ADAR promotes USP38 auto-deubiquitylation and stabilization in an RNA editing-independent manner in esophageal squamous cell carcinoma.

Esophageal cancer is mainly divided into esophageal adenocarcinoma and esophageal squamous cell carcinoma (ESCC). China is one of the high-incidence areas of esophageal cancer, of which about 90% are ESCC. The deubiquitinase USP38 has been reported to play significant roles in several biological processes, including inflammatory responses, antiviral infection, cell proliferation, migration, invasion, DNA damage repair, and chemotherapy resistance. However, the role and mechanisms of USP38 in ESCC development remain still unclear. Furthermore, although many substrates of USP38 have been identified, few upstream regulatory factors of USP38 have been identified. In this study, we found that USP38 was significantly upregulated in esophageal cancer tissues. Knockdown of USP38 inhibited ESCC growth. USP38 stabilized itself through auto-deubiquitylation. In addition, we demonstrate that adenosine deaminase acting on RNA (ADAR) could enhance the stability of USP38 protein and facilitate USP38 auto-deubiquitylation by interacting with USP38 in an RNA editing-independent manner. ADAR inhibition of ESCC cell proliferation depended on USP38. In summary, these results highlight that the potential of targeting the ADAR-USP38 axis for ESCC treatment.

The roles of cell wall polysaccharides in response to waterlogging stress in Brassica napus L. root.

BACKGROUND: Brassica napus L. (B. napus) is susceptible to waterlogging stress during different cultivation periods. Therefore, it is crucial to enhance the resistance to waterlogging stress to achieve a high and stable yield of B. napus. RESULTS: Here we observed significant differences in the responses of two B. napus varieties in root under waterlogging stress. The sensitive variety (23651) exhibited a more pronounced and rapid reduction in cell wall thickness and root integrity compared with the tolerant variety (Santana) under waterlogging stress. By module clustering analysis based on transcriptome data, we identified that cell wall polysaccharide metabolism responded to waterlogging stress in root. It was found that pectin content was significantly reduced in the sensitive variety compared with the tolerant variety. Furthermore, transcriptome analysis revealed that the expression of two homologous genes encoding polygalacturonase-inhibiting protein 2 (PGIP2), involved in polysaccharide metabolic pathways, was highly upregulated in root of the tolerant variety under waterlogging stress. BnaPGIP2s probably confer waterlogging resistance by inhibiting the activity of polygalacturonases (PGs), which in turn reduces the degradation of the pectin backbone polygalacturonic acid. CONCLUSIONS: Our findings demonstrate that cell wall polysaccharides in root plays a vital role in response to the waterlogging stress and provide a theoretical foundation for breeding waterlogging resistance in B. napus varieties.

BMP1 Promotes Keloid by Inducing Fibroblast Inflammation and Fibrogenesis.

Keloid is a typical fibrotic and inflammatory skin disease with unclear mechanisms and few therapeutic targets. In this study, we found that BMP1 was significantly increased in a collagen high-expressing subtype of fibroblast by reanalyzing a public single-cell RNA-sequence data set of keloid. The number of BMP1-positive fibroblast cells was increased in keloid fibrotic loci. Increased levels of BMP1 were further validated in the skin tissues and fibroblasts from keloid patients. Additionally, a positive correlation between BMP1 and the Keloid Area and Severity Index was found in keloid patients. In vitro analysis revealed collagen production, the phosphorylation levels of p65, and the IL-1ß secretion decreased in BMP1 interfered keloid fibroblasts. Besides, the knockdown of BMP1 inhibited the growth and migration of keloid fibroblast cells. Mechanistically, BMP1 inhibition downregulated the noncanonical TGF-ß pathways, including p-p38 and p-ERK1/2 signaling. Furthermore, we found the delivery of BMP1 siRNAs could significantly alleviate keloid in human keloid-bearing nude mice. Collectively, our results indicated that BMP1 exhibited various pathogenic effects on keloids as promoting cell proliferation, migration, inflammation, and ECM deposition of fibroblast cells by regulating the noncanonical TGF-ß/p38 MAPK, and TGF-ß/ERK pathways. BMP1-lowing strategies may appear as a potential new therapeutic target for keloid.

