RNAi technologies have been exploited to control viruses, pests, oomycetes, and fungal phytopathogens that cause disasters in host plants, including many agronomically significant crops. Double-stranded RNA (dsRNA) or small interfering RNA (siRNA) has been applied as a trigger for trans-kingdom RNAi between hosts and fungi. However, it is unclear what process mediates RNA uptake by fungi. In this study, by using live-cell imaging, we determined that exogenously synthesized RNA or small RNA (sRNA) was indiscriminately absorbed into , a notorious pathogenic fungus. Moreover, the application of endocytic inhibitors or deletion of endocytic-related genes reduced RNA uptake efficiency, showing that RNA absorption by fungal cells occurs mainly through endocytosis. In addition, we found that the endocytosed fluorescence-labeled RNAs were partly colocalized with endosome marker genes. Overall, our research concluded that exogenous RNA could be assimilated by through the endocytic pathway. Unraveling this cytological mechanism underlying trans-kingdom RNAi holds significant importance, especially considering the fact that RNAi-based strategies targeting pathogenic fungi are increasingly prevalent in the realm of crop protection.
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http://dx.doi.org/10.1002/mlf2.12149 | DOI Listing |
ACS Sens
March 2025
Centre for Innovative Materials for Health, School of Chemical Sciences, The University of Auckland, 23 Symonds Street, Auckland 1010, New Zealand.
Herein, a novel and simple electrospray (ES) printing technique was developed for the fabrication of ultrathin graphene layers with precisely controlled nanometer-scale thickness, where graphene oxide (GO) was electrosprayed on wafers and subsequently chemically reduced into reduced GO (rGO). Utilizing that technique, we prepared ultrathin rGO in-plane graphene field-effect transistor (GFET)-based biosensors coupled with a portable prototype measuring system for point-of-care detection of pathogens. We illustrate the use of such prepared GFETs to detect COVID-19, using the SARS-CoV-2 nucleocapsid protein antigen (N-protein) and genomic viral RNA as detection targets.
View Article and Find Full Text PDFIt is known that inhibition of the endoplasmic reticulum transmembrane signaling protein (ERN1) suppresses the glioblastoma cells proliferation. The present study aims to investigate the impact of inhibition of ERN1 endoribonuclease and protein kinase activities on the , , and gene expression in U87MG glioblastoma cells with an intent to reveal the role of ERN1 signaling in the regulation of expression of these genes. The U87MG glioblastoma cells with inhibited ERN1 endoribonuclease (dnrERN1) or both enzymatic activities of ERN1 (endoribonuclease and protein kinase; dnERN1) were used.
View Article and Find Full Text PDFThe development of targeted therapy for patients with multiple myeloma (MM) is hampered by the low frequency of actionable genetic abnormalities. Gain or amplification of chromosome 1q (1q+) is the most frequent arm-level copy number gain in patients with MM and is associated with higher risk of progression and death despite recent therapeutic advances. Thus, developing targeted therapy for MM patients with 1q+ stands to benefit a large portion of patients in need of more effective management.
View Article and Find Full Text PDFACS Nano
March 2025
School of Biomedical Sciences and Engineering, South China University of Technology, Guangzhou International Campus, Guangzhou 511442, P. R. China.
Mesenchymal stromal cell (MSC) therapy holds great promise for treating myocardial infarction (MI). However, the inflammatory and reactive oxygen species (ROS)-rich environment in infarcted myocardium challenges MSC survival, limiting its therapeutic impact. In this study, we demonstrate that chemical modification of MSCs with anti-VCAM1 and polydopamine (PD) significantly enhances MSC survival and promotes cardiac repair.
View Article and Find Full Text PDFHepatology
March 2025
Department of Liver Surgery and Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, China.
Background And Aims: Portal vein tumor thrombosis (PVTT), an indicator of clinical metastasis, significantly shortens hepatocellular carcinoma (HCC) patients' lifespan, and no effective treatment has been established. We aimed to illustrate mechanisms underlying PVTT formation and tumor metastasis, and identified potential targets for clinical intervention.
Approach And Results: Multi-omics data of 159 HCC patients (including 37 cases with PVTT) was analyzed to identify contributors to PVTT formation and tumor metastasis.
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