ArticleScience China. Life sciences2026
Mechanosensor YAP orchestrates human neural rosette morphogenesis via TEAD4-LEF1 transcriptional nexus.
Article in Science China. Life sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- hiPSC-derived Organoids and Organ-on-chip Systems: New Frontiers in Neural Tube Defect Research.Stem cell reviews and reports · 2026Review
- Single-nucleus interrogation of primate small intestinal aging reveals NCoR1 decline as a conserved feature that is reversed by metformin.Nature aging · 2026Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanical signaling plays a crucial yet poorly understood role in human neural tube morphogenesis. In this study, we elucidate how the Hippo pathway mechanosensor YAP converts apical tension into transcriptional programs to guide this process. Using human cortical organoids, we demonstrated that YAP accumulates and translocates to the nucleus within high-tension apical domains of neural rosettes. YAP depletion disrupted apicobasal epithelial polarity, manifested as disorganized cytoskeleton, compromised tight junctions, and impaired ciliogenesis, which ultimately resulted in defective rosette morphogenesis. Mechanistically, the YAP-TEAD4 complex transcriptionally activated LEF1, a central regulator of Wnt signaling. LEF1 deficiency phenocopied YAP loss, whereas its overexpression partially rescued rosette defects. Our findings establish the YAP-LEF1 axis as a critical integrator of mechanical and morphogenetic signals in neural tube development, thereby highlighting its potential as a therapeutic target for neural tube defects such as anencephaly.
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Registered trials
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