Characteristics of rhizosphere and bulk soil microbial community of Chinese cabbage (Brassica campestris) grown in Karst area.

Understanding the rhizosphere soil microbial community and its relationship with the bulk soil microbial community is critical for maintaining soil health and fertility and improving crop yields in Karst regions. The microbial communities in the rhizosphere and bulk soils of a Chinese cabbage (Brassica campestris) plantation in a Karst region, as well as their relationships with soil nutrients, were examined in this study using high-throughput sequencing technologies of 16S and ITS amplicons. The aim was to provide theoretical insights into the healthy cultivation of Chinese cabbage in a Karst area. The findings revealed that the rhizosphere soil showed higher contents of organic matter (OM), alkaline hydrolyzable nitrogen (AN), available phosphorus (AP), total phosphorus (TP), available potassium (AK), total potassium (TK), total nitrogen (TN), catalase (CA), urease (UR), sucrase (SU), and phosphatase (PHO), in comparison with bulk soil, while the pH value showed the opposite trend. The diversity of bacterial and fungal communities in the bulk soil was higher than that in the rhizosphere soil, and their compositions differed between the two types of soil. In the rhizosphere soil, Proteobacteria, Acidobacteriota, Actinobacteriota, and Bacteroidota were the dominant bacterial phyla, while Olpidiomycota, Ascomycota, Mortierellomycota, and Basidiomycota were the predominant fungal phyla. In contrast, the bulk soil was characterized by bacterial dominance of Proteobacteria, Acidobacteriota, Chloroflexi, and Actinobacteriota and fungal dominance of Ascomycota, Olpidiomycota, Mortierellomycota, and Basidiomycota. The fungal network was simpler than the bacterial network, and both networks exhibited less complexity in the rhizosphere soil compared with the bulk soil. Moreover, the rhizosphere soil harbored a higher proportion of beneficial Rhizobiales. The rhizosphere soil network was less complicated than the network in bulk soil by building a bacterial-fungal co-occurrence network. Furthermore, a network of relationships between soil properties and network keystone taxa revealed that the rhizosphere soil keystone taxa were more strongly correlated with soil properties than those in the bulk soil; despite its lower complexity, the rhizosphere soil contains a higher abundance of bacteria which are beneficial for cabbage growth compared with the bulk soil.

Types of vegetables shape composition, diversity, and co-occurrence networks of soil bacteria and fungi in karst areas of southwest China.

BACKGROUND: Microorganisms are of significant importance in soil. Yet their association with specific vegetable types remains poorly comprehended. This study investigates the composition of bacterial and fungal communities in soil by employing high-throughput sequencing of 16 S rRNA genes and ITS rRNA genes while considering the cultivation of diverse vegetable varieties. RESULTS: The findings indicate that the presence of cultivated vegetables influenced the bacterial and fungal communities leading to discernible alterations when compared to uncultivated soil. In particular, the soil of leafy vegetables (such as cabbage and kale) exhibited higher bacterial α-diversity than melon and fruit vegetable (such as cucumber and tomato), while fungal α-diversity showed an inverse pattern. The prevailing bacterial phyla in both leafy vegetable and melon and fruit vegetable soils were Proteobacteria, Acidobacteriota, Actinobacteriota, and Chloroflexi. In leafy vegetable soil, dominant fungal phyla included Ascomycota, Olpidiomycota, Mortierellomycota, and Basidiomycota whereas in melon and fruit vegetable soil. Ascomycota, Mortierellomycota, Basidiomycota, and Rozellomycota held prominence. Notably, the relative abundance of Ascomycota was lower in leafy vegetable soil compared to melon and fruit vegetable soil. Moreover, leafy vegetable soil exhibited a more complex and stable co-occurrence network in comparison to melon and fruit vegetable soil. CONCLUSION: The findings enhance our understanding of how cultivated soil bacteria and fungi respond to human disturbance, thereby providing a valuable theoretical basis for soil health in degraded karst areas of southwest China.

Unraveling the Mechanism of StWRKY6 in Potato (Solanum tuberosum)'s Cadmium Tolerance for Ensuring Food Safety.

