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Gene expression profile favoring phenotypic reversion: a clue for mechanism of tumor suppression by NF-IL6 3'UTR

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cell Research 2003年第6期13卷 509-514页

作者： DING GAN liu, QIU HONG JIANG, YUN Yl WEI, LI SUN, BEI BEI FU, Fu KUN zhao, QIONG ZHOU ’ state key laboratory of molecular biology and key laboratory of Proteomics, institute of biochemistryand cell biology, shanghai institutes for biological sciences, chinese academy of sciences, shanghai200031, china. E-mail: dgliu@*** state key laboratory of molecular biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China. dgliu@***

Transfection of cDNA in 3’untranslated region of human nuclear factor for interleukin-6 (NF-IL6 3’UTR) induced tumor suppression in a human hepatoma cell line. cDNA array analysis was used to reveal changes in gene expression profile leading to tumor suppression The results indicate that this suppression was not due to activation of dsRNA-dependent protein kinase, nor to inactivation of oncogenes; rather, all the changes in expression of known genes, induced by NF-IL6 3’UTR cDNA may be ascribed to the suppression of cellular malignancy. Therefore, our results imply that this 3’untranslated region may have played role of a regulator of gene expression profile.

关键词： cDNA array NF-IL6 hepatoma 3 ’UTR tumor suppression.

N端的改变对大肠杆菌精氨酰-tRNA合成酶的影响(英文)

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生物化学与生物物理学报 2002年第2期34卷 131-137页

作者：刘文刘默芳夏宪王恩多王应睐中国科学院上海生命科学研究院生物化学与细胞生物学研究所分子生物学国家重点实验室

得到了缺失Asn2 的大肠杆菌 (E .coli)精氨酰 tRNA合成酶 (ArgRS)的变种和在其N端添加酵母ArgRS的N端 2 3个氨基酸残基的嵌合变种。它们的基因在大肠杆菌中表达时 ,可能由于蛋白质误折叠 ,大部分产生了包涵体。与天然酶相比 ,缺失变种... 详细信息

得到了缺失Asn2 的大肠杆菌 (E .coli)精氨酰 tRNA合成酶 (ArgRS)的变种和在其N端添加酵母ArgRS的N端 2 3个氨基酸残基的嵌合变种。它们的基因在大肠杆菌中表达时 ,可能由于蛋白质误折叠 ,大部分产生了包涵体。与天然酶相比 ,缺失变种保留了全部的氨基酸活化活力 ,但氨基酰化活力下降了 2 6 % ;嵌合变种的以上两种活力下降了 90 %以上 ,不能氨基酰化酵母tRNAArg。缺失Asn2 和Ile3 的变种在E .coli中虽被表达 ,但不稳定。与天然酶相比 ,嵌合变种的荧光光谱的最大发射波长向长波移动 ,强度减小。表明变种酶的构象和天然酶不同 ,色氨酸更暴露。用远紫外CD光谱预测变种酶的二级结构表明 ,嵌合酶的α螺旋更少 ,β折叠更多 ,无规卷曲稍多。E .coliArgRS的N端结构域对活力和正确折叠是重要的

关键词：精氨酰-tRNA合成酶 N端活力突变

MicroRNA-155 functions as an oncomiR in breast cancer by targeting the suppressor of cytokine signaling-1 gene

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MicroRNA-155 functions as an oncomiR in breast cancer by tar...

Exploring noncoding variants in genetic diseases:from detection to functional insights

第三届细胞结构与功能的信号基础研讨会

作者： Shuai Jiang,Ming-Hua Lu,Xiao-Hong He,En-Duo Wang,mo-fang.liu state key laboratory of molecular biology,institute of biochemistry and cell biology,shanghai institutes for biological sciences,the chinese academy of sciences,320 Yueyang Road,shanghai 200031,china

