The underlying mechanism of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced alterations during development is thought to be mediated by a cytosolic aryl hydrocarbon receptor (Ahr). The specific role of Ahr-mediated changes in gene expression during embryonic development has not been elucidated. Recently, we reported that TCDD directly affects preimplantation embryo development in vitro, by accelerating differentiation of the blastocyst. In the work reported here, we provide evidence which suggests that Ahr mRNA and protein are present in mouse preimplantation embryos. Our results suggest that the embryo transcribes, rather than maternally - inherits Ahr mRNA. In addition, culturing embryos in medium with an Ahr antisense oligodeoxynucleotide resulted in a significantly lower incidence of blastocyst formation as well as mean embryo cell number. Results from this work suggest that Ahr may function in embryonic cell differentiation and proliferation independent of its known function in mediating TCDD toxicity in other systems.
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