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Although both protein arginine methylation (PRMT) and jasmonate (JA) signaling are crucial for regulating plant development, the relationship between these processes in the control of spikelet development remains unclear. In this study, we used the CRISPR/Cas9 technology to generate two OsPRMT6a loss-of-function mutants that exhibit various abnormal spikelet structures. Interestingly, we found that OsPRMT6a can methylate arginine residues in JA signal repressors OsJAZ1 and OsJAZ7. We showed that arginine methylation of OsJAZ1 enhances the binding affinity of OsJAZ1 with the JA receptors OsCOI1a and OsCOI1b in the presence of JAs, thereby promoting the ubiquitination of OsJAZ1 by the SCF complex and degradation via the 26S proteasome. This process ultimately releases OsMYC2, a core transcriptional regulator in the JA signaling pathway, to activate or repress JA-responsive genes, thereby maintaining normal plant (spikelet) development. However, in the osprmt6a-1 mutant, reduced arginine methylation of OsJAZ1 impaires the interaction between OsJAZ1 and OsCOI1a/OsCOI1b in the presence of JAs. As a result, OsJAZ1 proteins become more stable, repressing JA responses, thus causing the formation of abnormal spikelet structures. Moreover, we discovered that JA signaling reduces the OsPRMT6a mRNA level in an OsMYC2-dependent manner, thereby establishing a negative feedback loop to balance JA signaling. We further found that OsPRMT6a-mediated arginine methylation of OsJAZ1 likely serves as a switch to tune JA signaling to maintain normal spikelet development under harsh environmental conditions such as high temperatures. Collectively, our study establishes a direct molecular link between arginine methylation and JA signaling in rice.
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http://dx.doi.org/10.1016/j.molp.2024.04.014 | DOI Listing |
Free Radic Biol Med
September 2025
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center. Electronic address:
Background: Excessive oxidative stress is well known to participate in the pathogenesis of hypertension. A major regulator of oxidative stress is the transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2). However, the role of Nrf2 in the pathogenesis of hypertension is not completely understood, especially at the endothelial cell level.
View Article and Find Full Text PDFCell Death Differ
September 2025
Center of Growth, Metabolism and Aging, Key Laboratory of Bio-Resources and Eco-Environment of Ministry of Education, Southwest Bio-resources R&D Key Laboratory of Sichuan Province, College of Life Sciences, Sichuan University, Chengdu, China.
Tongue squamous cell carcinoma (TSCC) is a common oral malignancy prone to metastasis, whose underlying mechanism remains obscure. Here, we report the oncogenic roles of protein arginine methyltransferase 5 (PRMT5) in TSCC via inhibiting transcription factor ΔNp63α. We found that PRMT5 physically interacts with ΔNp63α, resulting in impairment of ΔNp63α-mediated transcriptional regulation.
View Article and Find Full Text PDFBiology (Basel)
July 2025
College of Physical Education, Yangzhou University, Yangzhou 225009, China.
Although exercise is known to exert anti-inflammatory effects in neurodegenerative diseases, its specific impact and underlying mechanisms in Parkinson's disease (PD) remain poorly understood. This study explores the effects of exercise on microglia-mediated neuroinflammation and apoptosis in a PD model, focusing on the role of irisin signaling in mediating these effects. Using a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model, we found that a 10-week treadmill exercise regimen significantly enhanced motor function, reduced dopaminergic neuron loss, attenuated neuronal apoptosis, and alleviated neuroinflammation.
View Article and Find Full Text PDFJ Med Chem
September 2025
Institute of Pharmacy, Faculty of Chemistry and Pharmacy, University of Regensburg, Universitätsstraße 31, Regensburg D-93053, Germany.
Labeled ligands for the neurotensin receptor 1 (NTSR), which is expressed in the CNS, the gastrointestinal tract, and in malignant tumors, are needed to investigate NTSR-ligand binding and NTSR expression. Aiming for fluorescence-labeled neurotensin(8-13)-derived NTSR ligands with high affinity and proteolytic stability, several previous approaches were combined: (1) replacement of Arg by an amino-functionalized carbamoylated arginine, allowing conjugation to a fluorophore, (2) -methylation of Arg and replacement of Tyr by β,β-dimethyl-l-Tyr, conferring proteolytic stability, and (3) replacement of Leu by trimethylsilyl-Ala, boosting binding affinity. This strategy gave fluorescent NTSR ligands with unprecedented NTSR binding affinity (5-TAMRA-labeled ligand : 0.
View Article and Find Full Text PDFLipids Health Dis
September 2025
Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Background: Heart failure with preserved ejection fraction (HFpEF), which accounts for more than half of all heart failure cases worldwide, has emerged as a major public health challenge characterized by substantial morbidity and mortality rates. As adropin is a key regulator of cardiovascular and metabolic homeostasis, this study investigated its therapeutic effects against HFpEF pathogenesis.
Methods: C57BL/6 mice were fed a high-fat diet (60% fat-derived calories) with NG-nitro-L-arginine methyl ester (L-NAME, 0.