonstrated that Bt infection causes the JH titer with a significant increase, which downregulates the expression of lipogenesis-related genes, SeFas3, SeFas4, and SeFas5, resulting in the delayed development of S. exigua larvae. In addition, the expression levels of SeFas genes were regulated by SeACC, indicating that SeFas genes were modulated by multiple pathways. Our findings reveal that novel insights into the molecular mechanisms underlying the impaired development caused by Bt infection which can inform the development of strategies for the sustainable pest control in the future.

The steroid 20-hydroxyecdysone (20E) is crucial in regulating ovarian development. However, the neuropeptidergic mechanisms underlying ovarian development via 20E are underexplored. In this study, we investigated myosuppressin (MS) signaling in the dominant fruit pest Grapholita molesta and revealed that MS signaling is necessary for 20E biosynthesis during ovarian maturation. Pharmacological and molecular docking analyses confirmed that the GmMS mature peptide could activate its receptor GmMSR. Additionally, transcript expression analyses of GmMS and GmMSR showed different distribution patterns in adults. Notably, GmMSR was also detected in the ovaries of sexually mature females. RNAi-mediated dysfunction of GmMS or GmMSR specifically decreased fertility in females. Furthermore, GmMS or GmMSR knockdown decreased vitellogenin synthesis and uptake, thereby delaying ovarian development. RNA-seq, gene expression validation, and hormone quantification further revealed that GmMS signaling depletion blocked 20E biosynthesis in the ovary. Finally, exogenous MS rescued most dsGmMS- or dsGmMSR-induced ovarian defects and 20E titers. These results suggest that MS/MSR-to-20E signaling regulates ovarian development through vitellogenesis, providing a new perspective on the development of neuroendocrine targets that suppress pest field populations.

The gray blight incited by Pestalotiopsis and allied genera is a prevalent disease affecting tea cultivation, and managing it with Trichoderma spp. is an alternative to synthetic fungicides. Plants modify their arsenal system against pathogens when they are exposed to Trichoderma spp., which produces proteins and enzymes associated with pathogenesis. Understanding the expression pattern of defense-related markers will help in developing gray blight resistance tea cultivars. Thus, this study intended to induce resistance against gray blight in tea by Trichoderma harzianum TIND02. For this, a total of eight Trichoderma isolates originated from organic tea rhizospheres were characterized and evaluated for their efficacy. Dual culture test revealed isolate TIND02 as the most potential candidate with 74.6% inhibitory activity against gray blight pathogen Pseudopestalotiopsis theae. Molecular characterization based on ITS and tef-1 alpha genes confirmed isolate TIND02 as T. harzianum. Scanning electron microscopic study showed the mycoparasitic nature of T. harzianum TIND02 (TH-TIND02) to Ps. theae. The ethyl acetate extract of TH-TIND02 at 100 and 200 μg mL⁻¹ showed potential inhibitory activity (>69.9%) against Ps. theae which confirmed the presence of higher volatile metabolites. Gas chromatography–Mass spectrometry study revealed that ethyl acetate extract of TH-TIND02 was composed of 21 major and minor volatile organic compounds with acetamide, 2, 2, 2-trifluoro-N, N-bis trimethyIsilyl–C (94.74%) as a major component. The isolate also produced chitinase, cellulase, β-1, 3 glucanase, and protease hydrolytic enzymes. Nursery experiments revealed that 2% and 5% doses (2 × 10⁶ CFU mL⁻¹) of TH-TIND02 significantly reduced respective 65.0% and 70.0% disease severity over control with improved plant growth. Besides, expressions of defense-related enzymes (chitinase, pHenolics, peroxidase, phenylalanine ammonia lyase, β-1, 3-glucanase, and polyphenol oxidase) and pathogenesis-related genes (chitinase and β-1, 3-glucanase) due to TH-TIND02 were determined. The secretion of defense-related enzymes was highly upregulated in plants applied with TH-TIND02 followed by Ps. theae inoculation compared to controls. The RT-qPCR analysis showed that the expression of both genes in co-inoculated plants was two-fold higher than in control after 21-day post incubation. These results suggest that TH-TIND02 application reduced gray blight severity by elevated enzyme activity and overexpressed pathogenesis-related genes in tea plants which offer for its eco-friendly and sustainable use as a bio-fungicide in tea gardens.