MicroR-155(miR-155) is overexpressed in many human cancers;however,the mechanisms by which miR-155 functions as a putative oncomiR are largely unknown. Here,we report that the tumor suppressor gene suppressor of cytokine signaling-1 (socsl) is an evolutionarily conserved target of miR-155 in breast cancer *** found that mir-155 expression is inversely correlated with socsl expression in breast cancer cell lines,as well as in a subset of primary breast *** also identified a 24A→G mutation in the miR-155 binding site of the SOCS1 3’UTR in a breast tumor that reduced miR-155 repression,implicating a mechanism for miRNA targets to avoid *** expression of miR-155 significantly promoted the proliferation of breast cancer cells,the formation of soft-agar foci in vitro,and the development of tumors in nude *** breast cancer cells,RNAi silencing of socs1 recapitulates the oncogenic effects of miR-155,whereas restoration of socs1 expression attenuates the pro-tumorigenesis function of miR-155,suggesting that miR-155 exerts its oncogenic role by negatively regulating *** of miR-155 in breast cancer cells leads to constitutive activation of STAT3 through the JAK pathway,and stimulation of breast cancer cells by the inflammatory cytokines INF-γand IL-6,lipopolysaccharide,and polyriboinosinic polyribocytidylic acid significantly upregulates mir-155 expression,suggesting that miR-155 may serve as a bridge between inflammation and *** together,our study reveals that miR-155 is an oncomiR in breast cancer and that miR-155 may be a potential target in breast cancer therapy.

关键词： microRNA-155 breast cancer SOCS1 STAT3 JAK2

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Journal of Genetics and Genomics 2024年第2期51卷 111-132页

作者： Ke Wu Fengxiao Bu Yang Wu Gen Zhang Xin Wang Shunmin He mo-fang.liu Runsheng Chen Huijun Yuan institute of Rare Diseases West China Hospital of Sichuan UniversityChengduSichuan 610041China key laboratory of Systems Health Science of Zhejiang Province School of Life ScienceHangzhou Institute for Advanced StudyUniversity of Chinese Academy of SciencesHangzhouZhejiang 310024China key laboratory of RNA biology Center for Big Data Research in HealthInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China University of chinese academy of sciences Beijing 100049China state key laboratory of molecular biology State Key Laboratory of Cell BiologyShanghai Key Laboratory of Molecular AndrologyShanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China

Previous studies on genetic diseases predominantly focused on protein-coding variations, overlooking the vast noncoding regions in the human genome. The development of high-throughput sequencing technologies and functional genomics tools has enabled the systematic identification of functional noncoding variants. These variants can impact gene expression, regulation, and chromatin conformation, thereby contributing to disease pathogenesis. Understanding the mechanisms that underlie the impact of noncoding variants on genetic diseases is indispensable for the development of precisely targeted therapies and the implementation of personalized medicine strategies. The intricacies of noncoding regions introduce a multitude of challenges and research opportunities. In this review, we introduce a spectrum of noncoding variants involved in genetic diseases, along with research strategies and advanced technologies for their precise identification and in-depth understanding of the complexity of the noncoding genome. We will delve into the research challenges and propose potential solutions for unraveling the genetic basis of rare and complex diseases.

关键词： Noncoding variation Genetic disease Research approach Challenge

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精子发生中小非编码RNA的新见解

Science Bulletin 2024年第11期69卷 1581-1585页

作者：王鑫张振翼赵爽刘默芳 key laboratory of Systems Health Science of Zhejiang Province School of Life ScienceHangzhou Institute for Advanced StudyUniversity of Chinese Academy of SciencesHangzhou 310024China New Cornerstone Science laboratory State Key Laboratory of Molecular BiologyState Key Laboratory of Cell BiologyShanghai Key Laboratory of Molecular AndrologyShanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai 200031China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China

Spermatogenesis is one of the most complicated cell differentiation processes in animals, which consists of mitosis, meiosis, and the post-meiotic phase of male germ cell development, i.e.,spermiogenesis. Mitosis is responsible for germline maintenance,while meiosis reduces the chromosome number by half and creates genetic diversity in the sperm.