Selection and Validation of Reliable Reference Genes for Liquidambar formosana Leaves with Different Leaf Colors.

Liquidambar formosana Hance is renowned for its rich leaf color and possesses notable advantages, such as robust adaptability, strong resistance to diseases and pests, and rapid growth, making it a preferred choice for urban greening and carbon sequestration forest initiatives. The completion of whole-genome sequencing of L. formosana has spurred an increased interest in exploring the molecular mechanisms underlying seasonal changes in leaf color, marking a significant focus in L. formosana breeding research. However, there is currently a lack of stable reference genes suitable for analyzing the expression patterns of functional genes in L. formosana exhibiting varying leaf colors. This study selected five L. formosana varieties with significant differences in leaf colors. Through the RT-qPCR analysis, and evaluation using BestKeeper, geNorm, NormFinder, Delta Ct, and RefFinder, the expression stability of 14 candidate reference genes was examined. Consequently, two reference genes (LifEF1-α and LifACT) with stable expression, suitable for RT-qPCR of L. formosana with diverse leaf colors, were identified. The stability of these selected reference genes was further validated by examining the LifbHLH137 gene, which promoted the biosynthesis of anthocyanins. This advancement facilitated molecular biology and genetic breeding investigations of L. formosana, providing essential data for the precise quantification of functional genes associated with leaf color variation.

Novel PLEC variants associated with infantile cholestasis.

Plectin is a cytoskeletal linker of intermediate filaments, encoded by the PLEC gene. Recently, plectin mutations have been identified in a pair of siblings with progressive familial intrahepatic cholestasis. Here, we reported two unrelated infants with plectinopathy causing cholestatic jaundice with novel variants in the PLEC gene. Trio exome sequencing identified compound heterozygous variants in the PLEC gene for each patient: c.71-11768C>T and c.4331G>T (p.Arg1444Leu) in Patient 1, and c.592C>T (p.Arg198Trp) and c.4322G>A (p.Arg1441His) in Patient 2. Immunofluorescence staining of liver samples from both patients revealed scattered signals of plectin in the cytoplasm of hepatocytes and reduced colocalization of plectin and cytokeratin 8. This study not only underscores the involvement of plectin in cholestasis but also highlights the utility of exome sequencing as a powerful diagnostic tool in identifying genetic underpinnings of infantile cholestasis.

The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases.

Pulmonary fibrosis (PF) is a severe pulmonary disease with limited available therapeutic choices. Recent evidence increasingly points to abnormal lipid metabolism as a critical factor in PF pathogenesis. Our latest research identifies the dysregulation of low-density lipoprotein (LDL) is a new risk factor for PF, contributing to alveolar epithelial and endothelial cell damage, and fibroblast activation. In this study, we first integrative summarize the published literature about lipid metabolite changes found in PF, including phospholipids, glycolipids, steroids, fatty acids, triglycerides, and lipoproteins. We then reanalyze two single-cell RNA-sequencing (scRNA-seq) datasets of PF, and the corresponding lipid metabolomic genes responsible for these lipids' biosynthesis, catabolism, transport, and modification processes are uncovered. Intriguingly, we found that macrophage is the most active cell type in lipid metabolism, with almost all lipid metabolic genes being altered in macrophages of PF. In type 2 alveolar epithelial cells, lipid metabolic differentially expressed genes (DEGs) are primarily associated with the cytidine diphosphate diacylglycerol pathway, cholesterol metabolism, and triglyceride synthesis. Endothelial cells are partly responsible for sphingomyelin, phosphatidylcholine, and phosphatidylethanolamines reprogramming as their metabolic genes are dysregulated in PF. Fibroblasts may contribute to abnormal cholesterol, phosphatidylcholine, and phosphatidylethanolamine metabolism in PF. Therefore, the reprogrammed lipid profiles in PF may be attributed to the aberrant expression of lipid metabolic genes in different cell types. Taken together, these insights underscore the potential of targeting lipid metabolism in developing innovative therapeutic strategies, potentially leading to extended overall survival in individuals affected by PF.

Correlation between the Systemic Immunoinflammatory Index and Platelet-Lymphocyte Ratio in Patients with Adenomyosis.

