The expression of insecticidal proteins under constitutive promoters in transgenic plants is fraught with problems like developmental abnormalities, yield drag, expression in unwanted tissues, and seasonal changes in expression. RbPCD1pro, a rapid, early acting wound-inducible promoter from rose that is activated within 5 min of wounding, was isolated and characterized. Wounding increased transcript levels up to 150 and 500 folds within 5 and 20 min coupled with high translation as seen by histochemical GUS enzyme activity within 5-20 min. RbPCD1pro was activated by both sucking and chewing insects and showed wound-inducible expression in various aerial tissues of plants representing commercially important dicot and monocot families. The promoter showed no expression in any vegetative tissue except upon wounding. Functionality of RbPCD1pro was tested by its ability to drive expression of the insecticidal protein gene cryIAc in transgenic Arabidopsis and tomato. Strong wound-inducible CryIAc expression was observed in both plants that increased 100-350 fold (Arabidopsis) and 280-600 fold (tomato) over the unwounded background within 5 min and over 1000-1600 fold within 20 min. The unwounded background level was just 3-6% of the CaMV35S promoter while wound-induced expression was 5-27 folds higher than the best CaMV35S line in just 5 min and 80-fold higher in 20 min. Transgenic plants showed strong resistance even to larger fourth instar larvae of H. armigera and no abnormalities in development and general plant growth. This is one of the earliest acting promoters with wide biotechnological application across monocot and dicot plants.
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http://dx.doi.org/10.1111/pbi.13071 | DOI Listing |
Elife
January 2025
Institut Pasteur, Université Paris Cité, Unité Plasticité du Génome Bactérien, Paris, France.
Tgt is the enzyme modifying the guanine (G) in tRNAs with GUN anticodon to queuosine (Q). is required for optimal growth of in the presence of sub-lethal aminoglycoside concentrations. We further explored here the role of the Q34 in the efficiency of codon decoding upon tobramycin exposure.
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January 2025
Department of Neurology, Baylor College of Medicine, Houston, United States.
variants in children with neurodevelopmental impairment are difficult to assess due to their heterogeneity and unclear pathogenic mechanisms. We describe a child with neonatal-onset epilepsy, developmental impairment of intermediate severity, and G256W heterozygosity. Analyzing prior KCNQ2 channel cryoelectron microscopy models revealed G256 as a node of an arch-shaped non-covalent bond network linking S5, the pore turret, and the ion path.
View Article and Find Full Text PDFTissue Eng Part A
January 2025
Orthopaedic and Bioengineering Research Laboratory, Colorado State University, Fort Collins, Colorado, USA.
The high failure rate of surgical repair for tendinopathies has spurred interest in adjunct therapies, including exosomes (EVs). Mesenchymal stromal cell (MSC)-derived EVs (MSCdEVs) have been of particular interest as they improve several metrics of tendon healing in animal models. However, research has shown that EVs derived from tissue-native cells, such as tenocytes, are functionally distinct and may better direct tendon healing.
View Article and Find Full Text PDFAntioxid Redox Signal
January 2025
Institute of Pharmacology, Max Rubner Center (MRC) for Cardiovascular Metabolic Renal Research, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.
Thyroid hormones (TH) are major regulators of cell differentiation, growth, and metabolic rate. TH synthesis in the thyroid gland requires high amounts of HO to oxidize iodide for the iodination of thyroglobulin (TG). Retinol Saturase (RetSat) is an oxidoreductase implicated in dihydroretinol formation and cellular sensitivity toward peroxides and ferroptosis.
View Article and Find Full Text PDFHepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
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