Enhancers stimulate transcription of several eukaryotic genes (for review see ref. 1). While some enhancers, like that of simian virus 40 (SV40), are active in a wide range of cell types, others are more cell-specific1. For example, the polyoma virus (Py) enhancer is not active in undifferentiated embryonal carcinoma (EC) cells, such as F9 cells, while it is active in differentiated cells2,3. In contrast, the SV40 enhancer is active in both undifferentiated and differentiated EC cells4. One possible explanation for this difference is that the two viral enhancers interact with different positively or negatively acting transcription factors, a notion supported by in vitro experiments showing that the Py enhancer interacts with proteins that do not bind to the SV40 enhancer5,6. Some viral7,8 and cellular9 enhancers, including the Py and SV40 enhancers, can be negatively regulated by the products of the E1A transcription unit of adenovirus-2. As it has been postulated that undifferentiated F9 cells contain an E1A-like activity10, it is possible that the latter is responsible for the lack of activity of the Py enhancer in these cells. We show here that the E1A products do not repress a point mutant of the Py enhancer (Py ECF9.1; ref. 11 and references therein) that is active in undifferentiated F9 cells3. This result is consistent with the idea that undifferentiated F9 cells contain a cellular represser that blocks the Py enhancer and that this represser has the same target sequence as the E1A proteins.
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A functionally inactive p53 protein interatocarcinoma cells is activated by either DNA damage or cellular differentiation
Nature Medicine (1996)
A point mutation in the last intron responsible for increased expression and transforming activity of the c-Ha-ras oncogene
Adenovirus E1A products suppress myogenic differentiation and inhibit transcription from muscle-specific promoters