生物谷：科學家直到最近才開始思考“垃圾DNA”（junk DNA）可能由于某個重要原因而存在于基因組中,。垃圾DNA是人類基因組中96%不編譯任何蛋白質的DNA,，它們過去被認為是無用的。現(xiàn)在,，來自加州大學San Diego分校（UCSD）醫(yī)學院的科學家們發(fā)現(xiàn)了它們的一項重要功能,。
基因是基因組中4%的編譯蛋白DNA－生命的構件（building blocks）。由UCSD醫(yī)學教授Michael G. Rosenfeld領導的小組發(fā)現(xiàn),，剩余的96%基因材料中的某些DNA對于幫助形成正確排布編譯DNA的邊界非常重要,。他們的結果發(fā)表在7月13日的Science上。
文章第一作者,，UCSD助理研究員Victoria Lunyak說：“一些垃圾DNA可以被視作標點符號,，以幫助基因組實現(xiàn)編譯。”
在老鼠中,，同樣只有約4%的基因擁有編譯蛋白的功能,，剩余的垃圾DNA不斷重復且沒有可編譯的序列,?？茖W家分析了一個重復的基因序列SINE B2,，它位于生長激素基因位置處，這一基因和衰老及壽命有關,。結果小組驚訝的發(fā)現(xiàn)SINE B2對于形成功能區(qū)域分界線至關重要,。
功能區(qū)域含有各種管理信號以及對于激活或是壓制特定基因很關鍵的信息。每個域都通過邊界劃分為實體,，就類似于通過標點符號劃分句子和單詞,。科學家的結果顯示,，重復的基因序列或許在哺乳動物中被廣泛用于組織功能區(qū)域,。
Rosenfeld說，沒有邊界元件,，基因組的編碼部分如同沒有標點的段落,。破譯“垃圾”DNA中的信息為醫(yī)學研究特別是基因治療開辟了新的領域，有助于尋找一種向患者移植不含多余遺傳序列（可能會使基因治療失效）的基因的方法,。
原文鏈接：http://www.physorg.com/news103469449.html
原始出處:
Science 13 July 2007:
Vol. 317. no. 5835, pp. 248 - 251
DOI: 10.1126/science.1140871
Developmentally Regulated Activation of a SINE B2 Repeat as a Domain Boundary in Organogenesis
Victoria V. Lunyak,1,2* Gratien G. Prefontaine,1 Esperanza Núñez,1 Thorsten Cramer,5 Bong-Gun Ju,1 Kenneth A. Ohgi,1 Kasey Hutt,1 Rosa Roy,4 Angel García-Díaz,4 Xiaoyan Zhu,1 Yun Yung,1 Lluís Montoliu,4 Christopher K. Glass,3 Michael G. Rosenfeld1*
The temporal and spatial regulation of gene expression in mammalian development is linked to the establishment of functional chromatin domains. Here, we report that tissue-specific transcription of a retrotransposon repeat in the murine growth hormone locus is required for gene activation. This repeat serves as a boundary to block the influence of repressive chromatin modifications. The repeat element is able to generate short, overlapping Pol II–and Pol III–driven transcripts, both of which are necessary and sufficient to enable a restructuring of the regulated locus into nuclear compartments. These data suggest that transcription of interspersed repetitive sequences may represent a developmental strategy for the establishment of functionally distinct domains within the mammalian genome to control gene activation.
1 Howard Hughes Medical Institute, School of Medicine, University of California, San Diego, 9500 Gilman Drive, Room 345, La Jolla, CA 92093–0648, USA.
2 Department of Medicine, Division of Endocrinology, University of California, San Diego, La Jolla, CA 92093, USA.
3 Department of Cellular and Molecular Medicine, Department and School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
4 Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus de Cantoblanco, C/Darwin 3, 28049 Madrid, Spain.
5 Department of Hepatology and Gastroenterology, Charité Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany.
These authors contributed equally to this work.
* To whom correspondence should be addressed. E-mail: [email protected] (M.G.R.); [email protected] (V.V.L.)