Background: The chronic inflammatory immune response is a significant factor in the pathogenesis of benign gynecological diseases. The systemic immunoinflammatory index (SII) and the platelet-to-lymphocyte ratio (PLR) are commonly available biomarkers of inflammation. However, evidence of the relationship between SII and PLR in patients with adenomyosis is limited. This study aimed to investigate the relationship between SII and PLR in patients with adenomyosis. Methods: This cross-sectional study included 483 patients with adenomyosis who were first diagnosed at our institution between January 2019 and December 2021. Basic patient clinical information and inflammatory factors were collected for univariate analysis, smoothed curve fitting, and multivariate segmented linear regression. Results: The results of the univariate analysis showed a significant positive correlation between PLR levels and SII (P < 0.001). In addition, a nonlinear relationship between PLR and SII was tested using a smoothed curve fit after adjusting for potential confounders. Multiple segmented linear regression models showed a significant relationship between SII and PLR in both SII < 1,326.47 (ß 0.14, 95% CI: 0.12, 0.16; P < 0.0001) and >1,326.47 (ß 0.02, 95% CI: -0.01, 0.05; P = 0.2461). Conclusions: In conclusion, this study showed a nonlinear relationship between SII and PLR in patients with uterine adenomyosis. An increase in serum PLR levels correlates with an increase in SII before SII levels reach an inflection point.

Molecular Mechanisms Underlying the Anticancer Properties of Pitavastatin against Cervical Cancer Cells.

Cervical cancer ranks as the fourth most prevalent form of cancer and is a significant contributor to female mortality on a global scale. Pitavastatin is an anti-hyperlipidemic medication and has been demonstrated to exert anticancer and anti-inflammatory effects. Thus, the purpose of this study was to evaluate the anticancer effect of pitavastatin on cervical cancer and the underlying molecular mechanisms involved. The results showed that pitavastatin significantly inhibited cell viability by targeting cell-cycle arrest and apoptosis in Ca Ski, HeLa and C-33 A cells. Pitavastatin caused sub-G1- and G0/G1-phase arrest in Ca Ski and HeLa cells and sub-G1- and G2/M-phase arrest in C-33 A cells. Moreover, pitavastatin induced apoptosis via the activation of poly-ADP-ribose polymerase (PARP), Bax and cleaved caspase 3; inactivated the expression of Bcl-2; and increased mitochondrial membrane depolarization. Furthermore, pitavastatin induced apoptosis and slowed the migration of all three cervical cell lines, mediated by the PI3K/AKT and MAPK (JNK, p38 and ERK1/2) pathways. Pitavastatin markedly inhibited tumor growth in vivo in a cancer cell-originated xenograft mouse model. Overall, our results identified pitavastatin as an anticancer agent for cervical cancer, which might be expanded to clinical use in the future.

Hesperetin Induces Autophagy and Delayed Apoptosis by Modulating the AMPK/Akt/mTOR Pathway in Human Leukemia Cells In Vitro.

BACKGROUND: Hesperetin has been reported to have anticancer properties. However, the molecular mechanisms underlying its action on leukemia cells remain unclear. This in vitro study evaluated the possible mechanisms of hesperetin in leukemia cells (HL-60 and U937). METHODS: Cell viability was evaluated using a cell counting kit-8 (CCK-8) assay. Apoptosis and autophagy assays were conducted through annexin V/PI staining and acidic vesicular organelle (AVO) staining. Cell cycle analysis was conducted through propidium iodide (PI) and flow cytometry. The expression of proteins related to apoptosis and autophagy, including cleaved-PARP-1, Bcl-2, Bax, LC3-I/II, Beclin-1, Atg5, p62, phospho-AMPK, AMPK, phospho-mTOR, mTOR, phospho-Akt, and Akt, in human leukemia cells were evaluated using Western blotting. RESULTS: Hesperetin dose-dependently inhibited leukemia cell viability. However, we found a low degree of apoptosis and cell cycle arrest induced by hesperetin in U937 cells. These findings imply the presence of additional mechanisms modulating hesperetin-induced cell death. Next, we evaluated autophagy, the possible mechanism modulating cell death or survival, to clarify the underlying mechanism of hesperetin-induced cell death. Hesperetin also dose-dependently increased the ratio of LC3II/I, Atg5, and Beclin 1 and decreased p62. Moreover, 3-methyladenine (3-MA) and bafilomycin A1 (Baf-A1) inhibited hesperetin-induced autophagy. We suggest that hesperetin can protect cancer cells during the transient period and may extend survival. Furthermore, a decrease in p-mTOR and p-Akt expression and an increase in p-AMPK expression were observed. Collectively, these findings suggest that hesperetin induces autophagy by modulating the AMPK/Akt/mTOR pathway. CONCLUSION: Hesperetin promoted cell death in the human leukemic cell line U937 by inducing a low degree of slight apoptosis, cell cycle arrest, and autophagy. It is therefore a potential adjuvant to antileukemia therapy and may be combined with other chemotherapeutic drugs to reduce chemoresistance and side effects.

