The mechanisms of viral diseases are a major focus of biology. Despite intensive investigations, how a plant virus interacts with host factors to cause diseases remains poorly understood. The Rice dwarf virus (RDV), a member of the genus Phytoreovirus, causes dwarfed growth phenotypes in infected rice (Oryza sativa) plants. The outer capsid protein P2 is essential during RDV infection of insects and thus influences transmission of RDV by the insect vector. However, its role during RDV infection within the rice host is unknown. By yeast two-hybrid and coimmunoprecipitation assays, we report that P2 of RDV interacts with entkaurene oxidases, which play a key role in the biosynthesis of plant growth hormones gibberellins, in infected plants. Furthermore, the expression of ent-kaurene oxidases was reduced in the infected plants. The level of endogenous GA 1 (a major active gibberellin in rice vegetative tissues) in the RDV-infected plants was lower than that in healthy plants. Exogenous application of GA 3 to RDV-infected rice plants restored the normal growth phenotypes. These results provide evidence that the P2 protein of RDV interferes with the function of a cellular factor, through direct physical interactions, that is important for the biosynthesis of a growth hormone leading to symptom expression. In addition, the interaction between P2 and rice ent-kaurene oxidase-like proteins may decrease phytoalexin biosynthesis and make plants more competent for virus replication. Moreover, P2 may provide a novel tool to investigate the regulation of GA metabolism for plant growth and development.

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In agriculture, loss of crop yield to pathogen damage seriously threatens efforts to achieve global food security. In the present work, “organic” elemental sulfur nanoparticles (SNPs) were investigated for management of the fungal pathogen Fusarium oxysporum f. sp. lycopersici on tomatoes. Foliar application and seed treatment with SNPs (30–100 mg/L, 30 and 100 nm) suppressed pathogen infection in tomatoes, in a concentration- and size-dependent fashion in a greenhouse experiment. Foliar application with 1 mg/plant of 30 nm SNPs (30-SNPs) exhibited the best performance for disease suppression, significantly decreasing disease incidence by 47.6% and increasing tomato shoot biomass by 55.6% after 10 weeks application. Importantly, the disease control efficacy with 30-SNPs was 1.43-fold greater than the commercially available fungicide hymexazol. Mechanistically, 30-SNPs activated the salicylic acid-dependent systemic acquired resistance pathway in tomato shoots and roots, with subsequent upregulation of the expression of pathogenesis-related and antioxidase-related genes (upregulated by 11–352%) and enhancement of the activity and content of disease-related biomolecules (enhanced by 5–49%). In addition, transmission electron microscopy imaging shows that SNPs were distributed in the tomato stem and directly inactivated in vivo pathogens. The oxidative stress in tomato shoots and roots, the root plasma membrane damage, and the growth of the pathogen in stem were all significantly decreased by SNPs. The findings highlight the significant potential of SNPs as an eco-friendly and sustainable crop protection strategy.

We systematically investigated the toxicity mechanism of three graphene-family materials (GFMs), graphene oxide (GO), reduced graphene oxide (rGO) and multi-layer graphene (MG), to algae (Chlorella pyrenoidosa). GFMs exhibited much higher toxicity than other carbon materials (carbon nanotube and graphite), with the 96 h median effective concentration (EC) values of 37.3 (GO), 34.0 (rGO), and 62.2 (MG) mg/L. Shading effect contributed approximately 16.4% of growth inhibition by GO due to its higher dispersibility and transformation while the other GFMs did not show any shading effect. Hydrophobic rGO and MG more readily heteroagglomerated with algae than GO, thus likely leading to more direct contacts with algae. Flow cytometry results showed significant decrease of membrane integrity after GFM exposure, and rGO caused the highest membrane damage, which was confirmed by the increased DNA and K efflux. The observed membrane damage was caused by a combination of oxidative stress and physical penetration/extraction. Moreover, all the three GFMs could adsorb macronutrients (N, P, Mg, and Ca) from the algal medium, thus leading to nutrient depletion-induced indirect toxicity. GO showed the highest nutrient depletion (53% of total toxicity) due to its abundant functional groups. The information provided in this work will be useful for understanding toxicity mechanism and environmental risk of different GFMs in aquatic environments.

Tumor suppressor Smad4 is the common signaling effector in the transforming growth factor β (TGF-β) superfamily. Phosphorylated regulatory Smads (R-Smads) interact with Smad4, and the complex translocates into the nucleus to regulate gene transcription. Proper TGF-β signaling requires precise control of Smad functions. Smurfs have been shown to mediate the degradation of R-Smads but not the commonpartner Smad4. We report a novel mechanism of Smad4 degradation. Jab1 interacts directly with Smad4 and induces its ubiquitylation for degradation. Jab1 was initially identified as a co-activator of c-Jun, and it also induces degradation of cell cycle inhibitor p27 and tumor suppressor p53. Ectopic expression of Jab1 decreased endogenous Smad4 steady-state levels. The 26S proteasome inhibitors lactacystin and MG132 reduced the degradation rate of Smad4 protein. Examination of the effects of JAB1-induced Smad4 degradation indicates that Jab1 inhibited TGF-β-induced gene transcription. Our data suggest that Jab1 antagonizes TGF-β function by inducing degradation of Smad4 through a distinct degradation pathway.