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NudC regulates actin dynamics and ciliogenesis by stabilizing cofilin 1
Emerging data indicate that actin dynamics is associated with ciliogenesis. However, the underlying mechanism remains unclear. Here we find that nuclear distribution gene C (NudC), an Hsp90 co-chaperone, is required for ac- tin organization and dynamics. Depletion of NudC promotes cilia elongation a...
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Published in: | Cell research 2016-02, Vol.26 (2), p.239-253 |
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description | Emerging data indicate that actin dynamics is associated with ciliogenesis. However, the underlying mechanism remains unclear. Here we find that nuclear distribution gene C (NudC), an Hsp90 co-chaperone, is required for ac- tin organization and dynamics. Depletion of NudC promotes cilia elongation and increases the percentage of ciliated cells. Further results show that NudC binds to and stabilizes cofilin 1, a key regulator of actin dynamics. Knockdown of cofilin 1 also facilitates ciliogenesis. Moreover, depletion of either NudC or cofilin 1 causes similar ciliary defects in zebrafish, including curved body, pericardial edema and defective left-right asymmetry. Ectopic expression of cofilin 1 significantly reverses the phenotypes induced by NudC depletion in both cultured cells and zebrafish. Thus, our data suggest that NudC regulates aetin cytoskeleton and ciliogenesis by stabilizing cofilin 1. |
doi_str_mv | 10.1038/cr.2015.152 |
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However, the underlying mechanism remains unclear. Here we find that nuclear distribution gene C (NudC), an Hsp90 co-chaperone, is required for ac- tin organization and dynamics. Depletion of NudC promotes cilia elongation and increases the percentage of ciliated cells. Further results show that NudC binds to and stabilizes cofilin 1, a key regulator of actin dynamics. Knockdown of cofilin 1 also facilitates ciliogenesis. Moreover, depletion of either NudC or cofilin 1 causes similar ciliary defects in zebrafish, including curved body, pericardial edema and defective left-right asymmetry. Ectopic expression of cofilin 1 significantly reverses the phenotypes induced by NudC depletion in both cultured cells and zebrafish. 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However, the underlying mechanism remains unclear. Here we find that nuclear distribution gene C (NudC), an Hsp90 co-chaperone, is required for ac- tin organization and dynamics. Depletion of NudC promotes cilia elongation and increases the percentage of ciliated cells. Further results show that NudC binds to and stabilizes cofilin 1, a key regulator of actin dynamics. Knockdown of cofilin 1 also facilitates ciliogenesis. Moreover, depletion of either NudC or cofilin 1 causes similar ciliary defects in zebrafish, including curved body, pericardial edema and defective left-right asymmetry. Ectopic expression of cofilin 1 significantly reverses the phenotypes induced by NudC depletion in both cultured cells and zebrafish. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Cheng</au><au>Zhang, Wen</au><au>Lu, Yi</au><au>Yan, Xiaoyi</au><au>Yan, Xiumin</au><au>Zhu, Xueliang</au><au>Liu, Wei</au><au>Yang, Yuehong</au><au>Zhou, Tianhua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NudC regulates actin dynamics and ciliogenesis by stabilizing cofilin 1</atitle><jtitle>Cell research</jtitle><stitle>Cell Res</stitle><addtitle>Cell Research</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>26</volume><issue>2</issue><spage>239</spage><epage>253</epage><pages>239-253</pages><issn>1001-0602</issn><eissn>1748-7838</eissn><abstract>Emerging data indicate that actin dynamics is associated with ciliogenesis. However, the underlying mechanism remains unclear. Here we find that nuclear distribution gene C (NudC), an Hsp90 co-chaperone, is required for ac- tin organization and dynamics. Depletion of NudC promotes cilia elongation and increases the percentage of ciliated cells. Further results show that NudC binds to and stabilizes cofilin 1, a key regulator of actin dynamics. Knockdown of cofilin 1 also facilitates ciliogenesis. Moreover, depletion of either NudC or cofilin 1 causes similar ciliary defects in zebrafish, including curved body, pericardial edema and defective left-right asymmetry. Ectopic expression of cofilin 1 significantly reverses the phenotypes induced by NudC depletion in both cultured cells and zebrafish. Thus, our data suggest that NudC regulates aetin cytoskeleton and ciliogenesis by stabilizing cofilin 1.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26704451</pmid><doi>10.1038/cr.2015.152</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/136/2432 631/80/128/1276 631/80/86 Actins - metabolism Animals Biomedical and Life Sciences Cell Biology Cells, Cultured Cilia - metabolism Cilia - physiology Cofilin 1 - metabolism Edema Hsp90 HSP90 Heat-Shock Proteins Life Sciences Morphogenesis - physiology Nuclear Proteins - metabolism Original original-article Zebrafish - metabolism Zebrafish - physiology 培养细胞 左右不对称 异位表达 稳定 纤毛细胞 组织动力学 肌动蛋白细胞骨架 |
title | NudC regulates actin dynamics and ciliogenesis by stabilizing cofilin 1 |
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