ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Gastrula-Premarked Posterior Enhancer Primes Posterior Tissue Development Through Cross-Talk with TGF-β Signaling Pathway.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integrated multi-omic atlas reveals the hierarchy of spatiotemporal regulatory networks of mouse gastrulation.Nature communications · 2026Article
- Emerging insights into enhancer RNAs: biogenesis, function, mechanism, and disease implication.Briefings in bioinformatics · 2026Review
- Posterior enhancer (p-Enh) maintains early neuromesodermal progenitors bi-potency during gastrulation.Cell regeneration (London, England) · 2025Article
- A dual enhancer-attenuator element ensures transient Cdx2 expression during mouse posterior body formation.Developmental cell · 2025Article
- Gastrula-Premarked Posterior Enhancer Primes Posterior Tissue Development Through Cross-Talk with TGF-β Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
The regulatory mechanisms governing cell fate determination, particularly lineage diversification during mammalian embryonic development, remain poorly understood with in-depth regulatory paradigms yet to be fully elucidated. Here, leveraging the epigenetic landscape of mouse gastrula, p-Enh is identified, an enhancer located within the first intron of Cdx2 and epigenetically pre-marked in the primitive streak region, as a pivotal regulator for posterior tissue development in mouse embryos. Morphological and single-cell transcriptomic analyses confirmed embryonic lethality phenotype with disrupted posterior tissue development trajectories in p-Enh-KO embryos. Molecularly, apart from regulating the neighboring coding-gene Cdx2 in cis, the findings suggest that p-Enh also modulates the global transcriptome and epigenomic landscape, which might through the transient production of eRNA in trans. Further investigation revealed p-Enh-derived eRNAs participate in the regulatory cascades of TGF-β signaling by directly interacting with SMAD4 protein. Combinatorial modulation of TGF-β signaling and p-Enh-eRNA abundance can largely rescue the posterior development deficiency in in vitro gastruloids through a Cdx2-independent mechanism. Thus, a potential model is proposed in which the broadly distributed p-Enh transcripts within the nucleus can serve as essential cross-modular coordinators, priming the posterior development of mouse embryo.
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