共查询到17条相似文献,搜索用时 62 毫秒
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以体细胞重编程技术为代表的诱导性多能干细胞(induced pluripotent stem cells,iPS)已成为干细胞研究的热点.表观遗传学研究发现,DNA甲基化、组蛋白修饰等在基因转录调控过程中扮演着重要角色,对维持干细胞多能性起着关键作用.本文主要综述细胞重编程中的特定转录因子引起的表观遗传学变化与肿瘤发生... 相似文献
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端粒酶与体细胞重编程是当今生物界最热门的研究领域之一。研究端粒酶能揭示生物体胚胎早期发育、衰老和癌症发生的机制;细胞重编程则有望从根本上解决体细胞克隆技术问题,从而开启生命再造新时代。文章通过对端粒酶与体细胞重编程及二者互作机制的最新研究进展进行详细阐述,发现细胞重编程面临的主要问题是效率低下,其根本原因是对其作用机制尚未完全了解;而最新研究证实,生殖细胞的端粒酶活性发生时序性变化可能在胚胎发育及细胞重编程过程中发挥重要调控作用。因此,揭示细胞重编程机制是今后研究工作的重心,尤其是揭示端粒酶在胚胎发育过程的分子调控机理及端粒酶调控细胞重编程可能开启的信号通路,对提高细胞重编程效率,推进克隆动物的生产实践并开启生命再造,以及为治疗癌症等人类重大疾病具有重要意义。 相似文献
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《中国农业科技导报》2011,(4):135-136
哺乳动物卵母细胞发育蛋白质组研究突破卵母细胞具有非常强的重编程能力,它可以在短短几个细胞周期内把高度分化的体细胞重编程为了具有全能性的克隆胚胎并可以进一步发育成为克隆动物。要想了解哪些蛋白是卵母细胞重编程过程所需要的蛋白,就需要对 相似文献
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[目的]检测克隆奶山羊(♀12003)和转基因克隆奶山羊(♂12001)作为供体细胞,对体细胞重编程效率的影响。[方法]采用慢病毒作为载体,携带多能因子来感染正常山羊(g2)、♀12003和♂12001体细胞,统计克隆形成率和碱性磷酸酶阳性克隆率。[结果]与普通山羊(g2)相比,转基因克隆奶山羊耳成纤维细胞的重编程效率低,出现的细胞克隆在传代之前容易分化;克隆奶山羊体细胞与普通山羊体细胞的重编程效率接近,转基因克隆奶山羊(♂12001)的重编程效率极显著低于克隆奶山羊(♀12003)和普通山羊(P0.01)。[结论]转基因克隆奶山羊体细胞可以被重编程为诱导性多能干细胞(Induced pluripotent stem cells,iPSCs),但效率较低。 相似文献
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选取健康、体重相近的15日龄双鬼头肉鸭480只,随机分成4个组,每个组6个重复,每个重复20羽,分别饲喂木薯添加量为0、10%、20%和30%的试验日粮,进行为期30 d的试验.结果表明:①随着木薯添加量的增加,肉鸭平均日采食量逐渐上升,30%木薯组显著高于10%木薯组(P<0.05),而肉鸭日增重呈现先上升后下降的趋势,其中20%木薯组的45日龄重(末重)和平均日增重均与对照组差异显著(P<0.05),当木薯添加量为20%时肉鸭增重效果最佳,料重比最低;②当木薯添加量为10%和20%时,日粮干物质表观消化率和表观代谢能显著高于其他2组(P<0.05),且有提高蛋白质表观消化率的趋势;除甘氨酸、精氨酸、苏氨酸、脯氨酸、缬氨酸和异亮氨酸外,其他氨基酸表观消化率各组间的差异均不显著(P>0.05).但10%木薯组和20%木薯组的蛋氨酸和赖氨酸表观消化率较其他2组均有提高的趋势.综合考虑,在肉鸭日粮中用木薯替代部分玉米,可以在一定程度上提高日粮中干物质和蛋白质的表观消化率,从而达到增重和降低料重比的效果.肉鸭日粮中木薯添加量以10%~20%为宜. 相似文献
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Molecular coupling of Xist regulation and pluripotency 总被引:2,自引:0,他引:2
Navarro P Chambers I Karwacki-Neisius V Chureau C Morey C Rougeulle C Avner P 《Science (New York, N.Y.)》2008,321(5896):1693-1695
During mouse embryogenesis, reversion of imprinted X chromosome inactivation in the pluripotent inner cell mass of the female blastocyst is initiated by the repression of Xist from the paternal X chromosome. Here we report that key factors supporting pluripotency-Nanog, Oct3/4, and Sox2-bind within Xist intron 1 in undifferentiated embryonic stem (ES) cells. Whereas Nanog null ES cells display a reversible and moderate up-regulation of Xist in the absence of any apparent modification of Oct3/4 and Sox2 binding, the drastic release of all three factors from Xist intron 1 triggers rapid ectopic accumulation of Xist RNA. We conclude that the three main genetic factors underlying pluripotency cooperate to repress Xist and thus couple X inactivation reprogramming to the control of pluripotency during embryogenesis. 相似文献
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Epigenetic reprogramming in plant and animal development 总被引:1,自引:0,他引:1
Epigenetic modifications of the genome are generally stable in somatic cells of multicellular organisms. In germ cells and early embryos, however, epigenetic reprogramming occurs on a genome-wide scale, which includes demethylation of DNA and remodeling of histones and their modifications. The mechanisms of genome-wide erasure of DNA methylation, which involve modifications to 5-methylcytosine and DNA repair, are being unraveled. Epigenetic reprogramming has important roles in imprinting, the natural as well as experimental acquisition of totipotency and pluripotency, control of transposons, and epigenetic inheritance across generations. Small RNAs and the inheritance of histone marks may also contribute to epigenetic inheritance and reprogramming. Reprogramming occurs in flowering plants and in mammals, and the similarities and differences illuminate developmental and reproductive strategies. 相似文献
