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DNA甲基化和组蛋白修饰在克隆动物发育过程中的作用

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  • 1. 中国科学院动物研究所计划生育生殖生物学国家重点实验室, 北京 100101; 2. 北京师范大学生命科学学院, 北京 100875

收稿日期: 2009-11-13

  修回日期: 2010-03-19

  网络出版日期: 2010-08-23

基金资助

国家自然科学基金项目(编号:30770245)和国家高技术研究发展计划项目(863计划)(编号:2008AA101006)资助

Effect of DNA methylation and histone modification during the de-velopment of cloned animals

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  • 1. State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China; 2. College of Life Sciences, Beijing Normal University, Beijing 100875, China

Received date: 2009-11-13

  Revised date: 2010-03-19

  Online published: 2010-08-23

摘要

体细胞核移植在农业应用、生产疾病模型动物、转基因家畜或产生人胚胎干细胞来治疗人类的疾病方面有巨大的应用潜力。虽然已经成功克隆出多种哺乳动物, 但该技术仍存在一些未解决的问题, 包括产生克隆动物的效率低和克隆动物的异常等。异常的表观遗传重编程是克隆胚胎发育失败的一个重要因素。文章重点论述了DNA甲基化、组蛋白修饰及其与克隆胚胎发育的关系。了解表观遗传调控机制有助于解决核移植技术中存在的问题, 有利于更好地应用这项技术。

本文引用格式

郭磊,李慧,韩之明 . DNA甲基化和组蛋白修饰在克隆动物发育过程中的作用[J]. 遗传, 2010 , 32(8) : 762 -768 . DOI: 10.3724/SP.J.1005.2010.00762

Abstract

Somatic cell nuclear transfer (SCNT) has great potential for agricultural applications, generation of medical model animals, transgenic farm animals or generating human embryonic stem cells for treatment of human diseases. Cloned animals derived from somatic cells have been generated in several mammal species, but there are still some unsolved problems with current cloning technology, for example, the low efficiency of animal cloning and the abnormal development of cloned animals. One critical factor of these developmental failures of cloned embryos is the aberrant epigenetic reprogramming. This review focuses on DNA methylation and histone modifications and the relationship between these two epigenetic modifications and the development of cloned embryos. Understanding the mechanisms of epigenetic regulation will be useful to solve the technical problems of SCNT and enable better applications of this technology.

参考文献

[1] Gurdon JB, Byrne JA. The first half-century of nuclear transplantation. Proc Natl Acad Sci USA, 2003, 100(14): 8048–8052. [2] Wilmut I, Schnieke AE, McWhir J, Kind AJ, Campbell KH. Viable offspring derived from fetal and adult mammalian cells. Nature, 1997, 385(6619): 810–813. [3] Yamanaka S. Pluripotency and nuclear reprogramming. Philos Trans R Soc Lond B Biol Sci, 2008, 363(1500): 2079–2087. [4] Han YM, Kang YK, Koo DB, Lee KK. Nuclear repro-gramming of cloned embryos produced in vitro. Therio-genology, 2003, 59(1): 33–44. [5] Cibelli JB, Campbell KH, Seidel GE, West MD, Lanza RP. The health profile of cloned animals. Nat Biotechnol, 2002, 20(1): 13–14. [6] Delcuve GP, Rastegar M, Davie JR. Epigenetic control. J Cell Physiol, 2009, 219(2): 243–250. [7] Bird A. DNA methylation patterns and epigenetic memory. Genes Dev, 2002, 16(1): 6–21. [8] Shi W, Zakhartchenko V, Wolf E. Epigenetic reprogramming in mammalian nuclear transfer. Differentiation, 2003, 71(2): 91–113. [9] Kurihara Y, Kawamura Y, Uchijima Y, Amamo T, Koba-yashi H, Asano T, Kurihara H. Maintenance of genomic methylation patterns during preimplantation development requires the somatic form of DNA methyltransferase 1. Dev Biol, 2008, 313(1): 335–346. [10] Suetake I, Morimoto Y, Fuchikami T, Abe K, Tajima S. Stimulation effect of Dnmt3L on the DNA methylation ac-tivity of Dnmt3a2. J Biochem, 2006, 140(4): 553–559. [11] Vaissiere T, Sawan C, Herceg Z. Epigenetic interplay be-tween histone modifications and DNA methylation in gene silencing. Mutat Res, 2008, 659(1–2): 40–48. [12] Strahl BD, Allis CD. The language of covalent histone modifications. Nature, 2000, 403(6765): 41–45. [13] Eilertsen KJ, Power RA, Harkins LL, Misica P. Targeting cellular memory to reprogram the epigenome, restore po-tential, and improve somatic cell nuclear transfer. Anim Reprod Sci, 2007, 98(1–2): 129–146. [14] Lucio-Eterovic AK, Cortez MA, Valera ET, Motta FJ, Queiroz RG, Machado HR, Carlotti CG, Jr., Neder L, Scrideli CA, Tone LG. Differential expression of 12 his-tone deacetylase (HDAC) genes in astrocytomas and nor-mal brain tissue: class II and IV are hypoexpressed in glioblastomas. BMC Cancer, 2008, 8243. [15] Wilson AJ, Byun DS, Popova N, Murray LB, L'Italien K, Sowa Y, Arango D, Velcich A, Augenlicht LH, Mariadason JM. Histone deacetylase 3 (HDAC3) and other class I HDACs regulate colon cell maturation and p21 expression and are deregulated in human colon cancer. J Biol Chem, 2006, 281(19): 13548–13558. [16] Witt O, Deubzer HE, Milde T, Oehme I. HDAC family: What are the cancer relevant targets? Cancer Lett, 2009, 277(1): 8–21. [17] Klose RJ, Zhang Y. Regulation of histone methylation by demethylimination and demethylation. Nat Rev Mol Cell Biol, 2007, 8(4): 307–318. [18] Misri S, Pandita S, Kumar R, Pandita TK. Telomeres, his-tone code, and DNA damage response. Cytogenet Genome Res, 2008, 122(3–4): 297–307. [19] Perez-Cadahia B, Drobic B, Davie JR. H3 phosphorylation: dual role in mitosis and interphase. Biochem Cell Biol, 2009, 87(5): 695–709. [20] Shukla A, Chaurasia P, Bhaumik SR. Histone methylation and ubiquitination with their cross-talk and roles in gene expression and stability. Cell Mol Life Sci, 2009, 66(8): 1419–1433. [21] Gill G. SUMO and ubiquitin in the nucleus: different functions, similar mechanisms? Genes Dev, 2004, 18(17): 2046–2059. [22] Nathan D, Ingvarsdottir K, Sterner DE, Bylebyl GR, Dok- manovic M, Dorsey JA, Whelan KA, Krsmanovic M, Lane WS, Meluh PB, Johnson ES, Berger SL. Histone sumoyla- tion is a negative regulator in Saccharomyces cerevisiae and shows dynamic interplay with positive-acting
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