Neuromesodermal axial progenitors (NMPs) give rise to both neurectoderm and presomitic mesoderm, driving the elongation of the mammalian body during embryogenesis. While Wnt and FGF signalling are established key players in NMP induction and differentiation, the role of Notch signalling, which is also active in the NMP niche, has been poorly understood. Now, Fay Cooper, Anestis Tsakiridis, Kim Dale and colleagues use human embryonic stem cell (hESC)-derived NMPs, together with chick embryo grafting experiments, to determine how Notch influences NMP induction/differentiation. They show that Notch signalling increases as hESCs differentiate into NMPs and that Notch inhibition skews NMPs to express neural markers (SOX2), reducing expression of pro-mesodermal genes (TBXT) and Hox genes, as well as FGF signalling. By co-culturing wild-type and TBXT knockdown cells, which exhibit reduced Notch activity and Hox gene expression, the authors determine that Notch acts partly in a non-cell autonomous manner, with wild-type cells restoring some Hox gene expression in the knockdowns. Finally, they show through grafting experiments that Notch inhibition reduces the frequency at which transplanted axial progenitors contribute to paraxial mesoderm in vivo. Together, these data demonstrate that Notch is part of the NMP signalling niche and regulates posterior body patterning through FGF signalling crosstalk.