Comparative genomics of the medicinal plants Lonicera macranthoides and L. japonica provides insight into genus genome evolution and hederagenin-based saponin biosynthesis.

Lonicera macranthoides (LM) and L. japonica (LJ) are medicinal plants widely used in treating viral diseases, such as COVID-19. Although the two species are morphologically similar, their secondary metabolite profiles are significantly different. Here, metabolomics analysis showed that LM contained ~86.01 mg/g hederagenin-based saponins, 2000-fold higher than LJ. To gain molecular insights into its secondary metabolite production, a chromosome-level genome of LM was constructed, comprising 9 pseudo-chromosomes with 40 097 protein-encoding genes. Genome evolution analysis showed that LM and LJ were diverged 1.30-2.27 million years ago (MYA). The two plant species experienced a common whole-genome duplication event that occurred ∼53.9-55.2 MYA before speciation. Genes involved in hederagenin-based saponin biosynthesis were arranged in clusters on the chromosomes of LM and they were more highly expressed in LM than in LJ. Among them, oleanolic acid synthase (OAS) and UDP-glycosyltransferase 73 (UGT73) families were much more highly expressed in LM than in LJ. Specifically, LmOAS1 was identified to effectively catalyse the C-28 oxidation of ß-Amyrin to form oleanolic acid, the precursor of hederagenin-based saponin. LmUGT73P1 was identified to catalyse cauloside A to produce α-hederin. We further identified the key amino acid residues of LmOAS1 and LmUGT73P1 for their enzymatic activities. Additionally, comparing with collinear genes in LJ, LmOAS1 and LmUGT73P1 had an interesting phenomenon of 'neighbourhood replication' in LM genome. Collectively, the genomic resource and candidate genes reported here set the foundation to fully reveal the genome evolution of the Lonicera genus and hederagenin-based saponin biosynthetic pathway.

Adenosine receptor A1 enhanced mitochondrial biogenesis and exerted neuroprotection after cerebral ischemia through PGC-1α.

Ischemic stroke is a common cause of morbidity and mortality worldwide. The current treatment fails to achieve satisfactory results, because interventional therapy as first-line treatment management has a strict time window. In recent years, a large number of studies have confirmed that adenosine, as an inhibitory neurotransmitter, has a protective effect on cerebral ischemic injury. Nevertheless, direct administration of adenosine has many side effects. Previous studies showed that adenosine exerted neuroprotective effects mainly through adenosine receptor A1 (A1 receptor). Therefore, further study on the mechanism of A 1 receptor induced neuroprotection may find new targets for stroke treament. Mitochondrial biogenesis (MB) is a therapeutic target for ischemic stroke, and the nuclear-encoded peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) is a major regulator of MB. However, the influence of A1 receptor on MB and PGC-1α is unclear. In this study, using the middle cerebral artery occlusion (MCAO) model of mice, we evaluated the temporal and spatial effects of A1 receptor after ischemic stroke and verified the neuroprotection of A1 receptor. Neurological scores were used to assess functional changes in mice. At the same time, we observed the effect of activating A1 receptor on MB and PGC-1α, and the effect of knockdown PGC-1α on A1 receptor induced MB in vitro. WB and immunofluorescence were used to detect relevant indicators of MB. In addition, we downregulated PGC-1α in vivo to observe the effects on A1 receptor induced MB and neuroprotection. The findings indicated that A1 receptor was increased and mainly expressed on neurons in the penumbra, further activated A1 receptor after stroke had neuroprotection. In vitro, activation of A1 promotes MB and increases the expression level of PGC-1α, while downregulation of PGC-1α partially reverses the effect of A1 receptor after OGD/R. Down regulation of PGC-1α in the penumbra neurons can reverse the effects of activation of A1 receptor on MB and neuroprotection. Taken together, these findings indicated that A1receptor promotes MB and improves neurological function after ischemic stroke via PGC-1α.

