β‐catenin regulates IRF3‐mediated innate immune signalling in colorectal cancer

Objective

β‐catenin is one of the most critical oncogenes associated with many kinds of human cancers, especially in the human CRC. Innate immunity recognizes tumour derived damage‐associated molecular patterns (DAMPs) and primes the anti‐tumour adaptive responses. While the function of β‐catenin in CRC tumourigenesis is well established, its impact on innate immune evasion is largely unknown. The aim of this study is to characterize the role of β‐catenin in inhibiting RIG‐I‐like receptor (RLR)‐mediated IFN‐β signalling in colorectal cancer.

Materials and Methods

Immunohistochemical staining and western blotting were conducted to study the expression of β‐catenin, IRF3 and phospho‐IRF3 (p‐IRF3) in CRC samples and cell lines. Plaque assay determining virus replication was performed to assess the regulation of β‐catenin on IFN‐β signalling. The inhibition of β‐catenin on RLR‐mediated IFN‐β signalling was further studied by real‐time analyses and reporter assays in the context of lentiviral‐mediated β‐catenin stably knocking down. Lastly, co‐immunoprecipitation and nuclear fractionation assay were conducted to monitor the interaction between β‐catenin and IRF3.

Results

We found that high expression of β‐catenin positively correlated with the expression of IRF3 in CRC cells. Overexpression of β‐catenin increased the viral replication. Conversely knocking down of β‐catenin inhibited viral replication. Furthermore, our data demonstrated that β‐catenin could inhibit the expression of IFN‐β and interferon‐stimulated gene 56 (ISG56). Mechanistically, we found that β‐catenin interacted with IRF3 and blocked its nuclear translocation.

Conclusion

Our study reveals an unprecedented role of β‐catenin in enabling innate immune evasion in CRC.

     

A nuclease‐toxin and immunity system for kin discrimination in Myxococcus xanthus

The use of toxin to attack neighbours and immunity proteins to protect against toxin has been observed in bacterial conflicts, including kin discrimination. Here, we report a novel nuclease‐toxin and its immunity protein function in the colony‐merger incompatibility, a kind of bacterial kin discrimination, in Myxococcus xanthus DK1622. The MXAN_0049 gene was determined to be a genetic determinant for colony‐merger incompatibility, and the incompatibility could be eliminated by deletion of the upstream co‐transcribed MXAN_0050 gene. We demonstrated that the MXAN_0050 protein was a nuclease, and MXAN_0049 protein was able to bind to MXAN_0050 to block nuclease activity in vitro. Expression of MXAN_0050 in Escherichia coli inhibited cellular growth, and the inhibition effect could be recovered by co‐expression of MXAN_0049. We found that deletion of the PAAR‐encoding gene (MXAN_0044) or the type VI secretion system led to the colony‐merger and co‐existence with the ΔMXAN_0049 mutant, suggesting that they were associated with colony‐merger incompatibility. Homologues of the nuclease‐toxin and cognate immunity pair are widely distributed in bacteria. We propose a simplified model to explain the kin discrimination mechanism mediated by the nuclease‐toxin and immunity protein.© 2018 Society for Applied Microbiology and John Wiley & Sons Ltd     

Reactivation of Partially Metallocluster-deficient MoFe Protein by Chromium-Containing Reconstituent Solution

By treating the reduced MoFe protein from Azotobacter vinelandii with o-phenanthroIi e and O2, partially deficient in both FeMoco and P-cluster and inactive protein could be o rained. After incubating the treated protein with a reconstituent solution containing K2CrO4, ferric homocitrate, Na2S and dithiothreitol, a reactivated protein could be obtained. The absorption spectrum, circular dichroism spectrum, and the C2H2 and proton reduction activities of the reactivated protein were remarkably recovered. However, the spectra were somewhat different from those of the reduced MoFe protein. The results showed that some of the reactivated protein might be Cr-containing protein (CrFe protein) which were similar in function, but somewhat different in structure from MoFe protein.     

球形红杆菌积累聚β-羟基链烷酸(PHA)的研究

通过对球形红杆菌(Rhodobacter sphaeroides)生长和积累聚卢-羟基链烷酸(PHA)条件的研究,确定采用两段培养法提高PHA的产量。第一阶段提供适合菌体生长的条件:以葡萄糖作碳源,尿素为氮源,光照微好氧培养。第二阶段则提供使菌体积累PHA的条件:补加乙酸钠厌氧光照培养。经两段培养后菌体PHA含量可占细胞干重的45％,PHA产量每升发酵液可达1.7g。     

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ＨａＳＮＰＶ蛋白激酶基因的核苷酸序列研究张传溪＊王根＊胡萃＊吴祥甫（中国科学院上海生物化学研究所,上海２０００３１;＊浙江农业大学应用昆虫学研究所,杭州３１００２９）关键词棉铃虫;核多角体病毒;蛋白激酶基因;核苷酸序列昆虫杆状病毒是重要的生物杀虫剂,...     

草原生态学研究方法学术讨论会在成都召开

中国植物学会于1981年11月21日至27日在四川省成都市召开了有61名代表参加的草原生态学研究方法学术讨论会。大会收到包括植物群落结构调查研究、第一性生产力测定、第二性生产力测定、光合作用测定、物质与水分循环、热值测定、数学生态等有关内容的研究方法论文和报告34篇。其中有18篇论文在大会上作了报告。在小组讨论中,代表们就第一性生产力测定、水分与物质循环、光合作用测定     

天蚕素A-马盖宁杂合肽对耐甲氧西林金黄色葡萄球菌抑菌机制的研究

【目的】研究天蚕素A-马盖宁杂合肽对耐甲氧西林金黄色葡萄球菌(MRSA)DNA作用的抑菌机制。【方法】利用激光扫描共聚焦显微镜(CLSM)、凝胶阻滞分析、紫外光谱分析、荧光光谱分析的方法。【结果】天蚕素A-马盖宁杂合肽对MRSA的最小抑菌浓度(MIC)为64 mg/L,杂合肽可以在细菌胞内形成累积,并能与体外基因组DNA发生结合作用。同时杂合肽可以引起DNA构象的改变,荧光光谱分析结果表明杂合肽能与溴化乙锭(EB)竞争性地嵌入基因组DNA中,作用方式类似于EB与DNA的结合方式,杂合肽与DNA的结合表现为混合式作用方式。【结论】天蚕素A-马盖宁进入细菌胞内,与MRSA基因组DNA结合,并以混合式作用方式与DNA发生了结合,通过胞内靶向机制发挥抑菌作用。