E3 ubiquitin ligase plays a vital role in the ubiquitin-mediated heat-related protein degradation pathway. Herein, we report that the expression of AtPPRT1, a C3HC4 zinc-finger ubiquitin E3 ligase gene, was induced by heat stress, and the β-glucuronidase (GUS) gene driven by the AtPPRT1 promoter has shown increased activity after basal and acquired thermotolerance. To further explore the function of AtPPRT1 in heat stress response (HSR), we used the atpprt1 mutant and AtPPRT1-overexpressing lines (OE2 and OE10) to expose in heat shock. In this study, the atpprt1 mutant had a lower germination and survival rate than those of Col-0 when suffered from the heat stress, whereas OEs enhanced basal and acquired thermotolerance in Arabidopsis seedlings. When compared to Col-0 and OEs, loss-of-function in AtPPRT1 resulted in lower chlorophyll retention and higher content of reactive oxygen species (ROS) after heat treatment. Moreover, the transcript levels of AtPPRT1 and several heat-related genes (AtZAT12, AtHSP21 and AtHSFA7a) were upregulated to greater extents in OEs and lower extents in atpprt1 compared to Col-0 after heat treated. Hence, we suggest that AtPPRT1 may act as a positive role in regulating the high temperature by mediating the degradation of unknown target proteins.

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Intracellular bacteria are the major contributor to the intractability of septic arthritis, which are sequestered in macrophages to undermine the innate immune response and avoid the antibacterial effect of antibiotics due to the obstruction of the cell membrane. Herein, we report a thermoresponsive nanoparticle, which consists of a phase-change material shell (fatty acids) and an oxygen-producing core (CaO 2 −vancomycin). Under external thermal stimulation, the shell of the nanoparticle transforms from a solid phase to a liquid phase. Then the CaO 2 −Vancomycin core is exposed to the surrounding aqueous solution to release vancomycin and generate Ca(OH) 2 and oxygen, thereby depleting accumulated lactate to mitigate lactateassociated immunosuppression, stabilizing hypoxia-inducible factor-1α (HIF-1α) to enhance M1-like polarization of macrophages, and increasing reactive oxygen species (ROS) and reactive nitrogen species (RNS) production. This combined effect between the controlled release of antibiotics and enhancement of host innate immunity provides a promising strategy to combat intracellular bacteria for septic arthritis therapy.