Gallic acid (GA), an important polyphenolic compound in the plant, is a well-known antioxidant, antihyperglycemic, and anti-lipid peroxidative agent. Recently, GA treatment exhibited ameliorative effects on plants in response to some abiotic stresses. However, the elicitation effect of GA on plant defense against herbivorous insects has not yet been reported. In this study, we found that the exogenous application of GA induced the direct defense of tea plant () against tea geometrid () larvae, through activating jasmonic acid (JA) signaling and phenylpropanoid pathways. These signaling cascades resulted in the efficient induction of several defensive compounds. Among them, astragalin, naringenin, and epigallocatechin-3-gallate were the three of the most active anti-feeding compounds. However, the exogenous GA treatment did not affect the preference of female moths and larval parasitoid sp. Our study suggests that GA may serve as an elicitor that triggers a direct defense response against tea geometrid larvae in tea plants. This study will help to deepen the understanding of the interaction between plants and phytophagous insects and also provide theoretical and technical guidance for the development of plant defense elicitors.
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http://dx.doi.org/10.3389/fpls.2022.833489 | DOI Listing |
BMC Vet Res
January 2025
Department of Veterinary Clinical Sciences, Clinic for Swine, Justus-Liebig-University, Frankfurter Strasse 112, D-35392, Giessen, Germany.
Background: The recently identified swine inflammation and necrosis syndrome (SINS) affects tail, ears, teats, coronary bands, claws and heels of affected individuals. The primarily endogenous syndrome is based on vasculitis, thrombosis, and intimal proliferation, involving defence cells, interleukins, chemokines, and acute phase proteins and accompanied by alterations in clinical chemistry, metabolome, and liver transcriptome. The complexity of metabolic alterations and the influence of the boar led to hypothesize a polygenic architecture of SINS.
View Article and Find Full Text PDFNat Protoc
January 2025
Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA.
The clinical potential of current chimeric antigen receptor-engineered T (CAR-T) cell therapy is hampered by its autologous nature that poses considerable challenges in manufacturing, costs and patient selection. This spurs demand for off-the-shelf therapies. Here we introduce an ex vivo feeder-free culture method to differentiate gene-engineered hematopoietic stem and progenitor (HSP) cells into allogeneic invariant natural killer T (NKT) cells and their CAR-armed derivatives (CAR-NKT cells).
View Article and Find Full Text PDFArch Rehabil Res Clin Transl
December 2024
Department of Orthopaedic Surgery, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
Objective: To estimate limb loss prevalence in the United States (US) by etiology and anatomical position and the trends of limb loss over 40 years.
Design: We used the National Inpatient Sample, Healthcare Cost and Utilization Project to estimate current and future limb loss prevalence in the US and by anatomical location. Prevalence estimates were based on the incidence and duration of the disease.
Pest Manag Sci
January 2025
Department of Plant Pathology, The Islamia University of Bahawalpur, Bahawalpur, Pakistan.
Background: Bacillus species produce antimicrobial lipopeptides (LPs) and methyl jasmonate (MeJA) induces resistance in harvested fruits against postharvest pathogens. However, there is limited evidence of the combined efficacy of Bacillus LPs and MeJA to suppress postharvest diseases.
Results: This study presents the combined effect of Bacillus LPs and MeJA to suppress P.
Oncogene
January 2025
Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA.
The functional activation of the androgen receptor (AR) and its interplay with the aberrant Hh/Gli cascade are pivotal in the progression of castration-resistant prostate cancer (CRPC) and resistance to AR-targeted therapies. Our study unveiled a novel role of the truncated form of Gli (t-Gli3) in advancing CRPC. Investigation into Gli3 regulation revealed a Smo-independent mechanism for its activation.
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