Nodal Promotes mir206 Expression to Control Convergence and Extension Movements During Zebrafish Gastrulation  

作　　者：Xiuli Liu Yuanqing Ma Congwei Zhang Shi Wei Yu Cao Qiang Wang 

机构地区：[1]State Key Laboratory of Biomembrane and Membrane Biotechnology,Institute of Zoology,Chinese Academy of Sciences [2]Department of Outpatient Surgery,Anguo City Hospital of Hebei Province

出　　处：《Journal of Genetics and Genomics》2013年第10期515-521,共7页遗传学报（英文版）

基　　金：supported by the grants from the Major Science Programs of China(Nos.2011CBA01101 and 2011CB943904);the National Natural Science Foundation of China(Nos.30971656 and 90919011)

摘　　要：Nodal, a member of the transforming growth factor β （TGF-β） superfamily, has been shown to play a role in mesendoderm induction and gastrulation movements. The activity of Nodal signaling can be modulated by microRNAs （miRNAs） as previously reported, but little is known about which miRNAs are regulated by Nodal during gastrulation. In the present study, we found that the expression of mir206, one of the most abundant miRNAs during zebrafish early embryo development, is regulated by Nodal signaling. Abrogation of Nodal signal activity results in defective convergence and extension （CE） movements, and these cell migration defects can be rescued by supplying an excess of mir206, suggesting that mir206 acts downstream of Nodal signaling to regulate CE movements. Furthermore, in mir206 morphants, the expression of cell adhesion molecule E-cadherin is significantly increased, while the key transcriptional repressor of E-cadherin, snailla, is depressed. Our study uncovers a novel mechanism by which Nodal-regulated mir206 modulates gastrulation movements in connection with the Snail/E-cadherin pathway.Nodal, a member of the transforming growth factor β （TGF-β） superfamily, has been shown to play a role in mesendoderm induction and gastrulation movements. The activity of Nodal signaling can be modulated by microRNAs （miRNAs） as previously reported, but little is known about which miRNAs are regulated by Nodal during gastrulation. In the present study, we found that the expression of mir206, one of the most abundant miRNAs during zebrafish early embryo development, is regulated by Nodal signaling. Abrogation of Nodal signal activity results in defective convergence and extension （CE） movements, and these cell migration defects can be rescued by supplying an excess of mir206, suggesting that mir206 acts downstream of Nodal signaling to regulate CE movements. Furthermore, in mir206 morphants, the expression of cell adhesion molecule E-cadherin is significantly increased, while the key transcriptional repressor of E-cadherin, snailla, is depressed. Our study uncovers a novel mechanism by which Nodal-regulated mir206 modulates gastrulation movements in connection with the Snail/E-cadherin pathway.

关 键 词：NODAL mir206 Convergence and extension snailla E-CADHERIN 

分 类 号：S917.4[农业科学—水产科学]