微RNAmiR-235将爆细胞静止状态与营养状态相结合
Hidefumi Kasuga1, Masamitsu Fukuyama, Aya Kitazawa
1Laboratory of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-0033, Japan.
Nature
|May 7, 2013
概括
在Caenorhabditis elegans中的microRNAmiR-235在L1隔离期中停止发育,通过胰岛素/IGF信号通路响应营养的可用性. 这项研究揭示了miR-92正义学家在调节基于营养的爆细胞行为的新角色.
科学领域:
- 发育生物学 发展生物学
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 干细胞和芽细胞的行为对于生长,再生和组织平衡至关重要.
- 虫幼虫进入L1隔膜,暂停发育,直到营养物质可用,由胰岛素/IGF信号传递 (IIS) 途径调节.
- 连接IIS信号与依赖营养物质的爆细胞静止的确切机制尚不清楚.
研究的目的:
- 阐明 IIS 途径调节发育静止以响应营养可用性的机制.
- 为了确定关键的分子参与者参与合爆细胞行为到C. elegans的营养状况.
主要方法:
- 研究了microRNA (miRNA) miR-235在C. elegans发育和L1 diapause中的作用.
- 分析了mir-235的表达及其对食和IIS通路活动的反应目标.
- 利用遗传分析来评估miR-235及其位nhr-91在调节神经母细胞和半母细胞中的功能.
主要成果:
- miR-235是一种哺乳动物miR-92的同类物,在皮下和质细胞中起作用,阻止神经母细胞和半母细胞的胚胎后发育.
- mir-235表达在L1隔断期间持续存在,并在食时减少,这取决于IIS通路.
- 作为miR-235的标的nhr-91的升级导致了在miR-235功能丧失突变体中观察到的缺陷.
结论:
- miR-235在协调爆细胞行为与L1隔断期间的营养可用性方面发挥着至关重要的作用.
- 这项研究确立了miR-92口腔科医生在调解基于营养状况的发育停止方面具有新的功能.
- 这些发现揭示了由miRNA和IIS信号控制的发育可塑性的新层调节.
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