Adaptation mechanism of three Impatiens species to different habitats based on stem morphology, lignin and MYB4 gene.

BACKGROUND: Impatiens is an important genus with rich species of garden plants, and its distribution is extremely extensive, which is reflected in its diverse ecological environment. However, the specific mechanisms of Impatiens' adaptation to various environments and the mechanism related to lignin remain unclear. RESULTS: Three representative Impatiens species,Impatiens chlorosepala (wet, low degree of lignification), Impatiens uliginosa (aquatic, moderate degree of lignification) and Impatiens rubrostriata (terrestrial, high degree of lignification), were selected and analyzed for their anatomical structures, lignin content and composition, and lignin-related gene expression. There are significant differences in anatomical parameters among the stems of three Impatiens species, and the anatomical structure is consistent with the determination results of lignin content. Furthermore, the thickness of the xylem and cell walls, as well as the ratio of cell wall thickness to stem diameter have a strong correlation with lignin content. The anatomical structure and degree of lignification in Impatiens can be attributed to the plant's growth environment, morphology, and growth rate. Our analysis of lignin-related genes revealed a negative correlation between the MYB4 gene and lignin content. The MYB4 gene may control the lignin synthesis in Impatiens by controlling the structural genes involved in the lignin synthesis pathway, such as HCT, C3H, and COMT. Nonetheless, the regulation pathway differs between species of Impatiens. CONCLUSIONS: This study demonstrated consistency between the stem anatomy of Impatiens and the results obtained from lignin content and composition analyses. It is speculated that MYB4 negatively regulates the lignin synthesis in the stems of three Impatiens species by regulating the expression of structural genes, and its regulation mechanism appears to vary across different Impatiens species. This study analyses the variations among different Impatiens plants in diverse habitats, and can guide further molecular investigations of lignin biosynthesis in Impatiens.

Reclaimable MoS2 Sponge Absorbent for Drinking Water Purification Driven by Solar Energy.

With the fast development of modern industries, scarcity of freshwater resources caused by heavy metal pollution (i.e., Hg2+) has become a severe issue for human beings. Herein, a 3D-MoS2 sponge as an excellent absorbent is fabricated for mercury removal due to its multidimensional adsorption pathways, which decreases the biomagnification effect of methylmercury in water bodies. Furthermore, a secondary water purification strategy is employed to harvest drinkable water with the exhausted adsorbents, thus alleviating the crisis of drinking water shortage. Compared to the conventional landfill treatment, the exhausted MoS2 sponge absorbents are further functionalized with a poly(ethylene glycol) (PEG) layer to prevent the heavy metals from leaking and enhance the hydrophilicity for photothermal conversion. The fabricated evaporator displays excellent evaporation rates of ∼1.45 kg m-2 h-1 under sunlight irradiation and produces freshwater with Hg2+ under the WHO drinking water standard at 0.001 mg L-1. These results not only assist in avoiding the biodeposition effect of mercury in water but also provide an environment-friendly strategy to recycle hazardous adsorbents for water purification.

The canonical Wnt/ß-catenin signaling pathway facilitates pseudorabies virus proliferation and enhances virus-induced autophagy.

Pseudorabies virus (PRV) is a swine herpesvirus with a broad host range that causes significant economic losses worldwide. The Wnt/ß-catenin signaling pathway is reportedly involved in multiple viruses' proliferation. In this study, we demonstrated that PRV infection significantly activated the Wnt/ß-catenin signaling and promoted the nuclear translocation of ß-catenin. Applying specific chemical inhibitors (FH535 and iCRT14) caused a remarkable decrease in PRV titers in various cell lines. Knockdown of ß-catenin by siRNA also reduced the proliferation of PRV. On the contrary, treatment with lithium chloride (LiCl), an inhibitor of GSK3ß, stimulated the Wnt/ß-catenin signaling pathway and enhanced the PRV proliferation. Similarly, overexpression of ß-catenin promoted PRV proliferation and reversed the antiviral effect of FH535. Moreover, LiCl promoted PRV-induced autophagy, whereas FH535 and iCRT14 showed converse effects. These findings suggest that PRV infection stimulates the canonical Wnt/ß-catenin signaling pathway, facilitating PRV proliferation and regulating virus-induced autophagy. These data also provide potential targets for developing antiviral agents against PRV.

Identification of pimavanserin tartrate as a potent Ca2+-calcineurin-NFAT pathway inhibitor for glioblastoma therapy.

