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K259-SUMOylation of DGCR8 promoted by p14ARF exerts a tumor-suppressive function Free
Changhong Zhu1,2,†, Cheng Chen2,†, Ran Chen2,†, Rong Deng2, Xian Zhao2, Hailong Zhang2, Jinzhuo Duo2, Qin Chen2, Hui Jin2, Yanli Wang2, Jian Huang2, Ming Xu1,2,*, and Jianxiu Yu1,2,3,*
1 Institute of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, 280 Mohe Road, Shanghai 201999, China
2 Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory of Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China
3 State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China *Correspondence to:Jianxiu Yu, E-mail: Jianxiu.Yu@gmail.com; Ming Xu, E-mail: mingxu.msu@gmail.com
J Mol Cell Biol, Volume 8, Issue 5, October 2016, 456-458,  https://doi.org/10.1093/jmcb/mjw030

DGCR8 is essential for the miRNA biogenesis (Han et al., 2004, 2006; Quick-Cleveland et al., 2014). We recently reported that at K707-SUMOylation of DGCR8 influences its affinity with pri-miRNAs and controls the direct functions of pri-miRNAs in gene silencing. However, the K707R mutation does not remove all SUMO1 modifications of DGCR8 (Zhu et al., 2015), suggesting that DGCR8 bears other SUMOylation sites. Here, we identified K259 as an alternative site for DGCR8 SUMOylation that was directly promoted by p14ARF in the nucleus. We also demonstrated a notable role of K259-SUMOylation in preventing DGCR8 nuclear export that is required for its function in the processing of pri-miRNAs into pre-miRNAs and tumor suppression.