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Although copper plays a critical role in the embryonic development and differentiation of mammals, the mo- lecular mechanism(s) by which copper deficiency during development leads to embryonic defects has not been sufficiently investigated. In this study, we have focused on the roles of copper in neurogenesis, using mouse embryo- nal carcinoma P19 cells as a model of neuronal differentiation. In morphological and immunofluorescence studies, we observed that the retinoic acid (RA)-induced neuronal differentiation of P19 cells was suppressed in copper- deficient conditions using a non-permeable copper chelator, BCS. Consistent with this result, minimum amounts of the neuron-specific marker dopamine β-hydroxylase and choline acetyltransferase mRNA were induced in the cop- per-deficit P19 cells. Furthermore, copper deficiency in P19 cells could suppress the activation of RA receptor (RAR) target genes, such as RARβ2 and cellular retinol binding protein 1 and p21waf1/cip1, and RA response element- driven reporter expression by RA. Consequently, our results indicate that intracellular copper is involved in RAR- dependent transcription, which may contribute to explaining the defect of neuronal differentiation in copper-deficit P19 cells.

Copper is Required for Retinoic Acid Receptor-Dependent Transcription and Neuronal Differentiation in P19 Embryonal Carcinoma Cells