TY - JOUR
T1 - Poised PABP–RNA hubs implement signal-dependent mRNA decay in development
AU - Modic, Miha
AU - Kuret, Klara
AU - Steinhauser, Sebastian
AU - Faraway, Rupert
AU - van Genderen, Emiel
AU - Ruiz de Los Mozos, Igor
AU - Novljan, Jona
AU - Vičič, Žiga
AU - Lee, Flora C.Y.
AU - ten Berge, Derk
AU - Luscombe, Nicholas M.
AU - Ule, Jernej
N1 - Publisher Copyright:
© The Author(s) 2024.
PY - 2024/9/1
Y1 - 2024/9/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85199564278&partnerID=8YFLogxK
U2 - 10.1038/s41594-024-01363-x
DO - 10.1038/s41594-024-01363-x
M3 - Article
C2 - 39054355
AN - SCOPUS:85199564278
SN - 1545-9993
VL - 31
SP - 1439
EP - 1447
JO - Nature Structural and Molecular Biology
JF - Nature Structural and Molecular Biology
IS - 9
ER -