The Francis Crick Institute, London, UK.
UK Dementia Research Institute at King's College London, London, UK.
Nat Struct Mol Biol. 2024 Sep;31(9):1439-1447. doi: 10.1038/s41594-024-01363-x. Epub 2024 Jul 25.
Signaling pathways drive cell fate transitions largely by changing gene expression. However, the mechanisms for rapid and selective transcriptome rewiring in response to signaling cues remain elusive. Here we use deep learning to deconvolve both the sequence determinants and the trans-acting regulators that trigger extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinase kinase (MEK)-induced decay of the naive pluripotency mRNAs. Timing of decay is coupled to embryo implantation through ERK-MEK phosphorylation of LIN28A, which repositions pLIN28A to the highly A+U-rich 3' untranslated region (3'UTR) termini of naive pluripotency mRNAs. Interestingly, these A+U-rich 3'UTR termini serve as poly(A)-binding protein (PABP)-binding hubs, poised for signal-induced convergence with LIN28A. The multivalency of AUU motifs determines the efficacy of pLIN28A-PABP convergence, which enhances PABP 3'UTR binding, decreases the protection of poly(A) tails and activates mRNA decay to enable progression toward primed pluripotency. Thus, the signal-induced convergence of LIN28A with PABP-RNA hubs drives the rapid selection of naive mRNAs for decay, enabling the transcriptome remodeling that ensures swift developmental progression.
信号通路主要通过改变基因表达来驱动细胞命运的转变。然而,对于响应信号线索的快速和选择性转录组重布线的机制仍然难以捉摸。在这里,我们使用深度学习来分解序列决定因素和反式作用调节剂,这些调节剂触发细胞外信号调节激酶 (ERK)-丝裂原激活蛋白激酶激酶 (MEK) 诱导的幼稚多能性 mRNA 的衰减。通过 ERK-MEK 对 LIN28A 的磷酸化,衰减的时间与胚胎着床相关联,LIN28A 将 pLIN28A 重新定位到幼稚多能性 mRNA 的富含 A+U 的 3'非翻译区 (3'UTR) 末端。有趣的是,这些富含 A+U 的 3'UTR 末端充当多聚 (A)-结合蛋白 (PABP) 结合枢纽,准备与 LIN28A 一起进行信号诱导的收敛。AUU 基序的多价性决定了 pLIN28A-PABP 收敛的效率,这增强了 PABP 3'UTR 结合,减少了 poly(A) 尾巴的保护,并激活了 mRNA 衰减,从而促进向初始多能性的进展。因此,LIN28A 与 PABP-RNA 枢纽的信号诱导收敛驱动了幼稚 mRNA 快速选择进行衰减,从而实现了确保快速发育进展的转录组重塑。