Department of Chemical and Systems Biology, Stanford University, Stanford, California, United States of America.
Department of Biochemistry and the Drukier Institute for Children's Health, Weill Cornell Medical College of Cornell University, New York, New York, United States of America.
PLoS Biol. 2022 Dec 5;20(12):e3001900. doi: 10.1371/journal.pbio.3001900. eCollection 2022 Dec.
How progenitor cells can attain a distinct differentiated cell identity is a challenging problem given the fluctuating signaling environment in which cells exist and that critical transcription factors are often not unique to a differentiation process. Here, we test the hypothesis that a unique differentiated cell identity can result from a core component of the differentiated state doubling up as a signaling protein that also drives differentiation. Using live single-cell imaging in the adipocyte differentiation system, we show that progenitor fat cells (preadipocytes) can only commit to terminally differentiate after up-regulating FABP4, a lipid buffer that is highly enriched in mature adipocytes. Upon induction of adipogenesis in mouse preadipocyte cells, we show that after a long delay, cells first abruptly start to engage a positive feedback between CEBPA and PPARG before then engaging, after a second delay, a positive feedback between FABP4 and PPARG. These sequential positive feedbacks both need to engage in order to drive PPARG levels past the threshold for irreversible differentiation. In the last step before commitment, PPARG transcriptionally increases FABP4 expression while fatty acid-loaded FABP4 increases PPARG activity. Together, our study suggests a control principle for robust cell identity whereby a core component of the differentiated state also promotes differentiation from its own progenitor state.
祖细胞如何获得独特的分化细胞身份是一个具有挑战性的问题,因为细胞所处的信号环境不断变化,而且关键转录因子通常不是分化过程所特有的。在这里,我们检验了这样一个假设,即分化状态的核心组成部分可以作为一种信号蛋白加倍,从而驱动分化,从而产生独特的分化细胞身份。我们在脂肪细胞分化系统中使用活细胞单细胞成像技术,表明前脂肪细胞(前脂肪细胞)只有在上调 FABP4 后才能终末分化,FABP4 是一种在成熟脂肪细胞中高度富集的脂质缓冲剂。在诱导小鼠前脂肪细胞的脂肪生成后,我们表明,在长时间延迟后,细胞首先突然开始在 CEBPA 和 PPARG 之间建立正反馈,然后在第二次延迟后,在 FABP4 和 PPARG 之间建立正反馈。这两个连续的正反馈都需要参与,以推动 PPARG 水平超过不可逆分化的阈值。在承诺之前的最后一步中,PPARG 转录增加 FABP4 的表达,而负载脂肪酸的 FABP4 增加 PPARG 的活性。总之,我们的研究提出了一个强大的细胞身份控制原则,即分化状态的核心组成部分也促进了自身祖细胞状态的分化。