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一个平行LIF信号通路的电路保持了小鼠ES细胞的多能性

Hitoshi Niwa¹, Kazuya Ogawa, Daisuke Shimosato

¹Laboratory for Pluripotent Cell Studies, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe 6500047, Japan. niwa@cdb.riken.jp

|July 3, 2009

概括

白血病抑制因子 (LIF) 信号通过 Klf4 和 Tbx3 转录因子维持小鼠胚胎干细胞的多能性. 这些因素将LIF信号与核心多能性基因联系起来,但对于维持多能性本身并不重要.

科学领域:

干细胞生物学干细胞生物学
分子信号传递是分子信号传递.
转录因子转录因子

背景情况:

白血病抑制因子 (LIF) 对于维持小鼠胚胎干细胞 (ESCs) 的多能性至关重要.
杰克-Stat3途径调解LIF信号,但其与核心多能转录因子 (Oct3/4,Sox2,Nanog) 的连接尚未完全理解.

研究的目的:

阐明LIF信号通路如何连接到小鼠ESC中的多能相关转录因子的核心电路.
确定Klf4和Tbx3在LIF信号中介和维持多能性的作用.

主要方法:

研究了小鼠ESC中的LIF信号通路.
通过不同的信号级联 (Jak-Stat3,PI3K-Akt,MAPK) 分析了Klf4和Tbx3的激活.
评估了Klf4,Tbx3和Nanog表达对ESC多能性和自我更新的影响,有或没有LIF.

主要成果:

Klf4主要由Jak-Stat3激活并激活Sox2,而Tbx3则由PI3K-Akt/MAPK通路调节并刺激NanoG.
在没有LIF的情况下,Klf4或Tbx3的人工表达可以保持Oct3/4表达和多能性.
在没有Klf4和Tbx3活动的情况下,Nanog的过度表达支持LIF独立的自我更新.

结论:

Klf4和Tbx3作为LIF向核心多能网络发送信号的媒介.
虽然Klf4和Tbx3对于信号传导很重要,但对于ESC多能性的内在维护并不重要.

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