Search

The bulk properties and chemical reactivity of disordered Pt-Ni alloys in the A1 (fcc) structure are investigated using different methods: Virtual Crystal Approximation (VCA), Korringa–Kohn–Rostoker Coherent Potential Approximation (KKR-CPA), and large explicit supercells generated using Super-Cell Random Approximates (SCRAPs). While VCA predicts lattice constants that closely follow Vegard's law, the large supercells and KKR-CPA predict lattice constants that are consistently larger than Vegard's law. KKR-CPA results closely agree with those from the large supercells for the disordered alloys, producing similar projected density of states and magnetic moment across the composition range. For instance, while VCA predicts the disordered alloys to be non-magnetic at a Pt concentration (xPt) ≥ 0.5, KKR-CPA and SCRAPs predict the disordered alloys to remain ferromagnetic to higher Pt concentrations. As xPt decreases, the adsorption of H becomes more exothermic on bulk-terminated (111) surfaces but less exothermic on Pt monolayer-terminated (111) surfaces due largely to strain effects. (111) surfaces cut from the large supercells predict average H adsorption energies on the disordered alloys similar to those on the ordered phases of the same compositions, while VCA predicts H adsorption to be more exothermic. [ABSTRACT FROM AUTHOR]

Poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) is a type of polyhydroxyalkanoates (PHA) that exhibits numerous outstanding properties and is naturally synthesized and elaborately regulated in various microorganisms. However, the regulatory mechanism involving the specific regulator PhaR in Haloferax mediterranei, a major PHBV production model among Haloarchaea, is not well understood. In our previous study, we showed that deletion of the phosphoenolpyruvate (PEP) synthetase-like (pps-like) gene activates the cryptic phaC genes in H. mediterranei, resulting in enhanced PHBV accumulation. In this study, we demonstrated the specific function of the PPS-like protein as a negative regulator of phaR gene expression and PHBV synthesis. Chromatin immunoprecipitation (ChIP), in situ fluorescence reporting system, and in vitro electrophoretic mobility shift assay (EMSA) showed that the PPS-like protein can bind to the promoter region of phaRP. Computational modeling revealed a high structural similarity between the rifampin phosphotransferase (RPH) protein and the PPS-like protein, which has a conserved ATP-binding domain, a His domain, and a predicted DNA-binding domain. Key residues within this unique DNA-binding domain were subsequently validated through point mutation and functional evaluations. Based on these findings, we concluded that PPS-like protein, which we now renamed as PspR, has evolved into a repressor capable of regulating the key regulator PhaR, and thereby modulating PHBV synthesis. This regulatory network (PspR-PhaR) for PHA biosynthesis is likely widespread among haloarchaea, providing a novel approach to manipulate haloarchaea as a production platform for high-yielding PHA. Key points: • The repressive mechanism of a novel inhibitor PspR in the PHBV biosynthesis was demonstrated • PspR is widespread among the PHA accumulating haloarchaea • It is the first report of functional conversion from an enzyme to a trans-acting regulator in haloarchaea [ABSTRACT FROM AUTHOR]

Poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) is a type of polyhydroxyalkanoates (PHA) that exhibits numerous outstanding properties and is naturally synthesized and elaborately regulated in various microorganisms. However, the regulatory mechanism involving the specific regulator PhaR in Haloferax mediterranei, a major PHBV production model among Haloarchaea, is not well understood. In our previous study, we showed that deletion of the phosphoenolpyruvate (PEP) synthetase-like (pps-like) gene activates the cryptic phaC genes in H. mediterranei, resulting in enhanced PHBV accumulation. In this study, we demonstrated the specific function of the PPS-like protein as a negative regulator of phaR gene expression and PHBV synthesis. Chromatin immunoprecipitation (ChIP), in situ fluorescence reporting system, and in vitro electrophoretic mobility shift assay (EMSA) showed that the PPS-like protein can bind to the promoter region of phaRP. Computational modeling revealed a high structural similarity between the rifampin phosphotransferase (RPH) protein and the PPS-like protein, which has a conserved ATP-binding domain, a His domain, and a predicted DNA-binding domain. Key residues within this unique DNA-binding domain were subsequently validated through point mutation and functional evaluations. Based on these findings, we concluded that PPS-like protein, which we now renamed as PspR, has evolved into a repressor capable of regulating the key regulator PhaR, and thereby modulating PHBV synthesis. This regulatory network (PspR-PhaR) for PHA biosynthesis is likely widespread among haloarchaea, providing a novel approach to manipulate haloarchaea as a production platform for high-yielding PHA. Key points: • The repressive mechanism of a novel inhibitor PspR in the PHBV biosynthesis was demonstrated • PspR is widespread among the PHA accumulating haloarchaea • It is the first report of functional conversion from an enzyme to a trans-acting regulator in haloarchaea [ABSTRACT FROM AUTHOR]

