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Clarification of cell polarity formation mechanism in archenteron formation

阐明archenteron形成中的细胞极性形成机制

基本信息

批准号：
17207015
负责人：
UENO Naoto
金额：
$ 31.28万
依托单位：
National Institute for Basic Biology
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (A)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2007
项目状态：
已结题

项目摘要

Remarkable study results were obtained for the control and the cell polarity formation of the cell migration in the archenteron formation in 2007 fiscal year. Research representative's Ueno identified positive restrictor ANR5 of the cellular adhesion as a negative controlling mechanism of the cell migration. ANR5 was one of the genes identified as a target gene of cellular growth factor FGF ANR5, and clarified that the cellular adhesion was exactly controlled by uniting directly with PAPC and controlling the RhoA revitalization in the downstream by excessive appearance and the functional inhibition that used [moruforinoanchisensuorigonukureochido]. Moreover, ANR5 was necessary for forming a film projection necessary so that the cell may move mutually in the group, and, as a result, it was clarified to play an indispensable role to the archenteron formation (Chung, H. A., et. al., Curr. Biol.). Moreover, Kinoshita, et al. clarified that the cell movement of the archenteron formation was adjusted by cellular growth factor's Wnt acting on the mesoblast cell, and controlling the ubiquitin related resolution of [pakishirin] with an indispensable role to the cell movement (Iioka, H., et. al., Nat Cell Biol.). These are important study results in which it is shown that the movement as the group of the cell is indispensable to the archenteron formation. In addition, Ueno clarified that the analysis that paid attention to the microtubule elongation about the initiation mechanism of a form and functional polarity making about the cell seen when the primitive gut was formed was done, and the boundary of the generation process between paragraphs had the polarity beginning signal (Shindo, A., et. al. PLoS ONE). I want to advance the research on the substance of this polarity beginning signal in the future.

2007财年在原肠段细胞迁移的控制和细胞极性的形成方面取得了显著的研究成果。研究代表的Ueno发现，细胞黏附的正向限制因子ANR5是细胞迁移的负向控制机制。ANR5是细胞生长因子FGFANR5的靶基因之一，阐明了细胞黏附是通过直接与PAPC结合，并通过过度的外观和使用[moruforinoancissusureOrigonureochido]的功能抑制来控制下游的RhoA活化而精确调控的。此外，ANR5是形成电影投影所必需的，因此细胞可以在群中相互移动，因此，它被阐明在原肠形成中起着不可或缺的作用(Chung，H.A.等)。Al.，Curr.Biol.)此外，Kinoshita，et al.阐明了细胞生长因子的Wnt作用于中胚层细胞，并控制与泛素相关的[pakishirin]对细胞运动起着不可或缺的作用，从而调节了原肠形成的细胞运动(Iioka，H.，et.Al.、NAT Cell Biol.)这些都是重要的研究结果，表明作为细胞群的运动对于原肠的形成是不可或缺的。此外，上野澄清说，在原始肠形成时看到的关于细胞形态起始机制和功能极性制造的微管延长的分析已经完成，段落之间发生过程的边界具有极性开始信号(Shindo，A.，et)。艾尔PLOS One)。我想在未来推进对这一极性开始信号的实质的研究。