Hancock R L
Departamento de Investigacion Cientifica, Facultad de Medicina, Universidad Autonoma de Tamaulipas, Mexico.
Med Hypotheses. 1989 Nov;30(3):187-94. doi: 10.1016/0306-9877(89)90060-1.
Embryonic gene enhancers may be controlled by deheterochromatization of genes of trans-acting factors caused by altered methylation states of hypersensitive chromatin. Such specific chromatin sites would have a certain required helical pitch (X-type DNA). Non-core regions surrounding the enhancer motif would allow interactions with specific cell type promoters. Differences in embryonic and adult type genes may be reduced to these enhancer activities and certain trans-acting proteins effecting these genic control elements. Furthermore all spurious embryonic gene activities of neoplasms may also be due to such factors. Even pleotrophic and cascade phenomena in dysdifferentiation processes may be described in terms of enhancer mechanisms. Duplications of enhancer sequences may be fundamental to the potential of hyperactivity by embryonic type genes. Examples of this would be alpha-fetoprotein correlations with enhancer activity and possibly increased nucleolar organizer activity of embryonic cells. The manner by which chemical carcinogens would be involved with enhancer processes would be via "key" mechanisms that have been presented previously.
胚胎基因增强子可能受由超敏染色质甲基化状态改变引起的反式作用因子基因去异染色质化的控制。此类特定染色质位点会具有一定所需的螺旋间距（X型DNA）。增强子基序周围的非核心区域会允许与特定细胞类型启动子相互作用。胚胎型和成体型基因的差异可能归结为这些增强子活性以及影响这些基因控制元件的某些反式作用蛋白。此外，肿瘤所有虚假的胚胎基因活性也可能归因于此类因素。甚至分化异常过程中的多效性和级联现象也可用增强子机制来描述。增强子序列的重复可能是胚胎型基因过度活跃潜能的基础。这方面的例子包括甲胎蛋白与增强子活性的相关性以及胚胎细胞可能增强的核仁组织区活性。化学致癌物参与增强子过程的方式将通过先前提出的“关键”机制。