The WRKY transcription factor plays a crucial role in plant stress adaptation. Our research has found that WRKY6 in Solanum tuberosum (potatoes) is closely related to cadmium (Cd) tolerance. Therefore, investigating the mechanism of StWRKY6 in plant resistance to Cd toxicity is of great scientific importance for food safety. This research further analyzed the gene structure and functional regions of the nuclear transcription factor WRKY6 in potatoes, discovering that StWRKY6 contains W box, GB/box, ABRE, and other elements that can act as a nuclear transcription regulatory factor to execute multiple functional regulations. The results of the heterologous expression of StWRKY6 in Arabidopsis under Cd stress showed that the overexpression line (StWRKY6-OE) had significantly higher SAPD values and content of reactive oxygen species scavenging enzymes than the wild type, indicating that StWRKY6 plays a crucial role in protecting the photosynthetic system and promoting carbohydrate synthesis. Transcriptome analysis also revealed that the Cd-induced expression of StWRKY6 up-regulated many potential gene targets, including APR2, DFRA, ABCG1, VSP2, ERF013, SAUR64/67, and BBX20, which are involved in Cd chelation (APR2, DFRA), plant defense (VSP2, PDF1.4), toxic substance efflux (ABCG1), light morphology development (BBX20), and auxin signal (SAUR64/67). These genes coordinate the regulation of Cd tolerance in the StWRKY6 overexpression line. In summary, this study identified a potential gene set of the co-expression module of StWRKY6, providing useful evidence for the remediation of Cd-contaminated soil and the genetic breeding of low Cd-accumulating crops, thereby ensuring food safety.

Fis1 phosphorylation by Met promotes mitochondrial fission and hepatocellular carcinoma metastasis.

Met tyrosine kinase, a receptor for a hepatocyte growth factor (HGF), plays a critical role in tumor growth, metastasis, and drug resistance. Mitochondria are highly dynamic and undergo fission and fusion to maintain a functional mitochondrial network. Dysregulated mitochondrial dynamics are responsible for the progression and metastasis of many cancers. Here, using structured illumination microscopy (SIM) and high spatial and temporal resolution live cell imaging, we identified mitochondrial trafficking of receptor tyrosine kinase Met. The contacts between activated Met kinase and mitochondria formed dramatically, and an intact HGF/Met axis was necessary for dysregulated mitochondrial fission and cancer cell movements. Mechanically, we found that Met directly phosphorylated outer mitochondrial membrane protein Fis1 at Tyr38 (Fis1 pY38). Fis1 pY38 promoted mitochondrial fission by recruiting the mitochondrial fission GTPase dynamin-related protein-1 (Drp1) to mitochondria. Fragmented mitochondria fueled actin filament remodeling and lamellipodia or invadopodia formation to facilitate cell metastasis in hepatocellular carcinoma (HCC) cells both in vitro and in vivo. These findings reveal a novel and noncanonical pathway of Met receptor tyrosine kinase in the regulation of mitochondrial activities, which may provide a therapeutic target for metastatic HCC.

AKT-mediated regulation of chromatin ubiquitylation and tumorigenesis through Mel18 phosphorylation.

Polycomb repressor complex 1 (PRC1) is linked to the regulation of gene expression and histone ubiquitylation conformation, which contributes to carcinogenesis. However, the upstream regulators of PRC1 biogenesis machinery remain obscure. Here, we report that the polycomb group-related mammalian gene Mel18 is a target of the protein kinase AKT. AKT phosphorylates Mel18 at T334 to disrupt the interaction between Mel18 and other PRC1 members, leading to attenuated PRC1-dependent ubiquitylation of histone H2A at Lys119. As such, PRC1 target genes, many of which are known oncogenes, are derepressed upon T334-Mel18 phosphorylation, which promotes malignant behaviours, including cell proliferation, tumour formation, migration and invasion, bone and brain metastatic lesion formation. Notably, a positive correlation between AKT activity and pT334-Mel18 is observed, and prognostic models based on p-AKT and pT334-Mel18 that predicted overall survival and distant metastasis-free survival in breast cancer patients are established. These findings have implications for understanding the role of AKT and its associated proteins in chromatin ubiquitylation, and also indicate the AKT-Mel18-H2AK119ub axis as a novel prognostic biomarker and therapeutic target for cancer patients.

Coupling Effect of Molecular Chain Displacement and Carrier Trap Characteristics on DC Breakdown of HDPE/LDPE Blend Insulation.

