Post-transcriptional gene silencing (PTGS) is characterized by the accumulation of short interfering RNAs that are proposed to mediate sequence-specific degradation of cognate and secondary target mRNAs. In plants, it is unclear to what extent endogenous genes contribute to this process. Here, we address the role of the endogenous target genes in transgene-mediated PTGS of beta-1,3-glucanases in tobacco. We found that mRNA sequences of the endogenous glucanase glb gene with varying degrees of homology to the Nicotiana plumbaginifolia gn1 transgene are targeted by the silencing machinery, although less efficiently than corresponding transgene regions. Importantly, we show that endogene-specific nucleotides in the glb sequence provide specificity to the silencing process. Consistent with this finding, small sense and antisense 21- to 23-nucleotide RNAs homologous to the endogenous glb gene were detected. Combined, these data demonstrate that a co-suppressed endogenous glucan ase gene is involved in signal amplification and selection of homologous targets, and show that endogenous genes can actively participate in PTGS in plants. The findings are introduced as a further sophistication of the post-transciptional silencing model.
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http://dx.doi.org/10.1093/emboj/cdf586 | DOI Listing |
Curr Biol
January 2025
Cornell Lab of Ornithology, Cornell University, Ithaca, NY 14850, USA; Actions@EBMF, New York, NY 10006, USA.
An emerging frontier in ecology explores how organisms integrate social information into movement behavior and the extent to which information exchange occurs across species boundaries. Most migratory landbirds are thought to undertake nocturnal migratory flights independently, guided by endogenous programs and individual experience. Little research has addressed the potential for social information exchange aloft during nocturnal migration, but social influences that aid navigation, orientation, or survival could be valuable during high-risk migration periods.
View Article and Find Full Text PDFActa Physiol (Oxf)
February 2025
Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada.
Purpose: Homoarginine (hArg) is an arginine metabolite that has been known for years, but its physiological role in the body remains poorly understood. For instance, it is well known that high hArg concentrations in the blood are protective against several disease states, yet the mechanisms behind these health benefits are unclear. This review compiles what is known about hArg, namely its synthetic pathways, its role in different diseases and conditions, and its proposed mechanisms of action in humans and experimental animals.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Division of Rheumatology, Center of Excellence for Intestinal and Immunology Research, University of Alberta, Edmonton, Alberta, Canada.
Superantigen-induced (Sag-induced) autoimmunity has been proposed as a mechanism for many human disorders, without a clear understanding of the potential triggers. In this issue of the JCI, McCarthy and colleagues used the SKG mouse model of rheumatoid arthritis to characterize the role of Sag activity in inflammatory arthritis by profiling arthritogenic naive CD4+ T cells. Within the diseased joints, they found a marked enrichment of T cell receptor-variable β (TCR-Vβ) subsets that were reactive to the endogenously encoded mouse mammary tumor virus (MMTV) Sag.
View Article and Find Full Text PDFTheranostics
January 2025
Department of biochemistry and molecular biology, College of Life Sciences, Central South University, Changsha, 410078, Hunan, China.
Stem cell transplantation is a promising strategy to establish neural relays in situ for spinal cord injury (SCI) repair. Recent research has reported short-term survival of exogenous cells, irrespective of immunosuppressive drugs (ISD), results in similar function recovery, though the mechanisms remain unclear. This study aims to validate this short-term repair effect and the potential mechanisms in large animals.
View Article and Find Full Text PDFPNAS Nexus
January 2025
Faculty of Medicine and Dentistry, William Harvey Research Institute, Barts and The London, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Metabolic dysfunction-associated steatotic liver disease (MASLD), hepatic fibrosis, and portal hypertension constitute an increasing public health problem due to the growing prevalence of obesity and diabetes. C-type natriuretic peptide (CNP) is an endogenous regulator of cardiovascular homeostasis, immune cell reactivity, and fibrotic disease. Thus, we investigated a role for CNP in the pathogenesis of MASLD.
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