关键词：精子发生 maintenance mitosis

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A dual role of the PIWI/pi RNA machinery in regulating mRNAs during mouse spermiogenesis

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Science china(Life sciences) 2020年第3期63卷 447-449页

作者： Peng Dai Xin Wang mo-fang.liu state key laboratory'of molecular biology、shanghai key laboratory of molecular Andrology CAS Center for Excellence in Molecular Cell ScienceShanghai Institute of Biochemistry and Cell BiologyChinese Academy of Sciences-University of Chinese Academy of SciencesShanghai 200031China

The post-meiotic phase of male germ cell development in mammals undergoes a series of dramatic morphological changes,including acrosome and flagellum formation,nuclear condensation,and cytoplasmic exclusion,which is driven by a highly regulated sequence of biochemical reactions(Meistrich and Hess,2013).Such differentiation process called spermiogenesis consists of at least 16 sequential transition steps in mice,including steps I to 8 for round spermatids,steps 9 to 11 for elongating spermatids,steps 12 to 14 for elongated or condensed spermatids,and final steps 15 to 16 for spermatozoa(Meistrich and Hess,2013).

关键词： steps condensed condensation

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Small RNAs:An expanding world with therapeutic promises

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Fundamental Research 2023年第5期3卷 676-682页

作者： Lan-Tao Gou Qifan Zhu mo-fang.liu state key laboratory of molecular biology Shanghai Key Laboratory of Molecular AndrologyShanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China School of Life Science Hangzhou Institute for Advanced StudyUniversity of Chinese Academy of SciencesHangzhou 310024China School of Life Science and Technology Shanghai Tech UniversityShanghai 201210China

Small non-coding RNAs(sncRNAs),such as microRNAs(miRNAs),small interfering RNAs(siRNAs),PIWIinteracting RNAs(piRNAs),and transfer RNA(tRNA)-derived small RNAs(tsRNAs),play essential roles in regulating various cellular and developmental *** the past three decades,researchers have identified novel sncRNA species from various *** molecules demonstrate dynamic expression and diverse functions,and they are subject to intricate regulation through RNA modifications in both healthy and diseased ***,certain sncRNAs in gametes,particularly sperm,respond to environmental stimuli and facilitate epigenetic ***,the in-depth understanding of sncRNA functions and mechanisms has accelerated the development of small RNA-based *** this review,we present the recent advances in the field,including new sncRNA species and the regulatory influences of RNA *** also discuss the current limitations and challenges associated with using small RNAs as either biomarkers or therapeutic drugs.

关键词： Small non-coding RNAs RNA modifications Human diseases RNA therapeutics Biomarkers

Methylation of PLK1 by SET7/9 ensures accurate kinetochore–microtubule dynamics

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Journal of molecular cell biology 2020年第6期12卷 462-476页

作者： Ruoying Yu Huihui Wu Hazrat Ismail Shihao Du Jun Cao Jianyu Wang Tarsha Ward Fengrui Yang Ping Gui Mahboob Ali Lingluo Chu Fei mo Qi Wang Youjun Chu Jianye Zang Yun zhao Mingliang Ye Guowei fang.Peng RChen Zhen Dou Xinjiao Gao Wenwen Wang Xing liu Xuebiao Yao moE key laboratory for cellular Dynamics&Anhui key laboratory for Chemical biology CAS Center for Excellence in Molecular Cell ScienceHefei National Science Center for Physical Sciences at Microscale&University of Science and Technology of ChinaHefei 230027China BUCM-MSM-USTC Joint Program on Global Health Equity Beijing University of Chinese MedicineBeijing 100029China Department of Physiology Morehouse School of MedicineAtlantaGA 30310USA Harvard Medical School BostonMA 02115USA Dalian institute for Physical Chemistry Dalian 116023China shanghai institute of biochemistry and cell biology Center for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China College of Chemistry and molecular Engineering Peking UniversityBeijing 100871China

