Further studies about Coactosin-like protein-1 affecting the migration of mouse neocortical neurons
Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protei...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Liu, Mengmeng [verfasserIn] Li, Guohong [verfasserIn] Wang, Mengli [verfasserIn] Cheng, Xinran [verfasserIn] Huang, Yinxue [verfasserIn] Xu, Mingrui [verfasserIn] Li, Kaikai [verfasserIn] Chen, Jiong [verfasserIn] Zhu, Xiaoyan [verfasserIn] Zhao, Shanting [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: The histochemical journal - Dordrecht [u.a.] : Springer Science + Business Media B.V., 1968, 49(2018), 5 vom: 20. Aug., Seite 519-530 |
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| Übergeordnetes Werk: |
volume:49 ; year:2018 ; number:5 ; day:20 ; month:08 ; pages:519-530 |
| Links: |
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| DOI / URN: |
10.1007/s10735-018-9790-3 |
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| Katalog-ID: |
SPR012837814 |
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| 520 | |a Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. | ||
| 650 | 4 | |a Coactosin-like protein 1 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Neuronal migration |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a F-actin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a In utero electroporation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Mitotic activity |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Li, Guohong |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Mengli |e verfasserin |4 aut | |
| 700 | 1 | |a Cheng, Xinran |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Yinxue |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Mingrui |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Kaikai |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Jiong |e verfasserin |4 aut | |
| 700 | 1 | |a Zhu, Xiaoyan |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Shanting |e verfasserin |4 aut | |
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10.1007/s10735-018-9790-3 doi (DE-627)SPR012837814 (SPR)s10735-018-9790-3-e DE-627 ger DE-627 rakwb eng 540 610 ASE 44.35 bkl 42.15 bkl Liu, Mengmeng verfasserin aut Further studies about Coactosin-like protein-1 affecting the migration of mouse neocortical neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. Coactosin-like protein 1 (dpeaa)DE-He213 Neuronal migration (dpeaa)DE-He213 F-actin (dpeaa)DE-He213 In utero electroporation (dpeaa)DE-He213 Mitotic activity (dpeaa)DE-He213 Li, Guohong verfasserin aut Wang, Mengli verfasserin aut Cheng, Xinran verfasserin aut Huang, Yinxue verfasserin aut Xu, Mingrui verfasserin aut Li, Kaikai verfasserin aut Chen, Jiong verfasserin aut Zhu, Xiaoyan verfasserin aut Zhao, Shanting verfasserin aut Enthalten in The histochemical journal Dordrecht [u.a.] : Springer Science + Business Media B.V., 1968 49(2018), 5 vom: 20. Aug., Seite 519-530 (DE-627)503327638 (DE-600)2210318-1 1573-6865 nnns volume:49 year:2018 number:5 day:20 month:08 pages:519-530 https://dx.doi.org/10.1007/s10735-018-9790-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 44.35 ASE 42.15 ASE AR 49 2018 5 20 08 519-530 |
| spelling |
10.1007/s10735-018-9790-3 doi (DE-627)SPR012837814 (SPR)s10735-018-9790-3-e DE-627 ger DE-627 rakwb eng 540 610 ASE 44.35 bkl 42.15 bkl Liu, Mengmeng verfasserin aut Further studies about Coactosin-like protein-1 affecting the migration of mouse neocortical neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. Coactosin-like protein 1 (dpeaa)DE-He213 Neuronal migration (dpeaa)DE-He213 F-actin (dpeaa)DE-He213 In utero electroporation (dpeaa)DE-He213 Mitotic activity (dpeaa)DE-He213 Li, Guohong verfasserin aut Wang, Mengli verfasserin aut Cheng, Xinran verfasserin aut Huang, Yinxue verfasserin aut Xu, Mingrui verfasserin aut Li, Kaikai verfasserin aut Chen, Jiong verfasserin aut Zhu, Xiaoyan verfasserin aut Zhao, Shanting verfasserin aut Enthalten in The histochemical journal Dordrecht [u.a.] : Springer Science + Business Media B.V., 1968 49(2018), 5 vom: 20. Aug., Seite 519-530 (DE-627)503327638 (DE-600)2210318-1 1573-6865 nnns volume:49 year:2018 number:5 day:20 month:08 pages:519-530 https://dx.doi.org/10.1007/s10735-018-9790-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 44.35 ASE 42.15 ASE AR 49 2018 5 20 08 519-530 |
| allfields_unstemmed |
10.1007/s10735-018-9790-3 doi (DE-627)SPR012837814 (SPR)s10735-018-9790-3-e DE-627 ger DE-627 rakwb eng 540 610 ASE 44.35 bkl 42.15 bkl Liu, Mengmeng verfasserin aut Further studies about Coactosin-like protein-1 affecting the migration of mouse neocortical neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. Coactosin-like protein 1 (dpeaa)DE-He213 Neuronal migration (dpeaa)DE-He213 F-actin (dpeaa)DE-He213 In utero electroporation (dpeaa)DE-He213 Mitotic activity (dpeaa)DE-He213 Li, Guohong verfasserin aut Wang, Mengli verfasserin aut Cheng, Xinran verfasserin aut Huang, Yinxue verfasserin aut Xu, Mingrui verfasserin aut Li, Kaikai verfasserin aut Chen, Jiong verfasserin aut Zhu, Xiaoyan verfasserin aut Zhao, Shanting verfasserin aut Enthalten in The histochemical journal Dordrecht [u.a.] : Springer Science + Business Media B.V., 1968 49(2018), 5 vom: 20. Aug., Seite 519-530 (DE-627)503327638 (DE-600)2210318-1 1573-6865 nnns volume:49 year:2018 number:5 day:20 month:08 pages:519-530 https://dx.doi.org/10.1007/s10735-018-9790-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 44.35 ASE 42.15 ASE AR 49 2018 5 20 08 519-530 |
