Francastel C, Walters M C, Groudine M, Martin D I
Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Cell. 1999 Oct 29;99(3):259-69. doi: 10.1016/s0092-8674(00)81657-8.
To explore the mechanism by which enhancers maintain gene expression, we have assessed the ability of an enhancer and derivative mutants to influence silencing and nuclear location of a transgene. Using site-specific recombination to place different constructs at the same integration sites, we find that disruption of core enhancer motifs impairs the enhancer's ability to suppress silencing. FISH analysis reveals that active transgenes linked to a functional enhancer localize away from centromeres. However, enhancer mutations that result in increased rates of transgene silencing fail to localize the transgene away from centromeric heterochromatin, even when the transgene is in an active state. These mutations thus dissociate transcriptional activity and subnuclear location. Together, our results suggest that the functional enhancer antagonizes gene silencing by preventing localization of a gene near centromeric heterochromatin.
为了探究增强子维持基因表达的机制,我们评估了一个增强子及其衍生突变体影响转基因沉默和核定位的能力。利用位点特异性重组将不同构建体置于相同整合位点,我们发现核心增强子基序的破坏会损害增强子抑制沉默的能力。荧光原位杂交(FISH)分析表明,与功能性增强子相连的活性转基因定位于远离着丝粒的位置。然而,导致转基因沉默率增加的增强子突变无法使转基因定位于远离着丝粒异染色质的位置,即使转基因处于活性状态。因此,这些突变使转录活性和亚核定位分离。我们的结果共同表明,功能性增强子通过阻止基因定位于着丝粒异染色质附近来拮抗基因沉默。