Knockdown of LIMD2 inhibits the progression of ovarian carcinoma through ERK1/2 pathway.

BACKGROUND: The incidence rate of ovarian carcinoma (OC) is the third of the female reproductive system malignant tumors, while its mortality rate ranks first among causes of female reproductive system tumor related death in the world. METHODS: In the present research, we investigated the specific role of LIMD2 through LIMD2 knockdown in OC cells. RESULTS: The results of online analysis and expression detection proved that LIMD2 was up-regulated in human OC tissues and cells. Knockdown of LIMD2 inhibited the proliferation, migration and invasion in OC cells. LIMD2 knockdown promoted the apoptosis, as well as the expression of Cleaved-Caspase3 and Bax. Importantly, knockdown of LIMD2 promotes cell autophagy. LC3-II/I ratio and Beclin1 expression increased in LIMD2 knockdown cells, while P62 expression declined in LIMD2 knockdown cells. Additionally, the phosphorylation of ERK1/2 was inhibited by the knockdown of LIMD2 in SKOV3 and OVCAR3 cells. CONCLUSION: Knockdown of LIMD2 inhibits cell proliferation, migration, invasion and autophagy, and promotes the apoptosis through the ERK1/2 signaling pathway, suggesting that LIMD2-siRNA may be an effective molecule to prevent OC progression.

Research Progress of MicroRNAs in Spinal Cord Injury.

Spinal cord injury is a serious and devastating condition. Recently, research into microRNAs (miRNAs) has become increasingly exhaustive and it has been determined that they are closely related to the pathophysiological processes of spinal cord injury. They participate in the regulation of the inflammatory response of spinal cord injury, the death of neuronal cells, and the repair of neural functions, which are related to the recovery of spinal cord injury. This review focuses on the relationship between miRNA and spinal cord injury, lists miRNA-324-5p, miRNA-221 and miRNA-124, which are helpful for the repair of spinal cord injury, and finally summarizes the current research progress of miRNA-based therapies, so as to provide a foundational reference for clinical and scientific researchers.

Effects of secondary release of chromium and vanadium on soil properties, nutrient cycling and bacterial communities in contaminated acidic paddy soil.

Although the contamination situation of chromium (Cr) and vanadium (V) have been revealed, the effects of their re-release on ecological risk in contaminated acidic paddy soil are unclear. To evaluate the effects, we assigned soil microcosms across three different concentration (100, 200, 300 mg/L) and introduced Cr and V alone or combination into an already slightly contaminated acidic soil. We found that Cr and V alone or interacted to increased soil bioavailable-metals, changed soil properties and nutrients to varying degrees. Meanwhile, soil ammoniacal nitrogen (NH4+-N) and nitrate nitrogen (NO3--N) contents, nitrogen (N) -cycling enzyme activities, microbial mass N were significantly influenced by Cr addition. Which demonstrated that Cr re-release may disturb soil N cycle. However, V alone significantly improved soil NO3--N contents, cellulase and dehydrogenase activities, soil respiration intensity and microbial mass carbon: nitrogen. Meanwhile, V addition also decreased bacterial diversity while Cr addition increased bacterial diversity and shaped new bacterial community, some V(V) and Cr (VI) reducing bacteria were identified. Heatmap of Pearson correlation and Redundancy analysis showed that NH4+-N, NO3--N, Potassium, Phosphorus, and Cr played an important role in bacterial community structure. These findings suggested that re-release of Cr and V disturbed soil function and raised ecological risks, and the power to destroy the ecosystem stability originated from Cr was much stronger than V. This study was contributed to understand the effects of Cr and V re-release on microecology in contaminated acidic agricultural soil.

ESIPT-Inspired Dual-Mode Photoswitches with Fast Molecular Isomerization in the Solid State.

