Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Department of Regenerative Medicine, Graduate School of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Cell Death Dis. 2021 Mar 17;12(4):285. doi: 10.1038/s41419-021-03537-7.
The RNA decay pathway plays key regulatory roles in cell identities and differentiation processes. Although adipogenesis is transcriptionally and epigenetically regulated and has been thoroughly investigated, how RNA metabolism that contributes to the stability of phenotype-shaping transcriptomes participates in differentiation remains elusive. In this study, we investigated Ddx6, an essential component of processing bodies (PBs) that executes RNA decay and translational repression in the cytoplasm and participates in the cellular transition of reprogramming. Upon adipogenic induction, Ddx6 dynamically accumulated to form PBs with a binding partner, 4E-T, at the early phase prior to emergence of intracellular lipid droplets. In contrast, preadipocytes with Ddx6 knockout (KO) or 4E-T knockdown (KD) failed to generate PBs, resulting in significant suppression of adipogenesis. Transcription factors related to preadipocytes and negative regulators of adipogenesis that were not expressed under adipogenic stimulation were maintained in Ddx6-KO and 4E-T-KD preadipocytes under adipogenic induction. Elimination of Dlk1, a major negative regulator of adipogenesis, in 3T3L1 Ddx6-KO cells did not restore adipogenic differentiation capacity to any extent. Similar to murine cells, human primary mesenchymal stem cells, which can differentiate into adipocytes upon stimulation with adipogenic cocktails, required DDX6 to maturate into adipocytes. Therefore, RNA decay of the entire parental transcriptome, rather than removal of a strong negative regulator, could be indispensable for adipogenesis.
RNA 降解途径在细胞身份和分化过程中发挥着关键的调节作用。尽管脂肪生成在转录和表观遗传水平上受到调控,并得到了深入的研究,但对于有助于表型形成转录组稳定性的 RNA 代谢如何参与分化仍然难以捉摸。在这项研究中,我们研究了 Ddx6,它是细胞质中执行 RNA 降解和翻译抑制的处理体(PBs)的必需组成部分,并参与细胞重编程的转变。在脂肪生成诱导后,Ddx6 在形成细胞内脂滴之前的早期阶段,与结合伙伴 4E-T 一起动态积累形成 PBs。相比之下,缺乏 Ddx6 或 4E-T 的前脂肪细胞无法形成 PBs,导致脂肪生成显著抑制。在脂肪生成诱导下,与前脂肪细胞相关的转录因子和脂肪生成的负调节剂在前脂肪细胞中没有表达。在 3T3L1 Ddx6-KO 细胞中消除主要的脂肪生成负调节剂 Dlk1,并不能在任何程度上恢复脂肪生成的分化能力。与鼠细胞类似,能够在脂肪生成鸡尾酒刺激下分化为脂肪细胞的人原代间充质干细胞也需要 DDX6 才能成熟为脂肪细胞。因此,整个亲本转录组的 RNA 降解,而不是去除强负调节剂,对于脂肪生成可能是必不可少的。