Faithful segregation of mitotic chromosomes requires bi-orientation of sister chromatids, which relies on the sensing of correct attachments between spindle microtubules and kinetochores. Although the mechanisms underlying PLK1 activation have been extensively studied, the regulatory mechanisms that couple PLK1 activity to accurate chromosome segregation are not well understood. In particular, PLK1 is implicated in stabilizing kinetochore–microtubule attachments, but how kinetochore PLK1 activity is regulated to avoid hyperstabilized kinetochore–microtubules in mitosis remains elusive. Here, we show that kinetochore PLK1 kinase activity is modulated by SET7/9 via lysine methylation during early mitosis. The SET7/9-elicited dimethylation occurs at the Lys191 of PLK1, which tunes down its activity by limiting ATP utilization. Overexpression of the non-methylatable PLK1 mutant or chemical inhibition of SET7/9 methyltransferase activity resulted in mitotic arrest due to destabilized kinetochore–microtubule attachments. These data suggest that kinetochore PLK1 is essential for stable kinetochore–microtubule attachments and methylation by SET7/9 promotes dynamic kinetochore–microtubule attachments for accurate error correction. Our findings define a novel homeostatic regulation at the kinetochore that integrates protein phosphorylation and methylation with accurate chromosome segregation for maintenance of genomic stability.

关键词： mitosis PLK1 kinase SET7/9 methylation kinetochore-microtubule attachment

The LRXs-RALFs-FER module controls plant growth and salt stress responses by modulating multiple plant hormones

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National Science Review 2021年第1期8卷 40-55页

作者： Chunzhao zhao Wei Jiang Omar Zayed Xin liu Kai Tang Wenfeng Nie Yali Li Shaojun Xie Yuan Li Tiandan Long Linlin liu Yingfang.Zhu Yang zhao Jian-Kang Zhu shanghai Center for Plant Stress biology and Center of Excellence in molecular Plant sciences Chinese Academy of Sciences Department of Horticulture and Landscape Architecture Purdue University key laboratory of Plant Stress biology School of Life SciencesHenan University National Center for Soybean Improvement Key Laboratory of Biology and Genetics and Breeding for Soybean Ministry of Agriculture State Key Laboratory of Crop Genetics and Germplasm Enhancement Nanjing Agricultural University Genetics Department Faculty of AgricultureMenofia University University of the chinese academy of sciences state key laboratory of Plant Physiology and biochemistry College of Biological SciencesChina Agricultural University state key laboratory of Crop Gene Exploration and Utilization in Southwest china Sichuan Agricultural University

Salt stress is a major environmental factor limiting plant growth and productivity. We recently discovered an important new salt tolerance pathway, where the cell wall leucine-rich repeat extensins LRX3/4/5, the RAPID ALKALINIZATION FACTOR (RALF) peptides RALF22/23 and receptor-like kinase FERONIA(FER) function as a module to simultaneously regulate plant growth and salt stress tolerance. However, the intracellular signaling pathways that are regulated by the extracellular LRX3/4/5-RALF22/23-FER module to coordinate growth, cell wall integrity and salt stress responses are still unknown. Here, we report that the LRX3/4/5-RALF22/23-FER module negatively regulates the levels of jasmonic acid (JA), salicylic acid(SA) and abscisic acid (ABA). Blocking JA pathway rescues the dwarf phenotype of the lrx345 and fer-4mutants, while disruption of ABA biosynthesis suppresses the salt-hypersensitivity of these mutants. Many salt stress-responsive genes display abnormal expression patterns in the lrx345 and fer-4 mutants, as well as in the wild type plants treated with epigallocatechin gallate (EGCG), an inhibitor of pectin methylesterases,suggesting cell wall integrity as a critical factor that determines the expression pattern of stress-responsive genes. Production of reactive oxygen species (ROS) is constitutively increased in the lrx345 and fer-4mutants, and inhibition of ROS accumulation suppresses the salt-hypersensitivity of these ***, our work provides strong evidence that the LRX3/4/5-RALF22/23-FER module controls plant growth and salt stress responses by regulating hormonal homeostasis and ROS accumulation.

关键词： salt stress cell wall integrity growth LRX RALF FER hormone