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GmSN1 enhances virus resistance in plants most likely by affecting the expression of signal transduction and immune response genes. Soybean mosaic virus (SMV) infection causes severe symptom and leads to massive yield loss in soybean (Glycine max). By comparative analyzing gene expression in the SMV-resistant soybean cultivar Rsmv1 and the susceptible cultivar Ssmv1 at a transcriptome level, we found that a subgroup of Gibberellic Acid Stimulated Transcript (GAST) genes were down-regulated in SMV inoculated Ssmv1 plants, but not Rsmv1 plants. Sequence alignment and phylogenetic analysis indicated that one of the GAST genes, GmSN1, was closely related to Snakin-1, a well-characterized potato microbial disease resistance gene. When over-expressed in Arabidopsis and soybean, respectively, under the control of the 35S promoter, GmSN1 enhanced turnip mosaic virus resistance in the transgenic Arabidopsis plants, and SMV resistance in the transgenic soybean plants, respectively. Transcriptome analysis results showed that the up-regulated genes in the 35S:GmSN1 transgenic Arabidopsis plants were largely enriched in functional terms including "signal transduction" and "immune response". Real-time PCR assay indicated that the expression of GmAKT2, a potassium channel gene known to enhance SMV resistance when over-expressed in soybean, was elevated in the 35S:GmSN1 transgenic soybean plants. Taken together, our results suggest that GmSN1 enhances virus resistance in plants most likely by affecting the expression of signal transduction and immune response genes.
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http://dx.doi.org/10.1007/s00299-017-2167-3 | DOI Listing |
Br J Haematol
September 2025
Department of Hematology, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Refractory cytomegalovirus (CMV) infection is a severe complication following umbilical cord blood transplantation (UCBT). Antiviral agents, the standard first-line therapy, are limited by toxicity and resistance without robust T-cell immunity. We evaluated third-party donor (TPD)-derived CMV-specific T cells (CMVSTs) as a treatment option.
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September 2025
State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 150069, Harbin, Heilongjiang, China.
Epizootic hemorrhagic disease virus (EHDV) causes severe disease in ruminants. We assessed the pathogenicity of the Chinese EHDV-7 isolate YN09 in mice lacking the type I interferon receptor and in sheep. In mice, YN09 infection resulted in 100% mortality, with histopathological lesions, viral replication, and immunoreactivity in multiple organs.
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September 2025
Unity Health Toronto, St. Joseph's Health Centre, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada; Unity Health Toronto, Li Ka Shing Knowledge Institute, Toronto, Ontario, Canada. Electronic address: Gregory.German@unityhe
Chronic urinary tract infections are persistent bacterial infections with the potential to drive antibiotic resistance. Like other persistent bacterial infections, intracellular bacterial reservoirs and biofilm formation hinder the clearance of pathogens despite long courses of antibiotic therapy. New strategies for treatment of these persistent infections are needed.
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August 2025
Dipartimento di Scienze degli Alimenti e del Farmaco (DipALIFAR), Università degli Studi di Parma, Viale delle Scienze, 27/A, 43124, Parma, Italy. Electronic address:
Cystic fibrosis (CF) is a multifaceted disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The resulting thick mucus accumulation increases the risk of microbial infections, leading to chronic lung inflammation, progressive tissue damage, and pulmonary exacerbations (PEs). Respiratory viruses may facilitate bacterial colonization, significantly contributing to PEs.
View Article and Find Full Text PDFSci Adv
September 2025
The Jackson Laboratory for Genomic Medicine, Farmington, CT 06032, USA.
Influenza A viruses remain a global health threat, yet no universal antibody therapy exists. Clinical programs have centered on neutralizing mAbs, only to be thwarted by strain specificity and rapid viral escape. We instead engineered three non-neutralizing IgG2a mAbs that target distinct, overlapping epitopes within the conserved N terminus of the M2 ectodomain (M2e).
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