Material-engineered bioartificial microorganisms enabling efficient scavenging of waterborne viruses.

Material-based tactics have attracted extensive attention in driving the functional evolution of organisms. In aiming to design steerable bioartificial organisms to scavenge pathogenic waterborne viruses, we engineer Paramecium caudatum (Para), single-celled microorganisms, with a semiartificial and specific virus-scavenging organelle (VSO). Fe3O4 magnetic nanoparticles modified with a virus-capture antibody (MNPs@Ab) are integrated into the vacuoles of Para during feeding to produce VSOs, which persist inside Para without impairing their swimming ability. Compared with natural Para, which has no capture specificity and shows inefficient inactivation, the VSO-engineered Para (E-Para) specifically gathers waterborne viruses and confines them inside the VSOs, where the captured viruses are completely deactivated because the peroxidase-like nano-Fe3O4 produces virus-killing hydroxyl radicals (•OH) within acidic environment of VSO. After treatment, magnetized E-Para is readily recycled and reused, avoiding further contamination. Materials-based artificial organelles convert natural Para into a living virus scavenger, facilitating waterborne virus clearance without extra energy consumption.

LncRNA MALAT-1 regulates the growth of interleukin-22-stimulated keratinocytes via the miR-330-5p/S100A7 axis.

Psoriasis is a chronic autoimmune disorder related to abnormal keratinocyte proliferation. Long noncoding RNAs (lncRNAs) are significant regulators in the progression of skin diseases. In this study, we explored how lncRNA MALAT-1 controls the pathogenesis of psoriasis by examining its impact on keratinocyte proliferation, inflammation, and apoptosis. A psoriasis cell model was established by treating HaCaT keratinocytes with the inflammatory factor, IL-22 (100 ng/ml), for 24 h. The MALAT-1 and S100A7 levels in psoriatic lesions, normal skin tissues, and IL-22-stimulated HaCaT cells were determined by RT-qPCR and western blotting. Cell proliferation, inflammation, and apoptosis were detected by the MTT assay, western blotting, and flow cytometry analysis, respectively. Bioinformatics analysis was used to identify the miRNAs that bind to MALAT-1 and S100A7. The relationships between MALAT-1 or miR-330-5p and S100A7 were assessed using a luciferase reporter assay. The MALAT-1 and S100A7 levels were upregulated in both psoriatic lesion samples and IL-22-stimulated HaCaT cells. Silencing MALAT-1 significantly reversed the IL-22-stimulated promotion of HaCaT proliferation and changes in Ki67 and KRT5/14/1/10 protein levels, and MALAT-1 deficiency also reversed the upregulation of TNF-α, IL-17, and IL-23 protein levels as well as suppression of cell apoptosis. As a ceRNA, MALAT-1 competed with S100A7 to prevent miR-330-5p-induced inhibition of S100A7 expression. There was a negative correlation between miR-330-5p and MALAT-1 (or S100A7) expression in psoriatic lesion tissues. In response to IL-22 treatment, miR-330-5p silencing eliminated the effects of MALAT-1 knockdown in HaCaT cells. Thus, these findings demonstrated that MALAT-1 modulates the IL-22-induced changes in HaCaT cells through the miR-330-5p/S100A7 axis.

The complete plastid genome of Thyrsostachys siamensis (Poaceae, Bambusoideae).

Thyrsostachys is oligotypic genus of Bambusinae, while its phylogenetic position had been unclear. Here, the complete plastid genome of the type species, T. siamensis, was sequenced and analyzed in this work. The complete genome is a typical quadripartite structure with 139,522 bp in length, comprising of a large single-copy region (LSC, 83,032 bp), a small single-copy region (SSC, 12,892 bp), and a pair of invert repeats regions (IR, 21,799 bp). The genome contains 138 genes, 89 protein-coding genes, 41 tRNA genes, and 8 rRNA genes. The GC content of genome was 38.9%. Phylogenetic analysis indicated T. siamensis was sister to Dendrocalamus birmanicus within Bambusinae.