Glioblastoma multiforme (GBM) is the most common and malignant type of primary brain tumor, and 95% of patients die within 2 years after diagnosis. In this study, aiming to overcome chemoresistance to the first-line drug temozolomide (TMZ), we carried out research to discover a novel alternative drug targeting the oncogenic NFAT signaling pathway for GBM therapy. To accelerate the drug's clinical application, we took advantage of a drug repurposing strategy to identify novel NFAT signaling pathway inhibitors. After screening a set of 93 FDA-approved drugs with simple structures, we identified pimavanserin tartrate (PIM), an effective 5-HT2A receptor inverse agonist used for the treatment of Parkinson's disease-associated psychiatric symptoms, as having the most potent inhibitory activity against the NFAT signaling pathway. Further study revealed that PIM suppressed STIM1 puncta formation to inhibit store-operated calcium entry (SOCE) and subsequent NFAT activity. In cellula, PIM significantly suppressed the proliferation, migration, division, and motility of U87 glioblastoma cells, induced G1/S phase arrest and promoted apoptosis. In vivo, the growth of subcutaneous and orthotopic glioblastoma xenografts was markedly suppressed by PIM. Unbiased omics studies revealed the novel molecular mechanism of PIM's antitumor activity, which included suppression of the ATR/CDK2/E2F axis, MYC, and AuroraA/B signaling. Interestingly, the genes upregulated by PIM were largely associated with cholesterol homeostasis, which may contribute to PIM's side effects and should be given more attention. Our study identified store-operated calcium channels as novel targets of PIM and was the first to systematically highlight the therapeutic potential of pimavanserin tartrate for glioblastoma.

Newcastle disease virus V protein interacts with hnRNP H1 to promote viral replication.

The interactions between host cellular proteins and viral proteins are important for successful infection by viruses. Previous studies from our group have identified various host cellular proteins that can interact with the Newcastle disease virus V protein (Chu et al., 2018a), but their function in NDV replication has not been fully determined. The present study reports that heterogenous nuclear ribonucleoprotein H1 (hnRNP H1) can interact with NDV V protein in yeast. The immunofluorescence results showed that hnRNP H1 and V protein could colocalize in the cytoplasm of a chicken embryo fibroblast cell line (DF-1 cells). Co-immunoprecipitation assays further verified the interaction of these two proteins. The effects of overexpression and knockdown of hnRNP H1 on NDV replication were evaluated in DF-1 cells through real time quantitative PCR (RT-qPCR) and plaque assays. The regulation of V protein on hnRNP H1 expression was also examined. The results indicated that overexpression of hnRNP H1 facilitated NDV replication, while knockdown of hnRNP H1 decreased NDV replication. It was also shown that V protein could regulate hnRNP H1 expression at the protein level instead of the transcription level. The effect of V protein and hnRNP H1 on the DF-1 cell cycle was also tested and the results revealed that V protein may regulate cell proliferation by controlling the expression of hnRNP H1. Taken together, these results suggest that NDV V protein could promote viral replication by interacting with hnRNP H1.

Musashi1 inhibit the release of Newcastle disease viruses through preventing apoptosis of DF-1 cells.

The efficient proliferation of Newcastle disease virus (NDV) depends on its inhibition of host cell innate immunity. V protein acts as a nonstructural protein which plays a significant role in virus replication, whereas its function remains to be further explored. In this study, Musashi RNA binding protein 1 (MSI1) was selected and its interaction with V protein was further verified by Co-immunoprecipitation (Co-IP) and Immuno-colocalization test. Through the transfection of pCMV-HA-MSI1 in DF-1 cells, the overexpression of MSI1 reduced virus particles in the cell supernatant but not reduced mRNA and virus protein in cells pellet, which suggests that MSI1may act as a new antiviral molecule by inhibiting viral release. Cell early apoptosis was detected by flow cytometry (FCM), the result shows that overexpression of MSI1 inhibit cell apoptosis, implying MSI1 Inhibit virus release may through this way. Taken together, MSI1 and NDV V protein has a detectable interaction, and may block apoptosis to inhibit the release of NDV. However, this is the first report about the interaction between MSI1 and V protein of NDV that can inhibit the NDV replicated.

Distinct assembly processes shape bacterial communities along unsaturated, groundwater fluctuated, and saturated zones.

The subsurface soil environment through the unsaturated (vadose) zone and saturated (below groundwater table) zone is one of the most active layers in the Earth's surface with biogeochemical interactions. Geochemical variables and geographic distance are key driving forces shaping the distribution of soil microbial communities, but our understandings are mainly limited to surface soil or shallow unsaturated zone (1-3 m beneath the ground). In this study, soil and sediment samples were collected from the unsaturated zone, through groundwater fluctuated zone, to saturated zone (up to 20 m) to unravel the assembly processes mediating vertical bacterial community succession across these three zones. Our results suggested both geochemical niches and bacterial diversity had different vertical patterns in each zone. With increased depth, pH increased and nutrient levels (C, N, P, K) and bacterial diversity declined in the unsaturated zone, and nutrients and bacterial diversity remained low levels after reaching the fluctuated and saturated zones. Nutrients were the key drivers shaping bacterial variation in the unsaturated zone, but limited nutrients and only 'depth' significantly explained the variations in the fluctuated zone and saturated zone, respectively. The co-occurrence network supported a more species co-existence pattern in the unsaturated zone than that in the other two zones. Due to the geochemical variations across three zones, the assembly of phylogenetically more clustered communities was observed through deterministic processes (e.g., 55% homogenizing selection) in the unsaturated zone, but the stochastic process (e.g., 50%-70% dispersal limitation) was more important in the fluctuated and saturated zones. These findings together suggested that the vertical distribution of soil bacterial community assembly was zone-specific and shaped by the degree of deterministic vs. stochastic processes. Our results provide a novel insight into the microbial community assembly across three different ecosystems in the Earth's critical zone and shed a light on subsurface biogeochemical processes.

