A pattern for the early, middle, and late phase of tea chrysanthemum response to Fusarium oxysporum.

Chrysanthemum morifolium is cultivated worldwide and has high ornamental, tea, and medicinal value. With the increasing area of chrysanthemum cultivation and years of continuous cropping, Fusarium wilt disease frequently occurs in various production areas, seriously affecting the quality and yield and causing huge economic losses. However, the molecular response mechanism of Fusarium wilt infection remains unclear, which limits the molecular breeding process for disease resistance in chrysanthemums. In the present study, we analyzed the molecular response mechanisms of 'Huangju,' one of the tea chrysanthemum cultivars severely infested with Fusarium wilt in the field at the early, middle, and late phases of F. oxysporum infestation. 'Huangju' responded to the infestation mainly through galactose metabolism, plant-pathogen interaction, auxin, abscisic acid, and ethylene signalling in the early phase; galactose metabolism, plant-pathogen interaction, auxin, salicylic acid signal, and certain transcription factors (e.g., CmWRKY48) in the middle phase; and galactose metabolism in the late phase. Notably, the galactose metabolism was important in the early, middle, and late phases of 'Huangju' response to F. oxysporum. Meanwhile, the phytohormone auxin was involved in the early and middle responses. Furthermore, silencing of CmWRKY48 in 'Huangju' resulted in resistance to F. oxysporum. Our results revealed a new molecular pattern for chrysanthemum in response to Fusarium wilt in the early, middle, and late phases, providing a foundation for the molecular breeding of chrysanthemum for disease resistance.

Heterografting enhances chrysanthemums resistance to Alternaria alternata via jasmonate-mediated increases in trichomes and terpenoids.

Trichomes, specialized hair-like structures in the epidermal cells of the aboveground parts of plants, protect plants from pests and pathogens and produce valuable metabolites. Chrysanthemum morifolium, used in tea products, has ornamental and medicinal value. However, it is susceptible to Alternaria alternata fungal infection, posing a threat to its production and use, resulting in substantial economic losses. Increasing the density of glandular trichomes enhances disease resistance and improves the production of medicinal metabolites in chrysanthemums. Jasmonate (JA), promotes the formation of glandular trichomes in various plants. However, it remains unclear whether glandular trichome in chrysanthemums are regulated by JA. Grafting, a technique to improve plant resistance to biotic stresses, has been insufficiently explored in its impact on glandular trichomes, terpenoids, and disease resistance. In this study, we demonstrated that grafting with Artemisia vulgaris rootstocks improves the resistance of chrysanthemum scions to A. alternata. Heterografted chrysanthemums exhibited higher trichome density and terpenoid content compared to self-grafted counterparts. Transcriptome analysis highlighted the significant role of CmJAZ1-like in disease resistance in heterografted chrysanthemums. Overexpressing CmJAZ1-like lines exhibited sensitivity to A. alternate, characterized by reduced glandular trichome density and limited terpenoids. Conversely, silencing lines exhibited resistance to A. alternata showcasing increased glandular trichome density and abundant terpenoids. Higher JA content was confirmed in heterografted chrysanthemum scions compared to self-grafted ones. Furthermore, we established that JA promotes the development of glandular trichomes and the synthesis of terpenoids while inducing the degradation of CmJAZ1-like proteins in chrysanthemums. These findings suggest that higher JA increases trichome density and terpenoid content, enhancing resistance to A. alternata by regulating CmJAZ1-like in heterografted chrysanthemums.

The protective effects of resveratrol, H2S and thermotherapy on the cell apoptosis induced by CdTe quantum dots.

Quantum dots (QDs) could be used in the field of biology and medicine as excellent nano-scale fluorescent probes due to their unique optical properties, but the adverse effects of QDs are always the obstruction for its usage in living organisms. In this study, we observed that CdTe QDs exposure decreased the cell viability while increased the apoptosis rates in the L929 cells. Apart from QD-induced oxidative stress indicated by excessive ROS generation, three signal transductions, including Akt, p38 and JNK, played important roles on the regulation of cell apoptosis by CdTe QDs exposure as well. In order to reduce the toxicity of CdTe QDs, we explored the protective effects of three treatments, i.e. resveratrol, H2S and thermotherapy at 43°C, against the cell apoptosis elicited by CdTe QDs. The results showed that resveratrol, H2S and thermotherapy at 43°C were capable of attenuating cell apoptosis and intercellular ROS production through inhibiting signal pathways of Akt, p38 and JNK, respectively. As there is only limited number of exogenous treatments reported to diminish the toxicity of QDs, our findings will provide a novel insight for researchers who try to reduce or even eliminate the adverse health effects of QDs.

Research advances on apoptosis caused by quantum dots.

Recently, quantum dots (QDs) have been widely applied in biological and biomedical fields such as cell labeling, living tissue imaging, and photodynamic therapy because of their superior optical properties. Meanwhile, the potential biological negative effects and/or toxic effects of QDs have become increasingly important, especially the cytotoxicity caused by QDs. One of the common cytotoxicity when living organisms are treated with QD is apoptosis, where many attempts have been made to explain the mechanisms of apoptosis caused by QDs' use. One of the mechanisms is the production of cadmium ion (Cd(2+)) and reactive oxygen species (ROS). Excess generation of ROS will result in oxidative stress that would mediate apoptosis. Furthermore, the activation of cell death receptors and mitochondria-dependent such as B cell lymphoma 2 (Bcl-2) family and the caspase family could onset apoptosis. Signal transduction such as some classical signal pathways of PI3K-AKT, NF-E2-related factor 2 (Nrf2)-antioxidant response element (ARE), mitogen-activated protein kinases (MAPKs), and nuclear factor kappa B (NF-κB) also plays an important role in the regulation of apoptosis. Several ways to reduce the apoptotic rate have been introduced, such as surface modification, controlling, the dose, size, and exposure time of QDs as well as using antioxidants or inhibitors. In this review, we attempted to review the most recent findings associated with apoptosis caused by QDs so as to provide some guidelines for a safer QD application in the future.