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Epigenetic reprogramming in mammalian development 总被引:1,自引:0,他引:1
DNA methylation is a major epigenetic modification of the genome that regulates crucial aspects of its function. Genomic methylation patterns in somatic differentiated cells are generally stable and heritable. However, in mammals there are at least two developmental periods-in germ cells and in preimplantation embryos-in which methylation patterns are reprogrammed genome wide, generating cells with a broad developmental potential. Epigenetic reprogramming in germ cells is critical for imprinting; reprogramming in early embryos also affects imprinting. Reprogramming is likely to have a crucial role in establishing nuclear totipotency in normal development and in cloned animals, and in the erasure of acquired epigenetic information. A role of reprogramming in stem cell differentiation is also envisaged. DNA methylation is one of the best-studied epigenetic modifications of DNA in all unicellular and multicellular organisms. In mammals and other vertebrates, methylation occurs predominantly at the symmetrical dinucleotide CpG (1-4). Symmetrical methylation and the discovery of a DNA methyltransferase that prefers a hemimethylated substrate, Dnmt1 (4), suggested a mechanism by which specific patterns of methylation in the genome could be maintained. Patterns imposed on the genome at defined developmental time points in precursor cells could be maintained by Dnmt1, and would lead to predetermined programs of gene expression during development in descendants of the precursor cells (5, 6). This provided a means to explain how patterns of differentiation could be maintained by populations of cells. In addition, specific demethylation events in differentiated tissues could then lead to further changes in gene expression as needed. Neat and convincing as this model is, it is still largely unsubstantiated. While effects of methylation on expression of specific genes, particularly imprinted ones (7) and some retrotransposons (8), have been demonstrated in vivo, it is still unclear whether or not methylation is involved in the control of gene expression during normal development (9-13). Although enzymes have been identified that can methylate DNA de novo (Dnmt3a and Dnmt3b) (14), it is unknown how specific patterns of methylation are established in the genome. Mechanisms for active demethylation have been suggested, but no enzymes have been identified that carry out this function in vivo (15-17). Genomewide alterations in methylation-brought about, for example, by knockouts of the methylase genes-result in embryo lethality or developmental defects, but the basis for abnormal development still remains to be discovered (7, 14). What is clear, however, is that in mammals there are developmental periods of genomewide reprogramming of methylation patterns in vivo. Typically, a substantial part of the genome is demethylated, and after some time remethylated, in a cell- or tissue-specific pattern. The developmental dynamics of these reprogramming events, as well as some of the enzymatic mechanisms involved and the biological purposes, are beginning to be understood. Here we look at what is known about reprogramming in mammals and discuss how it might relate to developmental potency and imprinting. 相似文献