Photoswitchable materials have attracted considerable attention in various fields. Developing excellent solid-state dual-mode photoswitches is an important but challenging task. Herein, we propose a new strategy to construct an excited-state intramolecular proton transfer (ESIPT) inspired photoswitch (DiAH-pht) that possesses aggregation-induced emission (AIE) features and displays a fast molecular isomerization process characterized by dual-mode behavior in the solid state. Mechanistic studies indicate that introduction of a bulky group can create a folded molecular conformation that provides adequate volume to facilitate photoisomerization and the enhanced ESIPT effect can boost the isomerization process. The feasibility of our strategy was further demonstrated by the activated photoisomerization performance of the Schiff base derivatives. Furthermore, DiAH-pht shows good performance in the fields of dual-mode information encryption and high-density data storage.

Janus-Type ESIPT Chromophores with Distinctive Intramolecular Hydrogen-bonding Selectivity.

Excited-state intramolecular proton transfer (ESIPT)-based solid luminescent materials with multiple hydrogen bond acceptors (HBAs) remain unexplored. Herein, we introduced a family of Janus-type ESIPT chromophores featuring distinctive hydrogen bond (H-bond) selectivity between competitive HBAs in a single molecule. Our investigations showed that the central hydroxyl group preferentially forms intramolecular H-bonds with imines in imine-modified 2-hydroxyphenyl benzothiazole (HBT) chromophores but tethers the benzothiazole moiety in hydrazone-modified HBT chromophores. Imine-derived HBTs generally exhibit higher fluorescence efficiency, while hydrazone-derived HBTs show a reduced overlap between the absorption and fluorescence bands. Quantum chemical calculations unveiled the molecular origins of the biased intramolecular H-bonds and their impact on the ESIPT process. This Janus-type ESIPT chromophore skeleton provides new opportunities for the design of solid luminescent materials.

High-throughput unmanned aerial vehicle-based phenotyping provides insights into the dynamic process and genetic basis of rapeseed waterlogging response in the field.

Waterlogging severely affects the growth, development, and yield of crops. Accurate high-throughput phenotyping is important for exploring the dynamic crop waterlogging response in the field, and the genetic basis of waterlogging tolerance. In this study, a multi-model remote sensing phenotyping platform based on an unmanned aerial vehicle (UAV) was used to assess the genetic response of rapeseed (Brassica napus) to waterlogging, by measuring morphological traits and spectral indices over 2 years. The dynamic responses of the morphological and spectral traits indicated that the rapeseed waterlogging response was severe before the middle stage within 18 d after recovery, but it subsequently decreased partly. Genome-wide association studies identified 289 and 333 loci associated with waterlogging tolerance in 2 years. Next, 25 loci with at least nine associations with waterlogging-related traits were defined as highly reliable loci, and 13 loci were simultaneously identified by waterlogging tolerance coefficients of morphological traits, spectral indices, and common factors. Forty candidate genes were predicted in the regions of 13 overlapping loci. Our study provides insights into the understanding of the dynamic process and genetic basis of rapeseed waterlogging response in the field by a high-throughput UAV phenotyping platform. The highly reliable loci identified in this study are valuable for breeding waterlogging-tolerant rapeseed cultivars.

Hepatitis B virus X gene impacts on the innate immunity and immune-tolerant phase in chronic hepatitis B virus infection.

BACKGROUND AND AIMS: The immunologic features involved in the immune-tolerant phase of chronic hepatitis B (CHB) virus (HBV) infection are unclear. The hepatitis B virus X (HBx) protein disrupts IFN-ß induction by downregulating MAVS and may destroy subsequent HBV-specific adaptive immunity. We aimed to analyse the impacts of genetic variability of HBx in CHB patients on the immune-tolerant phase during long-term follow-up. METHODS: Children with CHB in the immune-tolerant phase were recruited and followed longitudinally. HBx gene sequencing of infecting HBV strains was performed, and the effects of HBx mutations on the immune-tolerant phase were assessed. Restoration of the host immune response to end the immune-tolerant phase was investigated by immunoblotting, immunostaining, ELISA and reporter assays of MAVS/IFN-ß signalling in liver cell lines, patient liver tissues and the HBV plasmid replication system. RESULTS: A total of 173 children (median age, 6.92 years) were recruited. Patients carrying HBx R87G, I127V and R87G + I127V double mutations exhibited higher cumulative incidences of immune-tolerant phase breakthrough (p = .011, p = .006 and p = .017 respectively). Cells transfected with HBx R87G and I127V mutants and pHBV1.3-B6.3 replicons containing the HBx R87G and I127V mutations exhibited statistically increased levels of IFN-ß, especially under poly(I:C) stimulation or Flag-MAVS cotransfection. HA-HBx wild-type interacted with Flag-MAVS and enhanced its ubiquitination, but this ability was diminished in the R87G and I127V mutants. CONCLUSIONS: HBx suppresses IFN-ß induction. R87G and I127V mutation restored IFN-ß production by preventing MAVS degradation, contributing to curtailing the HBV immune-tolerant phase in CHB patients.

