Deacetylation of p53 induces autophagy by suppressing Bmf expression

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Deacetylation of p53 induces autophagy by suppressing Bmf expression

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Title: Deacetylation of p53 induces autophagy by suppressing Bmf expression
Author: Contreras, Amelia U.; Mebratu, Yohannes; Delgado, Monica; Montano, Gilbert; Hu, Chien-an A.; Ryter, Stefan W.; Choi, Augustine M.K.; Lin, Yuting; Xiang, Jialing; Chand, Hitendra; Tesfaigzi, Yohannes

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Citation: Contreras, A. U., Y. Mebratu, M. Delgado, G. Montano, C. A. Hu, S. W. Ryter, A. M. Choi, et al. 2013. “Deacetylation of p53 induces autophagy by suppressing Bmf expression.” The Journal of Cell Biology 201 (3): 427-437. doi:10.1083/jcb.201205064.
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Abstract: Interferon γ (IFN-γ)–induced cell death is mediated by the BH3-only domain protein, Bik, in a p53-independent manner. However, the effect of IFN-γ on p53 and how this affects autophagy have not been reported. The present study demonstrates that IFN-γ down-regulated expression of the BH3 domain-only protein, Bmf, in human and mouse airway epithelial cells in a p53-dependent manner. p53 also suppressed Bmf expression in response to other cell death–stimulating agents, including ultraviolet radiation and histone deacetylase inhibitors. IFN-γ did not affect Bmf messenger RNA half-life but increased nuclear p53 levels and the interaction of p53 with the Bmf promoter. IFN-γ–induced interaction of HDAC1 and p53 resulted in the deacetylation of p53 and suppression of Bmf expression independent of p53’s proline-rich domain. Suppression of Bmf facilitated IFN-γ–induced autophagy by reducing the interaction of Beclin-1 and Bcl-2. Furthermore, autophagy was prominent in cultured bmf−/− but not in bmf+/+ cells. Collectively, these observations show that deacetylation of p53 suppresses Bmf expression and facilitates autophagy.
Published Version: doi:10.1083/jcb.201205064
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