Hancock R L
Canadian Institute of Theoretical Biology, Scott's Bay, Nova Scotia.
Med Hypotheses. 1991 Sep;36(1):65-8. doi: 10.1016/0306-9877(91)90165-u.
A previous rendition of a mechanism for the induction of embryonic gene activity, derived from the viewpoint of agents capable of such inductions, concluded that a perturbed methylation pattern of DNA and/or chromatin proteins would be an essential feature. A more specific treatment of the mechanism centers on enhancer regions of proto-oncogenes as being the point of modification for any induction of new gene activity. DNA binding type proteins may be involved with deheterochromatization processes after complexing near long terminal repeat segments containing enhancer elements. Chemical carcinogens and steroids would modify the chromatin and directly or indirectly interfere with maintenance DNA methylation. The resulting hypomethylated enhancer and promoter regions would allow for enhancer mechanisms to activate repressed embryonic genes inappropriate to the developmental stage forcing embryonic features to be expressed by differentiating (or differentiated) cells.
从能够进行此类诱导的因子的角度推导出来的、关于胚胎基因活性诱导机制的先前版本得出结论，即DNA和/或染色质蛋白的甲基化模式紊乱将是一个基本特征。对该机制更具体的探讨集中在原癌基因的增强子区域，认为这是任何新基因活性诱导的修饰点。DNA结合型蛋白可能在与含有增强子元件的长末端重复序列片段附近结合后参与去异染色质化过程。化学致癌物和类固醇会修饰染色质，并直接或间接干扰维持性DNA甲基化。由此产生的低甲基化增强子和启动子区域将使增强子机制能够激活与发育阶段不相符的受抑制胚胎基因，迫使分化（或已分化）细胞表达胚胎特征。
