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Light exposure promotes COP1 export from the nucleus, preventing COP1-mediated degradation of transcription factors that regulate light-mediated development (photomorphogenesis). We report that, similar to its regulation in plants, mammalian COP1 localization is modulated by environment signals. Inactivation of a key mitogen-activated protein kinase (MAPK) signaling pathway (e.g., via exposure to anthrax lethal toxin) induces the rapid transit of COP1 from the nuclear envelope to the nucleoplasm. 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