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Open AccessArticle

RhoA-GTPase Modulates Neurite Outgrowth by Regulating the Expression of Spastin and p60-Katanin

by Dandan Tan 1,2,3, Haowen Zhang 1,2, Junyao Deng 1,2, Jingmin Liu 1,2, Jinkun Wen 1,2, Lixia Li 1,2, Xianghai Wang 1,2,4, Mengjie Pan 1,2, Xiaofang Hu 1,2 and Jiasong Guo 1,2,4,5,*
1
Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Southern Medical University, Guangzhou 510515, China
2
Department of Histology and Embryology, Southern Medical University, Guangzhou 510515, China
3
Department of Human Anatomy, Guangdong Medical University, Zhanjiang 524023, China
4
Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou 510515, China
5
Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Guangzhou 510515, China
*
Author to whom correspondence should be addressed.
Cells 2020, 9(1), 230; https://doi.org/10.3390/cells9010230 (registering DOI)
Received: 18 November 2019 / Revised: 10 January 2020 / Accepted: 14 January 2020 / Published: 16 January 2020
(This article belongs to the Section Cell Signaling and Regulated Cell Death)
RhoA-GTPase (RhoA) is widely regarded as a key molecular switch to inhibit neurite outgrowth by rigidifying the actin cytoskeleton. However, during neurite outgrowth, whether and how microtubule dynamics are regulated by RhoA remains to be elucidated. Herein, CT04 and Y27632 were used to inactivate RhoA and its downstream effector Rho-associated coiled coil-forming kinase (ROCK), while the RhoAQ63L lentiviral vector was utilized to overexpress the constitutively activated RhoA in dorsal root ganglion (DRG) neurons or neuronal differentiated PC12 cells. The current data illustrate that the RhoA signaling pathway negatively modulates neurite outgrowth and elevates the expression of Glu-tubulin (a marker for a stabilized microtubule). Meanwhile, the microtubule-severing proteins spastin and p60-katanin were downregulated by the RhoA signaling pathway. When spastin and p60-katanin were knocked down, the effects of RhoA inhibition on neurite outgrowth were significantly reversed. Taken together, this study demonstrates that the RhoA pathway-mediated inhibition of neurite outgrowth is not only related to the modulation of microfilament dynamics but is also attributable to the regulation of the expression of spastin and p60-katanin and thus influences microtubule dynamics.
Keywords: neurite outgrowth; RhoA signaling pathway; spastin; p60-katanin; microtubule-severing proteins; Glu-tubulin neurite outgrowth; RhoA signaling pathway; spastin; p60-katanin; microtubule-severing proteins; Glu-tubulin
MDPI and ACS Style

Tan, D.; Zhang, H.; Deng, J.; Liu, J.; Wen, J.; Li, L.; Wang, X.; Pan, M.; Hu, X.; Guo, J. RhoA-GTPase Modulates Neurite Outgrowth by Regulating the Expression of Spastin and p60-Katanin. Cells 2020, 9, 230.

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