This work focuses on the coupling effect of molecular chain displacement and trap characteristics on direct current (DC) breakdown properties of high density/low density polyethylene (HDPE/LDPE) blend insulation. Frequency domain spectroscopy (FDS) and isothermal discharge current (IDC) are used to characterize the dielectric relaxation and trap characteristics of HDPE/LDPE blends. A DC breakdown model is proposed to reveal the mechanisms of the molecular chain displacement and carrier trap on the DC breakdown strength. The dielectric relaxation α and δ present segmental motions and thermal ion polarization behaviours of HDPE/LDPE blends, respectively. α dielectric relaxation strength ( Δεα) increases as the amount of HDPE increases from 0 to 5 wt%, and then declines with a further increase of HDPE content to 20 wt%. According to the velocity equation, the increase of Δεα will increase the molecular chain displacement, resulting in a larger free volume, which will provide electrons with larger free path λ to form hot electrons. A positive correlation exists between the activation energy of the dielectric relaxation process δ and trap density, and the increase of δ dielectric relaxation strength (Δεδ) will adversely affect the breakdown strength of the specimen. HDPE/LDPE blends with 15 wt% HDPE content have lower Δεα and lowest Δεδ, which decreases the mean free path λ of molecular chain and thermal ion polarization. At the same time, it has the highest deep trap density, thus increasing the probability of hot electrons being captured and improving the DC breakdown strength. It is concluded the breakdown of the dielectric is synergistically affected by the molecular chain displacement and carrier trap.

Polo-Like Kinase 1 phosphorylates and stabilizes KLF4 to promote tumorigenesis in nasopharyngeal carcinoma.

Rationale: Advanced nasopharyngeal carcinoma (NPC) is an aggressive disease with no targeted therapies and poor outcomes. New innovative targets are urgently needed. KLF4 has been extensively studied in the context of tumors, and current data suggest that it can act as either a tissue-specific tumor-inhibiting or a tumor-promoting gene. Here, we found that KLF4 played as a tumor-promoting gene in NPC, and could be mediated by PLK1. Methods: Tissue immunohistochemistry (IHC) assay was performed to identify the role of KLF4 in NPC. Global gene expression experiments were performed to explore the molecular mechanisms underlying KLF4-dependent tumorigenesis. Small-molecule kinase inhibitor screening was performed to identify potential upstream kinases of KLF4. The pharmacologic activity of polo-like kinase inhibitor volasertib (BI6727) in vitro and in vivo was determined. Result: Our investigation showed that high expression of KLF4 was correlated with poor prognosis in NPC. Moreover, genome-wide profiling revealed that KLF4 directly activated oncogenic programmes, including gene sets associated with KRAS, VEGF, and MYC signalling. We further found that inhibition of polo-like kinase 1 could downregulate the expression of KLF4 and that PLK1 directly phosphorylated KLF4 at Ser234. Notably, phosphorylation of KLF4 by PLK1 caused the recruitment and binding of the E3 ligase TRAF6, which resulted in KLF4 K32 K63-linked ubiquitination and stabilization. Moreover, KLF4 could enhance TRAF6 expression at the transcriptional level, thus initiating a KLF4-TRAF6 feed-forward loop. Treatment with the PLK1 inhibitor volasertib (BI6727) significantly inhibited tumor growth in nude mice. Conclusion: Our study unveiled a new PLK1-TRAF6-KLF4 feed-forward loop. The resulting increase in KLF4 ubiquitination leads to stabilization and upregulation of KLF4, which leads to tumorigenesis in NPC. These results expand our understanding of the role of KLF4 in NPC and validate PLK1 inhibitors as potential therapeutic agents for NPC, especially cancer patients with KLF4 overexpression.

Astaxanthin acts via LRP-1 to inhibit inflammation and reverse lipopolysaccharide-induced M1/M2 polarization of microglial cells.

Microglia become activated during neuroinflammation and produce neurotoxic and neurotrophic factors, depending on whether they acquire M1 proinflammatory or M2 anti-inflammatory phenotypes. Astaxanthin (ATX), a natural carotenoid, has anti-inflammatory and neuroprotective effects. We investigated whether ATX could reverse M1/M2 polarization and suppress neuroinflammation via low-density lipoprotein receptor-related protein-1 (LRP-1). We observed increased expression of M1 (TNF-α, IL-1ß, and CD86) and decreased expression of M2 (Arg-1, IL-10, and CD206) markers in BV2 microglial cells stimulated with lipopolysaccharide (LPS). These alterations were reversed by pretreating the cells with ATX. Activation of the NF-κB and JNK pathways was observed upon LPS stimulation, which was reversed by ATX. ATX-induced M2 polarization was attenuated by inhibition of NF-κB and JNK. Pretreatment of LPS-stimulated BV2 cells with ATX resulted in increased LRP-1 expression. The addition of receptor-associated protein, an LRP-1 antagonist, ameliorated ATX-induced inactivation of NF-κB and JNK signaling, and M2 polarization. ATX promotes M2 polarization to suppress neuroinflammation via LRP-1 by inhibiting NF-κB and JNK signaling. This novel mechanism may suppress neuroinflammation in diseases such as Alzheimer's disease.