Tau acetylates and stabilizes β-catenin thereby promoting cell survival.

Enjie Liu, Qiuzhi Zhou, Ao-Ji Xie, Xiaoguang Li, Mengzhu Li, Jinwang Ye, Shihong Li, Dan Ke, Qun Wang, Zhi-Peng Xu, Li Li, Ying Yang, Gong-Ping Liu, Xiao-Chuan Wang, Hong-Lian Li, Jian-Zhi Wang

EMBO reports 2020 Mar 04

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Overexpressing Tau counteracts apoptosis and increases dephosphorylated β-catenin levels, but the underlying mechanisms are elusive. Here, we show that Tau can directly and robustly acetylate β-catenin at K49 in a concentration-, time-, and pH-dependent manner. β-catenin K49 acetylation inhibits its phosphorylation and its ubiquitination-associated proteolysis, thus increasing β-catenin protein levels. K49 acetylation further promotes nuclear translocation and the transcriptional activity of β-catenin, and increases the expression of survival-promoting genes (bcl2 and survivin), counteracting apoptosis. Mutation of Tau's acetyltransferase domain or co-expressing non-acetylatable β-catenin-K49R prevents increased β-catenin signaling and abolishes the anti-apoptotic function of Tau. Our data reveal that Tau preserves β-catenin by acetylating K49, and upregulated β-catenin/survival signaling in turn mediates the anti-apoptotic effect of Tau. © 2020 The Authors.

Citation

Enjie Liu, Qiuzhi Zhou, Ao-Ji Xie, Xiaoguang Li, Mengzhu Li, Jinwang Ye, Shihong Li, Dan Ke, Qun Wang, Zhi-Peng Xu, Li Li, Ying Yang, Gong-Ping Liu, Xiao-Chuan Wang, Hong-Lian Li, Jian-Zhi Wang. Tau acetylates and stabilizes β-catenin thereby promoting cell survival. EMBO reports. 2020 Mar 04;21(3):e48328