Authors
Rebecca Collier, Martina Bohuslavová, Michaela Vaškovičová, Aleksandar I Mihajlović, Andrea Hauserová, Valeriya Zabelina, Monika Fluks, Lenka Gahurová, Dávid Drutovič, Alexander W Bruce
Published in
Open biology. Volume 16. Issue 10. Oct 07, 2026.
Abstract
In mammalian preimplantation embryos, distinct cell lineages occupy defined spatial niches. The outer trophectoderm (TE) forms an epithelial monolayer surrounding the inner cell mass (ICM) and blastocyst cavity. In mice, the Tead4 gene encodes a polarity-dependent transcription factor required for TE specification. Here, we demonstrate that Tead4 also preserves TE integrity during blastocyst maturation. Clonal siRNA-mediated Tead4 knockdown (KD) disrupts outer cell apical domain morphology, causing abnormal allocation of these clones to an enlarged ICM, despite minimal impact on established polarity. Fixed sample and live embryo light-sheet microscopy imaging reveal that TEAD4-deficient outer cells atypically migrate into the blastocyst ICM, sometimes via apical domain abscission, or are repositioned post-division, linking disrupted apical domain morphology to altered spatial positioning and fate. Transcriptomic analysis indicates that TEAD4 regulates genes involved in cytoskeletal organization, particularly those related to actin and cell adhesion, which we propose are critical for maintaining outer cell TE positioning. Combined KD of Tead4 and two of its targets, the atypical GTPases Rnd1 and Rnd3, partially rescues misallocation but does not prevent apical morphological abnormalities. These findings indicate TEAD4 and its downstream regulatory network actively contribute to blastocyst TE maintenance, beyond initial specification, up until the peri-implantation stage, ensuring proper lineage segregation.
PMID:
42838532
Bibliographic data and abstract were imported from PubMed on 07 Oct 2026.
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