Efficiency of heterogeneous chelating agents on the phytoremediation potential and growth of Sasa argenteostriata (Regel) E.G. Camus on Pb-contaminated soil.

Ethylenediaminetetraacetic acid (EDTA) is one of the most effective chelating agents for enhancing lead (Pb) accumulation in various plant organs. However, it has a higher risk of causing secondary pollution than other chelating agents. To reduce such environmental risks and increase remediation efficiency, EDTA can be combined with degradable chelating agents for use in phytoremediation, but there are few reports on the combination of EDTA and nitrilotriacetic acid (NTA). This study evaluated the effects of combined EDTA and NTA application at different concentrations (900, 1200, or 1500 mg/kg) and with different methods (1 application or 3 applications) on dwarf bamboo (Sasa argenteostriata (Regel) E.G. Camus) growth and phytoremediation efficiency and on the soil environment in pot experiments with Pb-contaminated soil. Applying EDTA and NTA together resulted in lower soil water-soluble Pb concentrations than applying EDTA alone and therefore resulted in lower environmental risk. The increased availability of soil Pb produced a stress response in the dwarf bamboo plants, which increased their biomass significantly. Moreover, under the chelating treatments, the soil Pb availability increased, which promoted Pb translocation in plants. The Pb content in the aerial parts of the dwarf bamboo increased significantly in all treatments (translocation factors increased by 300~1500% compared with that in CK). The Pb content increase in the aerial parts caused high proline accumulation in dwarf bamboo leaves, to alleviate Pb toxicity. Maximum Pb accumulation was observed in the EN1500 treatment, which was significantly higher than that in the other treatments except the EN900 treatment. This study elucidates the choice of remediation techniques and the physiological characteristics of the plants used in such studies. In conclusion, the EN900 treatment resulted in the lowest environmental risk, greatest biomass production, and highest phytoremediation efficiency of all treatments, indicating that it has great potential for application in phytoremediation with dwarf bamboo in Pb-contaminated soil.

Analysis of Amino Acids in the Roots of Tamarix ramosissima by Application of Exogenous Potassium (K+) under NaCl Stress.

Soil salinization is one of the main environmental factors affecting plant growth worldwide. Tamarix ramosissima Ledeb. (T. ramosissima) is a halophyte representative that is widely grown in salinized soils. As an important nutrient element for plant growth, K+ plays an important role in improving the tolerance to salt stress, but the mechanism of reducing the damage caused by NaCl stress to T. ramosissima is less reported. Our results show that the proline content and the Log2 fold-change of proline's relative quantification in the roots of T. ramosissima increased over time with the application of exogenous potassium (K+) for 48 h and 168 h under NaCl stress. Moreover, 13 amino-acid-related metabolic pathways were involved in the resistance of T. ramosissima to salt stress. Mainly, the aldehyde dehydrogenase family genes and tryptophan-synthase-related genes were found at 48 h and 168 h with exogenous potassium applied to the roots of T. ramosissima under NaCl stress, and they regulated their related metabolic accumulation in the arginine and proline metabolism pathways, increasing the effectiveness of inducing NaCl tolerance of T. ramosissima. It is noteworthy that alpha-ketobutyric was produced in the roots of T. ramosissima under NaCl stress for 48 h with the application of exogenous potassium, which is one of the most effective mechanisms for inducing salt tolerance in plants. Meanwhile, we found three DEGs regulating alpha-ketobutyric acid. This study provides a scientific theoretical basis for further understanding the molecular mechanism of K+ alleviating the salinity damage to T. ramosissima caused by NaCl.