LINC00669 insulates the JAK/STAT suppressor SOCS1 to promote nasopharyngeal cancer cell proliferation and invasion.

Nasopharyngeal carcinoma (NPC) is an epithelial cancer emerging from the lining of nasopharyngeal mucosa, with extremely frequent occurrence in east and southeast Asia. For the purpose of exploring roles of the dysregulated long non-coding RNA (lncRNA) in NPC, we identified a novel lncRNA LINC00669 with an apparent negative correlation to the overall survival from human NPC mRNA expression profiling databases. We further performed RNA pulldown coupled with mass spectrum to find out its target protein, and applied a series of in vitro and in vivo loss-and-gain-of function assays to investigate its oncogenic roles in NPC tumor development and progression. Our results demonstrated that LINC00669 competitively binds to the key JAK/STAT signaling pathway suppressor SOCS1, and insulates it from imposing ubiquitination modification on the pathway component of STAT1, which leads to its abnormal stabilization and activation. The activated STAT1 is then transferred into the nucleus and initiates the transcription of genes related to proliferation and invasion. In summary, our study reveals that the cytoplasmic resident lncRNA LINC00669 confers malignant properties on NPC cancer cells by facilitating a persistent activation of the JAK/STAT signaling pathway. Findings in the current study shed lights on prospects for treating NPC using strategies targeting the novel regulator of the JAK/STAT signaling.

Screening and mechanistic study of key sites of the hemagglutinin-neuraminidase protein related to the virulence of Newcastle disease virus.

Newcastle disease is a kind of avian infectious disease caused by Newcastle disease virus (NDV). The virulence of NDV is dependent mainly on the fusion (F) protein and hemagglutinin-neuraminidase (HN) protein. The genomes of 2 viruses, NDV-Blackbird and NDV-Dove, are 99.9% similar, while NDV-Blackbird is a velogenic virus, and NDV-Dove is a lentogenic virus. Further analysis revealed that the F proteins of the 2 strains were identical, and only 5 amino acid sites on the HN proteins were inconsistent. Five different HN mutant plasmids were constructed and analyzed in this study. The results showed that the mutation F110L caused a significant increase in fusion-promotion activity caused by an increase in neuraminidase activity. Because of the increase in receptor-binding activity caused by G116R, there was a significant increase in fusion-promotion activity. The mutation G54S resulted in a slight decrease in the fusion-promotion activity caused by a slight decrease in receptor-binding activity. The slight increase in the fusion-promotion activity caused by A469V was associated with a significant increase in neuraminidase activity. Therefore, the amino acids L110 and R116 played a key role in determining the virulence difference between NDV-Blackbird and NDV-Dove, which could lay a foundation for illuminating the virulence differences of NDV strains, as well as the development of attenuated vaccines.

Thermo-Mechanical Performance of Polylactide Composites Reinforced with Alkali-Treated Bamboo Fibers.

In this study, polylactide acid (PLA) is filled with bamboo fibers (BFs) to fabricate a biodegradable natural composite for industrial applications. The influence of pre-treatment of BFs using 4 wt % sodium hydroxide (NaOH) solution at room temperature for 1 h on thermal and mechanical properties of resultant composites is systematically investigated. Differential scanning calorimetry and thermogravimetric analysis demonstrate that the incorporation of treated BFs promotes higher glass transition and crystallization temperatures of the resultant composites relative to untreated fiber composites, whereas alkali treatment results in superior thermal stability. Furthermore, the fracture surfaces are characterized by scanning electron microscopy. The changes in morphology reveal the possible dissolution of hemicellulose and lignin by alkalization with NaOH, indicative of an improved interfacial adhesion. An increment in the tensile strength of composites is achieved through the reinforcement with treated fibers. However, a lower tensile modulus is found for composites reinforced with chemically modified BFs, which might be due to the partial conversion of cellulose I into II. The results highlight that the use of BFs could be a feasible candidate as reinforcements for the development of biodegradable composites.

[Microbial community structure and distribution characteristics in oil contaminated soil].

Molecular biology methods such as PCR-DGGE combined with phylogenetic analysis were used for the soil microbial community structure and distribution profiling. Relationship of microbial community structure and distribution differed in a typical oil contaminated field was studied. Results showed that soil oil content was the main factor to the difference of microbial community structure similarity. The similarity index of microbial community structure and oil content had a significantly negative correlation. The contaminated soil microorganism genus had an uneven distribution. Thus, soil pollution had obvious stress and differentiation for microbial community structure and species relationship. Dominant species in oil contaminated soil were identified as Gulosibacter, Halomonas, Petrobacter, Methylocystis, and Pseudoalteromonas. The findings provide a basis for understanding the microbial characteristics of oil contaminated soil.