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首页> 外文期刊>Genomics >A 178-kb BAC transgene imprints the mouse Gtl2 gene and localizes tissue-specific regulatory elements.
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A 178-kb BAC transgene imprints the mouse Gtl2 gene and localizes tissue-specific regulatory elements.

机译：178 kb BAC转基因印记小鼠Gtl2基因并定位组织特异性调控元件。

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摘要

The regulation of genomic imprinting, the allele-specific expression of an autosomal gene, is complex and poorly understood. Imprinted genes are organized in clusters, where cis-acting regulatory elements are believed to interact to control multiple genes. We have used BAC transgenesis in the mouse to begin to delineate the region of DNA required for proper expression and imprinting of the mouse Delta-like1 (Dlk1) and Gene-trap locus2 (Gtl2) imprinted genes. We demonstrate that the Gtl2 gene is expressed from a BAC transgene in mouse embryo and placenta only upon maternal inheritance, as is the endogenous Gtl2 gene. Gtl2 is therefore properly imprinted on the BAC in an ectopic chromosomal location and must carry with it all necessary imprinting regulatory elements. Furthermore, we show that the BAC Gtl2 gene is expressed at levels approaching those of the endogenous gene only in the brain of adult animals, not in other sites of endogenous expression such as the pituitary, adrenal, and skeletal muscle. These data localize the enhancer(s) for brain Gtl2 expression, but not those for other tissues, to the DNA contained within the BAC clone. As the Dlk1 gene is not expressed from the BAC in any tissues, it must require additional elements that are different from those necessary for Gtl2 expression. Our data refine the interval for future investigation of Gtl2 imprinting and provide evidence for distinct regulation of the linked Dlk1 and Gtl2 genes.
机译：基因组印迹的调控，常染色体基因的等位基因特异性表达，是复杂的，人们对此知之甚少。印迹基因以簇的形式组织，其中顺式作用调节元件据信相互作用以控制多个基因。我们已经在小鼠中使用BAC转基因来开始描述正确表达和印迹小鼠Delta-like1（Dlk1）和Gene-trap locus2（Gtl2）印迹基因所需的DNA区域。我们证明，Gtl2基因是从BAC转基因在小鼠胚胎和胎盘中表达的，只有在内源性Gtl2基因才是母亲的遗传。因此，Gtl2被正确地印在异位染色体位置的BAC上，并且必须带有所有必需的印记调控元件。此外，我们显示BAC Gtl2基因仅在成年动物的大脑中以接近内源基因的水平表达，而在其他内源性表达部位（例如垂体，肾上腺和骨骼肌）中表达。这些数据将用于大脑Gtl2表达的增强子（而不是用于其他组织的增强子）定位到BAC克隆中包含的DNA。由于Dlk1基因在任何组织中都不从BAC表达，因此它必须需要与Gtl2表达所必需的其他元件不同的元件。我们的数据完善了Gtl2印迹未来研究的时间间隔，并为链接的Dlk1和Gtl2基因的不同调控提供了证据。

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