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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，在原肠形成中细胞迁移的控制和细胞极性形成方面获得了显着的研究结果。研究代表Ueno将细胞粘附的正限制因子ANR5确定为细胞迁移的负控制机制。ANR5是被鉴定为细胞生长因子FGF ANR5的靶基因的基因之一，并阐明了通过直接与PAPC结合并通过过度出现和使用[moruforinoanchisensuorigonukureochido]的功能抑制来控制下游的RhoA再生，从而精确地控制细胞粘附。此外，ANR 5对于形成必要的膜投影是必要的，以便细胞可以在群中相互移动，因此，已澄清ANR 5对原肠形成发挥着不可或缺的作用（Chung，H.一、et.例如，Curr. Biol.）。此外，Kinoshita等人阐明，原肠形成的细胞运动通过细胞生长因子的Wnt调节，Wnt作用于中胚层细胞，并控制对细胞运动具有不可或缺作用的[pakishirin]的泛素相关分解（Iioka，H.，et.例如，Nat Cell Biol.）。这些都是重要的研究结果，其中显示了作为细胞群的运动对于原肠的形成是不可或缺的。此外，Ueno阐明，进行了关注关于形成原肠时观察到的关于细胞的形式和功能极性的起始机制的微管伸长的分析，并且段落之间的产生过程的边界具有极性开始信号（Shindo，A.，et. PLoS ONE）。希望今后能进一步研究这种极性起始信号的实质。