Septin 14 is involved in cortical neuronal migration via interaction with Septin 4.
Septin 14 is involved in cortical neuronal migration via interaction with Septin 4.
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DOI:
10.1091/mbc.e09-10-0869
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发表时间:
2010-04-15
影响因子:
3.3
通讯作者:
Nagata K
中科院分区:
文献类型:
--
作者:
Shinoda T;Ito H;Sudo K;Iwamoto I;Morishita R;Nagata K
Septins are a family of conserved GTP/GDP-binding proteins implicated in a variety of cellular functions. We found that knockdown of Septin 14 or Septin 4 resulted in inhibition of cortical neuronal migration and defective leading process formation. These results suggest a novel function of septin in cortical development. Septins are a family of conserved guanosine triphosphate/guanosine diphosphate-binding proteins implicated in a variety of cellular functions such as cell cycle control and cytokinesis. Although several members of septin family, including Septin 14 (Sept14), are abundantly expressed in nervous tissues, little is known about their physiological functions, especially in neuronal development. Here, we report that Sept14 is strongly expressed in the cortical plate of developing cerebral cortex. Knockdown experiments by using the method of in utero electroporation showed that reduction of Sept14 caused inhibition of cortical neuronal migration. Whereas cDNA encoding RNA interference-resistant Sept14 rescued the migration defect, the C-terminal deletion mutant of Sept14 did not. Biochemical analyses revealed that C-terminal coiled-coil region of Sept14 interacts with Septin 4 (Sept4). Knockdown experiments showed that Sept4 is also involved in cortical neuronal migration in vivo. In addition, knockdown of Sept14 or Sept4 inhibited leading process formation in migrating cortical neurons. These results suggest that Sept14 is involved in neuronal migration in cerebral cortex via interaction with Sept4.
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影响因子:
2.7
作者:
Ito, H;Kamei, K;Kato, K
通讯作者:
Kato, K
DOI:
10.1016/j.bbrc.2005.03.132
发表时间:
2005-05-27
影响因子:
3.1
作者:
Kawauchi, T;Chihama, K;Hoshino, M
通讯作者:
Hoshino, M
影响因子:
3.5
作者:
Hanai, N;Nagata, K;Inagaki, M
通讯作者:
Inagaki, M
影响因子:
16.2
作者:
Fox, JW;Lamperti, ED;Walsh, CA
通讯作者:
Walsh, CA
影响因子:
3.3
作者:
Kremer, BE;Haystead, T;Macara, IG
通讯作者:
Macara, IG