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Development, Vol 107, Issue 4 945-956, Copyright © 1989 by Company of Biologists
JOURNAL ARTICLES |
TP Dooley, M Miranda, NC Jones and ML DePamphilis
Gene Regulation Laboratory, Imperial Cancer Research Fund, London, England.
Undifferentiated mouse embryonal carcinoma (EC) cells are capable of transactivating the adenovirus EIIa promoter in the absence of its normal transactivator, E1A protein, suggesting that EC cells contain an E1A-like activity. In an effort to identify where this activity appears during normal mouse development, mouse oocytes and preimplantation embryos were injected with plasmids containing the EIIa promoter coupled to various reporter genes. These expression vectors were fully active in human 293 cells where E1A is present, but were inactive in differentiated fibroblast cell lines unless cotransfected with the E1A gene. In mouse oocytes and preimplantation embryos, EIIa promoter activity in the absence of adenovirus E1A protein was equivalent to or greater than activity of the HSV thymidine kinase promoter coupled to a strong enhancer. Coinjection of the E1A gene failed to stimulate EIIa activity further, perhaps because c-myc protein, which has been reported to transactivate this promoter, was already present at high levels in mouse oocytes. Activation of the EIIa promoter in the absence of E1A was unique to mouse oocytes and preimplantation embryos because gene expression from an EIIa promoter introduced into transgenic mice was observed only in the adult ovary, and particularly in the oocytes. In addition, post-implantation transgenic embryos failed to express the E1A-activatable reporter gene, thereby indicating that expression from the EIIa promoter is restricted to the relatively undifferentiated stages of oogenesis and preimplantation development. These data suggest that cellular promoters of the class that can be transactivated by E1A may serve uniquely to initiate transcription of genes that are needed for preimplantation development.
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