Aurora B-dependent phosphorylation of Ataxin-10 promotes the interaction between Ataxin-10 and Plk1 in cytokinesis

作者：Tian, Jie; Tian, Chuan; Ding, Yuehe; Li, Zhe; Geng, Qizhi; Xiahou, Zhikai; Wang, Jue; Hou, Wenya; Liao, Ji; Dong, Meng-Qiu; Xu, Xingzhi^*; Li, Jing

来源：Scientific Reports, 2015, 5(1): 8360.

DOI：10.1038/srep08360

• KINASE 1
• PROTEIN
• TYPE-10
• COMPLEX
• IDENTIFICATION
• TRANSFERASE
• SUBUNIT
• MITOSIS
• REPEAT
• CANCER

Spinocerebellar ataxia type 10 (SCA10) is an autosomal dominant neurologic disorder caused by ATTCT expansion in the ATXN10 gene. Previous investigations have identified that depletion of Ataxin-10, the gene product, leads to cellular apoptosis and cytokinesis failure. Herein we identify the mitotic kinase Aurora B as an Ataxin-10 interacting partner. Aurora B interacts with and phosphorylates Ataxin-10 at S12, as evidenced by in vitro kinase and mass spectrometry analysis. Both endogenous and S12-phosphorylated Ataxin-10 localizes to the midbody during cytokinesis, and cytokinetic defects induced by inhibition of ATXN10 expression is not rescued by the S12A mutant. Inhibition of Aurora B or expression of the S12A mutant renders reduced interaction between Ataxin-10 and polo-like kinase 1 (Plk1), a kinase previously identified to regulate Ataxin-10 in cytokinesis. Taken together, we propose a model that Aurora B phosphorylates Ataxin-10 at S12 to promote the interaction between Ataxin-10 and Plk1 in cytokinesis. These findings identify an Aurora B-dependent mechanism that implicates Ataxin-10 in cytokinesis.

• 出版日期2015-2-10
• 单位北京生命科学研究所; 首都师范大学