title: Aurora B-dependent phosphorylation of Ataxin-10 promotes the interaction between Ataxin-10 and Plk1 in cytokinesis.
abstract: 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.
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Jie
authors: J
authors: Tian
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Chuan
authors: C
authors: Tian
authors: National Institute of Biological Sciences, Beijing 102206, China.
authors: Yuehe
authors: Y
authors: Ding
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Zhe
authors: Z
authors: Li
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Qizhi
authors: Q
authors: Geng
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Zhikai
authors: Z
authors: Xiahou
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Jue
authors: J
authors: Wang
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Wenya
authors: W
authors: Hou
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Ji
authors: J
authors: Liao
authors: National Institute of Biological Sciences, Beijing 102206, China.
authors: Meng-Qiu
authors: MQ
authors: Dong
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Xingzhi
authors: X
authors: Xu
authors: Beijing Key Laboratory of DNA Damage Response, College of Life Sciences, Capital Normal University, Beijing 100048, China.
authors: Jing
authors: J
authors: Li
mesh_terms: D019943:Amino Acid Substitution; D000067736:Ataxin-10 / Q000235:genetics / Q000378:metabolism*; D064107:Aurora Kinase B / Q000235:genetics / Q000378:metabolism*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D048749:Cytokinesis / Q000502:physiology*; D006367:HeLa Cells; D006801:Humans; D020125:Mutation, Missense; D010766:Phosphorylation / Q000502:physiology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D000097869:Polo-Like Kinase 1
chemical_list: D000067736:Ataxin-10; D064107:Aurora Kinase B; D018797:Cell Cycle Proteins; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D000097869:Polo-Like Kinase 1; C503889:ATXN10 protein, human; C576921:AURKB protein, human