JAK/STAT3 signalling is sufficient and dominant over antagonistic cues for the establishment of naive pluripotency.
JAK/STAT3 signalling is sufficient and dominant over antagonistic cues for the establishment of naive pluripotency.
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JAK/STAT3信号传导在拮抗性线索上足以建立幼稚的多能性。
DOI：
10.1038/ncomms1822
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发表时间：
2012-05-08
影响因子：
16.6
通讯作者：
中科院分区：
文献类型：
--
作者：
诱导多能性依赖于特定因子的表达与培养环境之间的协同作用。后者也决定了多能细胞的状态，即幼稚或启动。Lif-JAK/STAT3信号通路最近被证明是重新编程为天真多能性的限制因素。在这里，我们表明，JAK/STAT3的充分激活克服了细胞中间体的重编程障碍，并使体细胞在缺乏其他必要的多能性介质的情况下进行重编程。激活成纤维细胞生长因子-ERK信号，促进原始多能细胞退出自我更新，但不能阻止JAK/STAT3诱导植入后外胚源干细胞转化为原始多能干细胞。此外，即使在指示和维持启动状态的成纤维细胞生长因子加激活素存在的情况下，JAK/STAT3也加强了上皮细胞的幼稚多能性。我们得出的结论是，JAK/STAT3信号足以并主导于拮抗信号，从而能够诱导一种天真的多能性状态。
Induced pluripotency depends on cooperativity between expression of defined factors and the culture environment. The latter also determines the pluripotent cell state, that is, naïve or primed. LIF-JAK/sTAT3 signalling was recently shown to be a limiting factor for reprogramming to naïve pluripotency. Here we show that sufficient activation of JAK/sTAT3 overcomes the reprogramming block of cell intermediates and enables somatic cell reprogramming in absence of otherwise essential pluripotency medium requisites. Activation of FGF-ERK signalling, which promotes exit of naïve pluripotent cells from self-renewal, does not prevent JAK/sTAT3 induced post-implantation epiblast-derived stem cell conversion into naïve pluripotency. Moreover, even in the presence of FGF plus Activin, which instructs and maintains the primed state, JAK/sTAT3 enforces naïve pluripotency in epiblast stem cells. We conclude that JAK/sTAT3 signalling can be sufficient and dominant over antagonistic cues to enable the induction of a naïve pluripotent state.
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