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(PeVYV) is a newly recognized extracted from Chinese pepper. The symptoms of PeVYV-infested pepper plants comprise intervein yellow staining, leaf curl formation and other malformations, and leaf internodal shrinkage, but the roles of the viral proteins remain undetermined. The P0 protein of the genus has established post-transcriptional gene silencing (PTGS) activity. This investigation focused on the PeVYV-encoded P0 protein and assessed its potential virulence capacity, PTGS activity, and tendencies to localize in the nucleus. This study revealed that P0 influenced the pathogenic properties of a specific heterologous . In addition, P0 proteins impaired local gene silencing, although they did not regulate generalized gene silencing within 16c plants. Furthermore, P0 proteins localized mainly in the nucleus, particularly in the nucleolus. P0 deletion mutagenesis demonstrated that the F-box motif (56-72 amino acids, AAs) of P0 was essential for symptom determination, inhibition of PTGS, and subcellular localization. Mutation analysis of the F-box motif of P0 protein indicated that AA 57 of the P0 protein was a pivotal site in symptom development and that AA 56 of the P0 protein was indispensable for inhibiting PTGS and subcellular localization. The outcomes obtained here suggest that further studies should be conducted on the molecular mechanisms of amino acids of the F-box domain of P0 protein in the interaction of PeVYV with plants.
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http://dx.doi.org/10.3389/fmicb.2021.680658 | DOI Listing |
High Blood Press Cardiovasc Prev
September 2025
Center for Translational and Experimental Cardiology, Department of Cardiology, University Hospital Zurich and University of Zürich, Wagistrasse 12, 8952, Schlieren, Switzerland.
Introduction: Epigenetic changes are important modulators of gene expression. The histone acetyltransferase gene non-derepressible 5 (Gcn5) is emerging as a pivotal epigenetic player in metabolism and cancer, yet its role in obesity and cardiovascular disease remains elusive.
Aims: To investigate Gcn5 role in obesity-related endothelial dysfunction.
Acta Parasitol
September 2025
Ministry of Education Key Laboratory of Molecular and Cellular Biology, Hebei Collaborative Innovation Center for Eco-Environment, Hebei Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, Shijiazhuang, 050024, China.
Purpose: This study aimed to identify and analyze the role of Ferric reductase inBlastocystis sp. subtype 2 (ST2) and explore the relationship between the parasite and iron metabolism.
Methods: The location of Ferric reductase in Blastocystis sp.
Nucleic Acids Res
September 2025
Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208, United States.
DDX6 is known to repress messenger RNA (mRNA) translation and promote mRNA decay in microRNA-mediated silencing. In embryonic stem cells (ESCs), DDX6 primarily functions at the translation level, independent of mRNA destabilization; however, the precise molecular mechanism of how DDX6 represses translation remains unclear. Here, we identify DDX3X as a key downstream target of DDX6-mediated translational repression in ESCs.
View Article and Find Full Text PDFNucleic Acids Res
September 2025
Division of Chromatin Regulation, National Institute for Basic Biology, Okazaki 444-8585, Japan.
Methylation of histone H3 at lysine 9 (H3K9me), a hallmark of heterochromatin, is catalyzed by Clr4/Suv39. Clr4/Suv39 contains two conserved domains-an N-terminal chromodomain and a C-terminal catalytic domain-connected by an intrinsically disordered region (IDR). Several mechanisms have been proposed to regulate Clr4/Suv39 activity, but how it is regulated under physiological conditions remains largely unknown.
View Article and Find Full Text PDFAllergol Immunopathol (Madr)
September 2025
Department of Respiratory and Critical Care Medicine, the Wenzhou Central Hospital and Dingli Clinical Institute of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Background: Acute lung injury (ALI) is a critical clinical condition with high mortality, necessitating the development of more effective therapeutic strategies. Rho Guanine nucleotide dissociation inhibitor (GDP) beta (ARHGDIB) has been shown to exert protective effects against noxious stimuli in various disease models.
Objective: In this study, we investigated whether ARHGDIB knockdown had a protective effect on lipopolysaccharide (LPS)-induced injury in alveolar epithelial cells and elucidated its underlying molecular mechanisms.