关于DNA甲基化的研究

DNA甲基化是表观遗传学中最重要的机制之一,是主要发生在CpG双核苷酸序列中胞嘧啶上的一种表观遗传修饰。本文就DNA甲基化的涵义、检测方法、在植物研究中的应用、面临的问题以及未来的前景进行综述,从而为DNA甲基化在表观遗传学中的研究提供理论参考。     

关于DNA甲基化的研究

DNA甲基化是表观遗传学中最重要的机制之一,是主要发生在CpG双核苷酸序列中胞嘧啶上的一种表观遗传修饰。本文就DNA甲基化的涵义、检测方法、在植物研究中的应用、面临的问题以及未来的前景进行综述,从而为DNA甲基化在表观遗传学中的研究提供理论参考。     

表观遗传学及其研究进展

表观遗传学是指以不涉及到核苷酸序列的改变、但可以通过有丝分裂和减数分裂进行遗传的生物现象为内容的生命学科.它通过DNA的甲基化、组蛋白修饰、染色质重塑和非编码RNA调控4种方式来控制表观遗传的沉默.据此,对表观遗传学涉及的机制、改变的特征及表观遗传学的相关研究进展等方面问题进行综述.     

DNA甲基化及检测方法研究进展

DNA甲基化是一种重要的遗传修饰,是表观遗传学（epigenetics）研究的重要内容。综述了目前常用的甲基化检测方法的原理及其在检测DNA甲基化中的优缺点,如MSAP检测方法、亚硫酸氢盐法、基因芯片技术等。随着对表观遗传学研究的深入,DNA甲基化检测方法也有了快速的发展,将有利于科学工作者更快更好的检测出DNA甲基化。     

DNA甲基化及检测方法研究进展

DNA甲基化是一种重要的遗传修饰,是表观遗传学(epigenetics)研究的重要内容.综述了目前常用的甲基化检测方法的原理及其在检测DNA甲基化中的优缺点,如MSAP检测方法、哑硫酸氢盐法、基因芯片技术等.随着对表观遗传学研究的深入,DNA甲基化检测方法也有了快速的发展,将有利于科学工作者更快更好的检测出DNA甲基化.     

肿瘤相关基因的表观遗传修饰研究进展

表观遗传学是遗传学的分支学科，研究非DNA序列改变所导致的可遗传的基因表达水平的变化。与肿瘤相关的表观基因改变主要是DNA甲基化和组蛋白修饰．该文分别从这两方面阐述了肿瘤相关基因的表观遗传学改变的研究进展。     

肿瘤表观基因组学药物治疗研究进展

表观基因组学（Epigenomics）是在基因组水平上对表观遗传学改变的探讨,与肿瘤相关的表观基因改变主要是DNA甲基化和组蛋白修饰,综述了与肿瘤相关表观基因药物治疗的研究进展。     

巴西橡胶树表观遗传研究进展

表观遗传是指在不涉及基因组DNA序列改变的情况下,基因功能发生了可逆的、可遗传的改变。研究表明,表观遗传调控在植物的生长发育及逆境胁迫应答反应中起着重要的作用。目前,表观遗传学研究主要集中在DNA甲基化、小RNA调控、组蛋白修饰、染色质重塑及基因组印迹等。与模式植物相比,橡胶树表观遗传的研究相对滞后,主要涉及DNA甲基化及miRNAs研究这2个方面。本文就橡胶树DNA甲基化及miRNAs的相关研究进行了简要综述,并对表观遗传在橡胶树中的研究前景提出展望。     

表观遗传的优势

表观遗传修饰主要包括DNA甲基化和组蛋白修饰,它具有不改变DNA序列而能够导致遗传变化的特点,为生物应对环境快速变化和外力胁迫提供了一种应变机制,具有明显的遗传学优势。     

水产养殖环境胁迫对鱼类表观遗传的影响研究进展

表观遗传学是研究基因核苷酸序列不发生改变的情况下,基因表达的可遗传的变化的一门遗传学分支学科。表观遗传的现象较多,已有DNA甲基化、组蛋白修饰、染色质重塑、非编码RNA调控、基因组印记、基因沉默、母体效应、核仁显性、休眠转座子激活等。在集约化的水产养殖模式中,养殖密度提高,投喂过量等均会产生刺激鱼类生长的环境因素。已有文献报道,环境胁迫因素刺激可影响鱼类表观遗传修饰,但并未涉及遗传信息的变化,所以在一定范围内可以解释为表型变化。本研究围绕环境胁迫因素对鱼类表观遗传产生的影响进行了综述,为进一步阐释环境因素与基因互作关系提供了参考。     

Epigenetic reprogramming in mammalian development

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.     

