MEC-17 Deficiency Leads to Reduced alpha-Tubulin Acetylation and Impaired Migration of Cortical Neurons | |
Li, L; Wei, D; Wang, Q; Pan, J; Liu, R; Zhang, X; Bao, L | |
刊名 | JOURNAL OF NEUROSCIENCE |
2012 | |
卷号 | 32期号:37页码:12673-12683 |
通讯作者 | Bao, L (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, State Key Lab Cell Biol, Shanghai 200031, Peoples R China.,baolan@sibs.ac.cn |
英文摘要 | Neuronal migration is a fundamental process during the development of the cerebral cortex and is regulated by cytoskeletal components. Microtubule dynamics can be modulated by posttranslational modifications to tubulin subunits. Acetylation of alpha-tubulin at lysine 40 is important in regulating microtubule properties, and this process is controlled by acetyltransferase and deacetylase. MEC-17 is a newly discovered alpha-tubulin acetyltransferase that has been found to play a major role in the acetylation of alpha-tubulin in different species in vivo. However, the physiological function of MEC-17 during neural development is largely unknown. Here, we report that MEC-17 is critical for the migration of cortical neurons in the rat. MEC-17 was strongly expressed in the cerebral cortex during development. MEC-17 deficiency caused migratory defects in the cortical projection neurons and interneurons, and perturbed the transition of projection neurons from the multipolar stage to the unipolar/bipolar stage in the intermediate zone of the cortex. Furthermore, knockdown of alpha-tubulin deacetylase HDAC6 or overexpression of tubulin(K40Q) to mimic acetylated alpha-tubulin could reduce the migratory and morphological defects caused by MEC-17 deficiency in cortical projection neurons. Thus, MEC-17, which regulates the acetylation of alpha-tubulin, appears to control the migration and morphological transition of cortical neurons. This finding reveals the importance of MEC-17 and alpha-tubulin acetylation in cortical development. |
学科主题 | Neurosciences & Neurology |
类目[WOS] | Neurosciences |
关键词[WOS] | RADIAL MIGRATION ; INTERNEURON MIGRATION ; CEREBRAL-CORTEX ; ACETYLTRANSFERASE ; DOUBLECORTIN ; NEOCORTEX ; MOTILITY ; PROTEIN ; HDAC6 ; NUCLEOKINESIS |
收录类别 | SCI |
语种 | 英语 |
WOS记录号 | WOS:000308805800004 |
内容类型 | 期刊论文 |
版本 | 出版稿 |
源URL | [http://202.127.25.143/handle/331003/693] |
专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
推荐引用方式 GB/T 7714 | Li, L,Wei, D,Wang, Q,et al. MEC-17 Deficiency Leads to Reduced alpha-Tubulin Acetylation and Impaired Migration of Cortical Neurons[J]. JOURNAL OF NEUROSCIENCE,2012,32(37):12673-12683. |
APA | Li, L.,Wei, D.,Wang, Q.,Pan, J.,Liu, R.,...&Bao, L.(2012).MEC-17 Deficiency Leads to Reduced alpha-Tubulin Acetylation and Impaired Migration of Cortical Neurons.JOURNAL OF NEUROSCIENCE,32(37),12673-12683. |
MLA | Li, L,et al."MEC-17 Deficiency Leads to Reduced alpha-Tubulin Acetylation and Impaired Migration of Cortical Neurons".JOURNAL OF NEUROSCIENCE 32.37(2012):12673-12683. |
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