3 years ago

SUMO2/3 modification of activating transcription factor 5 (ATF5) controls its dynamic translocation at the centrosome.

Bin Wang, David Liu, Kathy Lengel, Kari Gaither, Henning Knipprath, Edward Liu, Dongmeng Qian, Ming Hu, Yidi Xu, Eugene Kim, Yunsheng Yuan
Activating transcription factor 5 (ATF5) is a member of the ATF/CREB family of transcription factors. ATF5 regulates stress responses and cell survival, proliferation, and differentiation and also plays a role in viral infections, cancer, diabetes, schizophrenia, and the olfactory system. Moreover, it was found to also have a critical, cell cycle-dependent structural function at the centrosome. However, the mechanism that controls ATF5's localization at the centrosome is unclear. Here, we report that ATF5 is SUMO2/3- modified at a conserved SUMO-targeting consensus site in various types of mammalian cells. We found that SUMOylation of ATF5 is elevated in the G1 phase of the cell cycle and diminished in the G2/M phase. ATF5 SUMOylation disrupted ATF5's interaction with several centrosomal proteins and dislodged ATF5 from the centrosome at the end of the M phase. Of note, blockade of ATF5 SUMOylation deregulated the centrosome cycle, impeded ATF5 translocation from the centrosome, and caused genomic instability and G2/M arrest in HeLa cells. Our results indicate that ATF5 SUMOylation is an essential mechanism that regulates ATF5 localization and function at the centrosome.

Publisher URL: http://doi.org/10.1074/jbc.RA117.001151

DOI: 10.1074/jbc.RA117.001151

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