Epigenetic transgenerational actions of endocrine disruptors and male fertility

Transgenerational effects of environmental toxins require either a chromosomal or epigenetic alteration in the germ line. Transient exposure of a gestating female rat during the period of gonadal sex determination to the endocrine disruptors vinclozolin (an antiandrogenic compound) or methoxychlor (an estrogenic compound) induced an adult phenotype in the F1 generation of decreased spermatogenic capacity (cell number and viability) and increased incidence of male infertility. These effects were transferred through the male germ line to nearly all males of all subsequent generations examined (that is, F1 to F4). The effects on reproduction correlate with altered DNA methylation patterns in the germ line. The ability of an environmental factor (for example, endocrine disruptor) to reprogram the germ line and to promote a transgenerational disease state has significant implications for evolutionary biology and disease etiology.     

Role for piRNAs and noncoding RNA in de novo DNA methylation of the imprinted mouse Rasgrf1 locus

Genomic imprinting causes parental origin-specific monoallelic gene expression through differential DNA methylation established in the parental germ line. However, the mechanisms underlying how specific sequences are selectively methylated are not fully understood. We have found that the components of the PIWI-interacting RNA (piRNA) pathway are required for de novo methylation of the differentially methylated region (DMR) of the imprinted mouse Rasgrf1 locus, but not other paternally imprinted loci. A retrotransposon sequence within a noncoding RNA spanning the DMR was targeted by piRNAs generated from a different locus. A direct repeat in the DMR, which is required for the methylation and imprinting of Rasgrf1, served as a promoter for this RNA. We propose a model in which piRNAs and a target RNA direct the sequence-specific methylation of Rasgrf1.     

鱼类原始生殖细胞与鱼类性别分化的关系

在鱼类的性别分化中,原始生殖细胞在雌雄二性中的增殖方式不同,而且在部分鱼类中原始生殖细胞的缺失能导致其发育为单一雄性表型。在此过程中,生殖细胞的特有基因vasa的剪接变体的二态性分布与鱼类原始生殖细胞的分化关系密切。     

菜心茎尖DNA甲基化水平及GA、蛋白质含量的变化与花芽分化

研究了菜心花芽分化起始前后茎尖部位DNA甲基化水平、赤霉素(GA)含量和蛋白质(Pr)含量的变化.结果表明:花芽分化前夕,即一级分化之前DNA甲基化水平就开始下降,且随着花芽分化的进行进一步下降;GA含量在花芽将要分化时,稍有下降,但花芽开始分化后又有所回升;蛋白质含量从花芽分化前夕开始伴随着花芽分化的进行呈逐步上升的趋势.     

Imprinting and the epigenetic asymmetry between parental genomes

Genomic imprinting confers a developmental asymmetry on the parental genomes, through epigenetic modifications in the germ line and embryo. These heritable modifications regulate the monoallelic activity of parental alleles resulting in their functional differences during development. Specific cis-acting regulatory elements associated with imprinted genes carry modifications involving chromatin structural changes and DNA methylation. Some of these modifications are initiated in the germ line. Comparative genomic analysis at imprinted domains is emerging as a powerful tool for the identification of conserved elements amenable to more detailed functional analysis, and for providing insight into the emergence of imprinting during the evolution of mammalian species. Genomic imprinting therefore provides a model system for the analysis of the epigenetic control of genome function.     

Hypoxia triggers meiotic fate acquisition in maize

Evidence from confocal microscopic reconstruction of maize anther development in fertile, mac1 (excess germ cells), and msca1 (no germ cells) flowers indicates that the male germ line is multiclonal and uses the MAC1 protein to organize the somatic niche. Furthermore, we identified redox status as a determinant of germ cell fate, defining a mechanism distinct from the animal germ cell lineage. Decreasing oxygen or H(2)O(2) increases germ cell numbers, stimulates superficial germ cell formation, and rescues germinal differentiation in msca1 flowers. Conversely, oxidizing environments inhibit germ cell specification and cause ectopic differentiation in deeper tissues. We propose that hypoxia, arising naturally within growing anther tissue, acts as a positional cue to set germ cell fate.     

植物体与植物体细胞无性系发育中的DNA甲基化及其表达调控研究进展

从DNA甲基化与基因表达调控模式、DNA甲基化形式、植物发育中DNA甲基化调控、体细胞无性系发育中的DNA甲基化等方面,阐述DNA甲基化在植物体与植物体细胞无性系发育中的相关机制,评述植物体与植物体细胞无性系发育、繁殖等的相关分子机制及表观遗传机制。