2012年10月12日 訊 /生物谷BIOON/ --近日,，刊登在國(guó)際著名雜志PNAS上的一篇研究報(bào)告中,，來(lái)自麥吉爾大學(xué)的研究者揭示了人類(lèi)大腦DNA和動(dòng)物大腦DNA在對(duì)早期生命多樣性反應(yīng)上出現(xiàn)的驚人的相似性，這也就表明,，對(duì)早期生命多樣性的進(jìn)化保守機(jī)制效應(yīng)可以影響基因組中的一系列基因,，文章強(qiáng)調(diào)了兒童期社會(huì)環(huán)境的重要性，并且也揭示了兒童逆境對(duì)于DNA的影響是可程序化的,。
在這項(xiàng)研究中，研究者檢測(cè)了濫用藥物兒童和對(duì)照組兒童大腦海馬體區(qū)域甲基化DNA的差異性,，DNA甲基化的和其早期經(jīng)歷直接相關(guān),。人類(lèi)的早期生活經(jīng)歷，尤其是社會(huì)經(jīng)驗(yàn),，可以對(duì)未來(lái)其身心健康產(chǎn)生深遠(yuǎn)的影響,。目前，研究者并不知道這些早期的逆境或經(jīng)歷是如何在生物學(xué)上影響機(jī)體的發(fā)育的,。
此前的研究揭示了早期生活經(jīng)歷可以對(duì)個(gè)體的健康產(chǎn)生深遠(yuǎn)的影響,，也就是說(shuō)引起健康影響的一系列基因在早期生活經(jīng)歷中都已經(jīng)被不斷修飾過(guò)了。
這項(xiàng)研究揭示了,，將社會(huì)經(jīng)驗(yàn)嵌合入大腦DNA中可以影響不僅僅一些基因,，而是影響整個(gè)基因組網(wǎng)絡(luò)的基因。研究者Syzf說(shuō),，我們的研究揭示了兒童期社會(huì)環(huán)境對(duì)機(jī)體健康的重要性,，如今通過(guò)我們的研究就可以理解如何預(yù)防并且治療個(gè)體的身心疾病。（生物谷Bioon.com）
編譯自：Evidence of biological process that embeds social experience in DNA that affects entire networks of genes
doi:10.1073/pnas.1121260109
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Conserved epigenetic sensitivity to early life experience in the rat and human hippocampus
Matthew Sudermana,b,c,1, Patrick O. McGowand,1, Aya Sasakid,1, Tony C. T. Huangb, Michael T. Hallettc, Michael J. Meaneya,e,f,g, Gustavo Tureckie, and Moshe Szyfa,b,g,2
Early life experience is associated with long-term effects on behavior and epigenetic programming of the NR3C1 (GLUCOCORTICOID RECEPTOR) gene in the hippocampus of both rats and humans. However, it is unlikely that such effects completely capture the evolutionarily conserved epigenetic mechanisms of early adaptation to environment. Here we present DNA methylation profiles spanning 6.5 million base pairs centered at the NR3C1 gene in the hippocampus of humans who experienced abuse as children and nonabused controls. We compare these profiles to corresponding DNA methylation profiles in rats that received differential levels of maternal care. The profiles of both species reveal hundreds of DNA methylation differences associated with early life experience distributed across the entire region in nonrandom patterns. For instance, methylation differences tend to cluster by genomic location, forming clusters covering as many as 1 million bases. Even more surprisingly, these differences seem to specifically target regulatory regions such as gene promoters, particularly those of the protocadherin α, β, and γ gene families. Beyond these high-level similarities, more detailed analyses reveal methylation differences likely stemming from the significant biological and environmental differences between species. These results provide support for an analogous cross-species epigenetic regulatory response at the level of the genomic region to early life experience.
