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The phytohormone auxin plays crucial roles in nearly every aspect of plant growth and development. Auxin signaling is activated through the phytohormone-induced proteasomal degradation of the Auxin/INDOLE-3-ACETIC ACID (Aux/IAA) family of transcriptional repressors. Notably, many auxin-modulated physiological processes are also regulated by nitric oxide (NO) that executes its biological effects predominantly through protein S-nitrosylation at specific cysteine residues. However, little is known about the molecular mechanisms in regulating the interactive NO and auxin networks. Here, we show that NO represses auxin signaling by inhibiting IAA17 protein degradation. NO induces the S-nitrosylation of Cys-70 located in the intrinsically disordered region of IAA17, which inhibits the TIR1–IAA17 interaction and consequently the proteasomal degradation of IAA17. The accumulation of a higher level of IAA17 attenuates auxin response. Moreover, an IAA17C70Wnitrosomimetic mutation renders the accumulation of a higher level of the mutated protein, thereby causing partial resistance to auxin and defective lateral root development. Taken together, these results suggest that S-nitrosylation of IAA17 at Cys-70 inhibits its interaction with TIR1, thereby negatively regulating auxin signaling. This study provides unique molecular insights into the redox-based auxin signaling in regulating plant growth and development.

Three lanthanide-based coordination polymers (Ln-CPs) with layered structure, {[La2(L)3(DMF) (H2O)3]·H2O}n(1), {[Eu2(L)3(DMF)2(H2O)]·(H2O)}n(2) {[Tb2(L)3(DMF)2(H2O)]·H2O}n(3) were successfully synthesized from H2L(N,N′-bis(4-carbozylbenzyl)aniline). Remarkably, compound 3has extremely high sensitivity to 4-nitrophenol. When the concentration of 4-nitrophenol reaches 5.98 × 10−3 mmol/L, the fluorescence intensity of compound 3is quenched by 59%. The calculated KSVis 7.56 × 104and limit of detection (LOD) is 4.73 μg/L. 3exhibits a highly sensitive detection towards Fe3+and compound 2shows outstanding antibacterial effects on Staphylococcus aureus, respectively. The white light emission was also investigated by changing the mixing ratio of LaNO3, EuNO3and TbNO3during the preparation of coordination polymers.

Superantigens can induce cell-mediated cytotoxicity preferentially against MHC II-positive target cells with large amounts of inflammatory cytokines releasing. In this study, superantigen staphylococcal enterotoxin C (SEC) 1 was investigated to evaluate its potential in bladder cancer immunotherapy in vitroand in vivo. Our results revealed that SEC1 could stimulate the proliferation of human peripheral blood mononuclear cells (PBMCs) in a dose-dependent manner, accompanied with the release of interleukin-2, interferon-γ, and tumor necrosis factor-α, and increased the population of CD4+T cells and CD8+T cells. PBMCs stimulated by SEC1 could initiate significant cytotoxicity towards human bladder cancer cells in vitro. The results of in vivoantitumor experiment indicated that SEC1 could decrease the rate of tumor formation and prolong the survival time of tumor-bearing mice. Our study demonstrated that SEC1 inhibited the growth of bladder cancer. And it is also suggested that SEC1 may become a candidate for bladder cancer immunotherapy.