Microorganisms play an essential role in sulfide removal. Alkaline absorption solution facilitates the sulfide's dissolution and oxidative degradation, so haloalkaliphile is a prospective source for environmental-friendly and cost-effective biodesulfurization. In this research, 484 sulfide oxidation genes were identified from the metagenomes of the soda-saline lakes and a haloalkaliphilic heterotrophic bacterium Halomonas salifodinae IM328 (=CGMCC 22183) was isolated from the same habitat as the host for expression of a representative sequence. The genetic manipulation was successfully achieved through the conjugation transformation method, and sulfide: quinone oxidoreductase gene (sqr) was expressed via pBBR1MCS derivative plasmid. Furthermore, a whole-cell catalyst system was developed by using the engineered strain that exhibited a higher rate of sulfide oxidation under the optimal alkaline pH of 9.0. The whole-cell catalyst could be recycled six times to maintain the sulfide oxidation rates from 41.451 to 80.216 µmol·min−1·g−1 dry cell mass. To summarize, a whole-cell catalyst system based on the engineered haloalkaliphilic bacterium is potentiated to be applied in the sulfide treatment at a reduced cost. [ABSTRACT FROM AUTHOR]

Background: Potential target genes of microRNA (miR)-494 have been reported in many types of cancers. However, the role of miR-494 in esophageal squamous cell carcinoma (ESCC) remains unknown. Aim: This study focused on the expression and biological function of miR-494 in ESCC. Methods: Using bioinformatics analyses, we found that cleft lip and palate transmembrane 1-like (CLPTM1L) was a potential target of miR-494. We performed quantitative real-time (qRT) PCR assays in 37 ESCC tumor tissues to determine the expression of miR-494 and CLPTM1L mRNA, and we analyzed the correlation between both of these factors and clinical characteristics. The cell counting kit-8 and colony formation assays were used to evaluate the effects of miR-494 expression on the proliferation of ESCC cells. The transwell migration assay and flow cytometric apoptosis assay were performed to study the influence of miR-494 on the invasion and apoptosis of ESCC cells. Western blotting, luciferase assays, and CLPTM1L knockdown experiments were used to determine whether CLPTM1L was a target of miR-494. Results: The qRT-PCR assays showed significant downregulation of miR-494 ( P < 0.05) and upregulation of CLPTM1L mRNA ( P < 0.05), both of which were significantly associated with lymph node metastases ( P < 0.05). High expression of miR-494 inhibited cell proliferation and invasion and promoted cell apoptosis ( P < 0.05). The results also showed that CLPTM1L was a target of miR-494. Conclusion: These results show that the expression of miR-494, which can regulate cell growth, invasion and apoptosis of ESCC cells by targeting CLPTM1L, is downregulated in ESCC tumor tissues. The miR-494-CLPTM1L pathway could be further exploited to develop a new approach to treat ESCC. [ABSTRACT FROM AUTHOR]

A novel Gram-stain-negative bacterium, designated as IM2376T, was isolated from the sediment of Hutong Qagan Lake in the Ordos, Inner Mongolia Autonomous Region of China. Phylogenetic analysis based on 16S rRNA gene sequence revealed that the strain IM2376T had the highest similarity with Roseinatronobacter thiooxidans DSM 13087T (96.2%) and Rhodobaca bogoriensis LBB1T (96.2%) of the family Rhodobacteraceae. Genomic relatedness analyses showed that strain IM2376T was clearly distinguished from other species in the family Rhodobacteraceae, with average nucleotide identities, average amino acid identities, and in silico DNA–DNA hybridization values not more than 74.1, 68.5, and 20.2%, respectively. The fatty acids were mainly composed of C18:1ω7c (64.9%), iso-C16:0 (16.3%), and C16: 1ω7c/C16:1ω6c (6.0%). The major polar lipids were diphosphatidylglycerol, phosphatidylglycerol, and phosphatidylcholine. The predominant ubiquinone was Q-10 (94.9%). The genomic DNA G + C content was 66 mol%. Based on all these results, strain IM2376T was considered a novel species of a new genus in the family Rhodobacteraceae, for which the name Rhabdonatronobacter sediminivivens gen. nov., sp. nov. is proposed. The type strain of Rhabdonatronobacter sediminivivens is IM2376T (= CGMCC 1.17852T = KCTC 92134T). [ABSTRACT FROM AUTHOR]

Activation of hypoxia-inducible factor 1α (HIF1α) controls the transcription of genes governing angiogenesis under hypoxic condition during tumorigenesis. Here we show that hypoxia-responsive miR-182 is regulated by HIF1α at transcriptional level. Prolyl hydroxylase domain enzymes (PHD) and factor inhibiting HIF-1 (FIH1), negative regulators of HIF1 signaling, are direct targets of miR-182. Overexpression of miR-182 in prostate cancer cells led to a reduction of PHD2 and FIH1 expression and an increase in HIF1α level either under normoxic or hypoxic condition. Consistently, inhibition of miR-182 could increase PHD2 and FIH1 levels, thereby reducing the hypoxia-induced HIF1α expression. Matrigel plug assay showed that angiogenesis was increased by miR-182 overexpression, and vice versa. miR-182 overexpression in PC-3 prostate cancer xenografts decreased PHD2 and FIH1 expression, elevated HIF1α protein levels, and increased tumor size. Lastly, we revealed that the levels of both miR-182 and HIF1α were elevated, while the expression PHD2 and FIH1 was downregulated in a mouse model of prostate cancer. Together, our results suggest that the interplay between miR-182 and HIF1α could result in a sustained activation of HIF1α pathway, which might facilitate tumor cell adaption to hypoxic stress during prostate tumor progression. [ABSTRACT FROM AUTHOR]