Ultraviolet-C (UV-C) radiation has been reported to induce defence responses to pathogens in growing crops and described as a new environmentally friendly method for disease control. However, whether the effect of the induced defence mechanisms will persist after the stress imposed by UV-C is alleviated and how these mechanisms interact with pathogen elicitors upon infection have not yet been investigated. Thus, we inoculated strawberry plants with Mycosphaerella fragariae, the causal agent of leaf spot disease, after 5 weeks of repeated UV-C irradiation treatment (cumulative dose of 10.2 kJ m −2 ) and investigated the alteration of gene expression and biochemical phenotypes. The results revealed that UV-C treatment had a significant impact on gene expression in strawberry leaves and led to the overexpression of a set of genes involved in plant-pathogen interaction. UV-C-treated leaves displayed a stronger response to infection after inoculation, with reduced symptoms and increases in accumulation of total phenolics and volatile terpenes, higher expression of pathogenesis-related proteins and the activity of several defence enzymes. This study presumptively describe, for the first time, the involvement of terpenes, reactive oxygen species, and abscisic acid, salicylic acid, jasmonic acid, and their transduction factors, in the network underpinning UV-C priming of growing crops for improved protection against pathogens.

Natural ventilation (NV) is a key sustainable solution for reducing the energy use in buildings, improving thermal comfort, and maintaining a healthy indoor environment. However, the energy savings and environmental benefits are affected greatly by ambient air pollution in China. Here we estimate the NV potential of all major Chinese cities based on weather, ambient air quality, building configuration, and newly constructed square footage of office buildings in the year of 2015. In general, little NV potential is observed in northern China during the winter and southern China during the summer. Kunming located in the Southwest China is the most weatherfavorable city for natural ventilation, and reveals almost zero loss due to air pollution. Building Energy Simulation (BES) is conducted to estimate the energy savings of natural ventilation in which ambient air pollution and total square footage must be taken into account. Beijing, the capital city, displays limited per-square-meter saving potential due to the unfavorable weather and air quality for natural ventilation, but its largest total square footage of office buildings makes it become the city with the greatest energy saving opportunity in China. Our analysis 1 † These authors contributed equally to this work.

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Targeting the PI3K pathway has achieved limited success in cancer therapy. One reason for the disappointing activity of drugs that interfere with molecules that are important player in this pathway is the induction of multiple feedback loops that have been only partially understood. To understand these limitations and develop improved treatment strategies, we comprehensively characterized molecular mechanisms of PI3K pathway signaling in bladder cancer cell lines upon using small molecule inhibitors and RNAi technologies against all key molecules and protein complexes within the pathway and analyzed functional and molecular consequences. When targeting either mTORC1, mTOR, AKT or PI3K, only S6K1 phosphorylation was affected in most cell lines examined. Dephosphorylation of 4E-BP1 required combined inhibition of PI3K and mTORC1, independent from AKT, and resulted in a robust reduction in cell viability. Long-term inhibition of PI3K however resulted in a PDK1-dependent, PIP3 and mTORC2 independent rephosphorylation of AKT. AKT rephosphorylation could also be induced by mTOR or PDK1 inhibition. Combining PI3K/mTOR inhibitors with AKT or PDK1 inhibitors suppressed this rephosphorylation, induced apoptosis, decreased colony formation, cell viability and growth of tumor xenografts. Our findings reveal novel molecular mechanisms that explain the requirement for simultaneous targeting of PI3K, AKT and mTORC1 to achieve effective tumor growth inhibition.