Sall4 regulates neuromesodermal progenitors and their descendants during body elongation in mouse embryos.

摘要: Bi-potential neuromesodermal progenitors (NMPs) produce both neural and paraxial mesodermal in the trunk tail during vertebrate body elongation. We show that Sall4, a pluripotency-related transcription factor gene, has multiple roles regulating NMPs their descendants post-gastrulation mouse embryos. Sall4 deletion using TCre caused body/tail truncation, reminiscent of early depletion NMPs, suggesting role NMP maintenance. This phenotype became significant at time trunk-to-tail transition, maintenance enables formation. mutants exhibit expanded reduced tissues, indicating differentiation balance. Mechanistically, we promotion WNT/β-catenin signaling contributes to RNA-Seq SALL4 ChIP-Seq analyses support notion regulates development. Furthermore, compartment, genes presomitic mesoderm are downregulated mutants. In towards post-mitotic neuron is accelerated Our results collectively provide evidence supporting descendants.