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MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons
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| Zeitschriftentitel: | The Journal of Neuroscience |
|---|---|
| Personen und Körperschaften: | , , , , , , |
| In: | The Journal of Neuroscience, 32, 2012, 37, S. 12673-12683 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Society for Neuroscience
|
| Schlagwörter: |
| author_facet |
Li, Lei Wei, Dan Wang, Qiong Pan, Jing Liu, Rong Zhang, Xu Bao, Lan Li, Lei Wei, Dan Wang, Qiong Pan, Jing Liu, Rong Zhang, Xu Bao, Lan |
|---|---|
| author |
Li, Lei Wei, Dan Wang, Qiong Pan, Jing Liu, Rong Zhang, Xu Bao, Lan |
| spellingShingle |
Li, Lei Wei, Dan Wang, Qiong Pan, Jing Liu, Rong Zhang, Xu Bao, Lan The Journal of Neuroscience MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons General Neuroscience |
| author_sort |
li, lei |
| spelling |
Li, Lei Wei, Dan Wang, Qiong Pan, Jing Liu, Rong Zhang, Xu Bao, Lan 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.0016-12.2012 <jats:p>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 α-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 α-tubulin acetyltransferase that has been found to play a major role in the acetylation of α-tubulin in different species<jats:italic>in vivo</jats:italic>. 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 α-tubulin deacetylase HDAC6 or overexpression of tubulin<jats:sup>K40Q</jats:sup>to mimic acetylated α-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 α-tubulin, appears to control the migration and morphological transition of cortical neurons. This finding reveals the importance of MEC-17 and α-tubulin acetylation in cortical development.</jats:p> MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons The Journal of Neuroscience |
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Society for Neuroscience, 2012 |
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Society for Neuroscience, 2012 |
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0270-6474 1529-2401 |
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The Journal of Neuroscience |
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49 |
| title |
MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_unstemmed |
MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_full |
MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_fullStr |
MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_full_unstemmed |
MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_short |
MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_sort |
mec-17 deficiency leads to reduced α-tubulin acetylation and impaired migration of cortical neurons |
| topic |
General Neuroscience |
| url |
http://dx.doi.org/10.1523/jneurosci.0016-12.2012 |
| publishDate |
2012 |
| physical |
12673-12683 |
| description |
<jats:p>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 α-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 α-tubulin acetyltransferase that has been found to play a major role in the acetylation of α-tubulin in different species<jats:italic>in vivo</jats:italic>. 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 α-tubulin deacetylase HDAC6 or overexpression of tubulin<jats:sup>K40Q</jats:sup>to mimic acetylated α-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 α-tubulin, appears to control the migration and morphological transition of cortical neurons. This finding reveals the importance of MEC-17 and α-tubulin acetylation in cortical development.</jats:p> |
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| author | Li, Lei, Wei, Dan, Wang, Qiong, Pan, Jing, Liu, Rong, Zhang, Xu, Bao, Lan |
| author_facet | Li, Lei, Wei, Dan, Wang, Qiong, Pan, Jing, Liu, Rong, Zhang, Xu, Bao, Lan, Li, Lei, Wei, Dan, Wang, Qiong, Pan, Jing, Liu, Rong, Zhang, Xu, Bao, Lan |
| author_sort | li, lei |
| container_issue | 37 |
| container_start_page | 12673 |
| container_title | The Journal of Neuroscience |
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| description | <jats:p>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 α-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 α-tubulin acetyltransferase that has been found to play a major role in the acetylation of α-tubulin in different species<jats:italic>in vivo</jats:italic>. 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 α-tubulin deacetylase HDAC6 or overexpression of tubulin<jats:sup>K40Q</jats:sup>to mimic acetylated α-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 α-tubulin, appears to control the migration and morphological transition of cortical neurons. This finding reveals the importance of MEC-17 and α-tubulin acetylation in cortical development.</jats:p> |
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| imprint | Society for Neuroscience, 2012 |
| imprint_str_mv | Society for Neuroscience, 2012 |
| institution | DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229 |
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| publisher | Society for Neuroscience |
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| spelling | Li, Lei Wei, Dan Wang, Qiong Pan, Jing Liu, Rong Zhang, Xu Bao, Lan 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.0016-12.2012 <jats:p>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 α-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 α-tubulin acetyltransferase that has been found to play a major role in the acetylation of α-tubulin in different species<jats:italic>in vivo</jats:italic>. 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 α-tubulin deacetylase HDAC6 or overexpression of tubulin<jats:sup>K40Q</jats:sup>to mimic acetylated α-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 α-tubulin, appears to control the migration and morphological transition of cortical neurons. This finding reveals the importance of MEC-17 and α-tubulin acetylation in cortical development.</jats:p> MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons The Journal of Neuroscience |
| spellingShingle | Li, Lei, Wei, Dan, Wang, Qiong, Pan, Jing, Liu, Rong, Zhang, Xu, Bao, Lan, The Journal of Neuroscience, MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons, General Neuroscience |
| title | MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_full | MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_fullStr | MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_full_unstemmed | MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_short | MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| title_sort | mec-17 deficiency leads to reduced α-tubulin acetylation and impaired migration of cortical neurons |
| title_unstemmed | MEC-17 Deficiency Leads to Reduced α-Tubulin Acetylation and Impaired Migration of Cortical Neurons |
| topic | General Neuroscience |
| url | http://dx.doi.org/10.1523/jneurosci.0016-12.2012 |