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SNX17 Recruits USP9X to Antagonize MIB1-Mediated Ubiquitination and Degradation of PCM1 during Serum-Starvation-Induced Ciliogenesis

by Pengtao Wang 1,2,3,4, Jianhong Xia 2,3, Leilei Zhang 2,3, Shaoyang Zhao 2,3, Shengbiao Li 2,3, Haiyun Wang 2,3, Shan Cheng 4, Heying Li 2,3, Wenguang Yin 2,3, Duanqing Pei 2,3,5,* and Xiaodong Shu 2,3,4,5,6,*
1
School of Life Sciences, University of Science and Technology of China, Hefei 230027, China
2
CAS Key Laboratory of Regenerative Biology, South China Institutes for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China
3
Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, Guangzhou 510530, China
4
Hefei Institute of Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China
5
Guangzhou Regenerative Medicine and Health Guangdong Laboratory (GRMH-GDL), Guangzhou 510005, China
6
Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou Medical University, Guangzhou 511436, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Tomer Avidor-Reiss
Cells 2019, 8(11), 1335; https://doi.org/10.3390/cells8111335
Received: 13 September 2019 / Revised: 15 October 2019 / Accepted: 27 October 2019 / Published: 29 October 2019
(This article belongs to the Section Organelle Function)
Centriolar satellites are non-membrane cytoplasmic granules that deliver proteins to centrosome during centrosome biogenesis and ciliogenesis. Centriolar satellites are highly dynamic during cell cycle or ciliogenesis and how they are regulated remains largely unknown. We report here that sorting nexin 17 (SNX17) regulates the homeostasis of a subset of centriolar satellite proteins including PCM1, CEP131, and OFD1 during serum-starvation-induced ciliogenesis. Mechanistically, SNX17 recruits the deubiquitinating enzyme USP9X to antagonize the mindbomb 1 (MIB1)-induced ubiquitination and degradation of PCM1. SNX17 deficiency leads to enhanced degradation of USP9X as well as PCM1 and disrupts ciliogenesis upon serum starvation. On the other hand, SNX17 is dispensable for the homeostasis of PCM1 and USP9X in serum-containing media. These findings reveal a SNX17/USP9X mediated pathway essential for the homeostasis of centriolar satellites under serum starvation, and provide insight into the mechanism of USP9X in ciliogenesis, which may lead to a better understating of USP9X-deficiency-related human diseases such as X-linked mental retardation and neurodegenerative diseases. View Full-Text
Keywords: SNX17; USP9X; PCM1; MIB1; centriolar satellite; cilia SNX17; USP9X; PCM1; MIB1; centriolar satellite; cilia
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MDPI and ACS Style

Wang, P.; Xia, J.; Zhang, L.; Zhao, S.; Li, S.; Wang, H.; Cheng, S.; Li, H.; Yin, W.; Pei, D.; Shu, X. SNX17 Recruits USP9X to Antagonize MIB1-Mediated Ubiquitination and Degradation of PCM1 during Serum-Starvation-Induced Ciliogenesis. Cells 2019, 8, 1335.

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