| allfieldsGer |
10.1007/s10735-018-9790-3 doi (DE-627)SPR012837814 (SPR)s10735-018-9790-3-e DE-627 ger DE-627 rakwb eng 540 610 ASE 44.35 bkl 42.15 bkl Liu, Mengmeng verfasserin aut Further studies about Coactosin-like protein-1 affecting the migration of mouse neocortical neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. Coactosin-like protein 1 (dpeaa)DE-He213 Neuronal migration (dpeaa)DE-He213 F-actin (dpeaa)DE-He213 In utero electroporation (dpeaa)DE-He213 Mitotic activity (dpeaa)DE-He213 Li, Guohong verfasserin aut Wang, Mengli verfasserin aut Cheng, Xinran verfasserin aut Huang, Yinxue verfasserin aut Xu, Mingrui verfasserin aut Li, Kaikai verfasserin aut Chen, Jiong verfasserin aut Zhu, Xiaoyan verfasserin aut Zhao, Shanting verfasserin aut Enthalten in The histochemical journal Dordrecht [u.a.] : Springer Science + Business Media B.V., 1968 49(2018), 5 vom: 20. Aug., Seite 519-530 (DE-627)503327638 (DE-600)2210318-1 1573-6865 nnns volume:49 year:2018 number:5 day:20 month:08 pages:519-530 https://dx.doi.org/10.1007/s10735-018-9790-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 44.35 ASE 42.15 ASE AR 49 2018 5 20 08 519-530 |
| allfieldsSound |
10.1007/s10735-018-9790-3 doi (DE-627)SPR012837814 (SPR)s10735-018-9790-3-e DE-627 ger DE-627 rakwb eng 540 610 ASE 44.35 bkl 42.15 bkl Liu, Mengmeng verfasserin aut Further studies about Coactosin-like protein-1 affecting the migration of mouse neocortical neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. Coactosin-like protein 1 (dpeaa)DE-He213 Neuronal migration (dpeaa)DE-He213 F-actin (dpeaa)DE-He213 In utero electroporation (dpeaa)DE-He213 Mitotic activity (dpeaa)DE-He213 Li, Guohong verfasserin aut Wang, Mengli verfasserin aut Cheng, Xinran verfasserin aut Huang, Yinxue verfasserin aut Xu, Mingrui verfasserin aut Li, Kaikai verfasserin aut Chen, Jiong verfasserin aut Zhu, Xiaoyan verfasserin aut Zhao, Shanting verfasserin aut Enthalten in The histochemical journal Dordrecht [u.a.] : Springer Science + Business Media B.V., 1968 49(2018), 5 vom: 20. Aug., Seite 519-530 (DE-627)503327638 (DE-600)2210318-1 1573-6865 nnns volume:49 year:2018 number:5 day:20 month:08 pages:519-530 https://dx.doi.org/10.1007/s10735-018-9790-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 44.35 ASE 42.15 ASE AR 49 2018 5 20 08 519-530 |
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English |
| source |
Enthalten in The histochemical journal 49(2018), 5 vom: 20. Aug., Seite 519-530 volume:49 year:2018 number:5 day:20 month:08 pages:519-530 |
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Enthalten in The histochemical journal 49(2018), 5 vom: 20. Aug., Seite 519-530 volume:49 year:2018 number:5 day:20 month:08 pages:519-530 |
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Coactosin-like protein 1 Neuronal migration F-actin In utero electroporation Mitotic activity |
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Liu, Mengmeng @@aut@@ Li, Guohong @@aut@@ Wang, Mengli @@aut@@ Cheng, Xinran @@aut@@ Huang, Yinxue @@aut@@ Xu, Mingrui @@aut@@ Li, Kaikai @@aut@@ Chen, Jiong @@aut@@ Zhu, Xiaoyan @@aut@@ Zhao, Shanting @@aut@@ |
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Further studies about Coactosin-like protein-1 affecting the migration of mouse neocortical neurons |
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Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. |
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Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. |
| abstract_unstemmed |
Abstract During the development of mammalian cortex, late neurons generated by neuronal progenitors bypass earlier-born neurons and migrate to reach upper layers of cortical plate in an inner-to-outer fashion. Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. Therefore, These results demonstrated that Cotl1 played an important role in mouse neocortical development. |
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Filamentous-actin (F-actin) can regulate neuronal migration, whereas Coactosin-like protein 1 (Cotl1) modulates F-actin. Lys 75 and Arg 73 of Cotl1 play an important role in binding F-actin; when they are mutated to Glu, Cotl1 cannot bind F-actin, called as a non-actin-binding mutant (ABM). The Lys 131 site of Cotl1, the 5-Lipoxygenase (5LO) binding site, is spatially close to Lys 75, leading to impact the binding of Cotl1 to F-actin. When Lys 131 is mutated to Ala (K131A), Cotl1 cannot bind to 5LO. We have demonstrated that overexpression of Cotl1 inhibited neuronal migration and increased the length of neuronal leading processes. To further explore cellular and molecular mechanisms of Cotl1’s effect on neuronal migration, we constructed two mutant vectors—Cotl1-ABM and Cotl1-K131A and studied using in utero electroporation and primary neuronal culture technique. Results indicated that in the Cotl1-ABM group, the neuronal migration and length of the leading process both recovered as control neurons at the postnatal day 1 (P1), while in the Cotl1-K131A group, numerous neurons remained in deeper layers of cortical plate or intermediate zone. However, at P7, most Cotl1-K131A transfected neurons reached their destination. Moreover, we found that overexpression of Cotl1 inhibited the proliferation and mitotic activity of NPs. 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