In the elongating mouse embryo, posteriorly located neuromesodermal progenitors (NMPs) have the ability to either self-renew or give rise to the precursors of the spinal cord and paraxial mesoderm. The balance between proliferation and differentiation of NMPs must be coordinated with the process of somitogenesis which generates the segmented body plan. The molecular mechanisms driving NMP self-renewal, and the differential regulation of NMP output as progressively more posterior structures are being laid down, is not well characterised. Here we propose Nuclear receptor subfamily 6 group A member 1 (Nr6a1) as a critical regulator of axial elongation through its control of NMP self-renewal. We show that the expression of Nr6a1 drops dramatically in the posterior region from embryonic day (E)8.5 to E9.5, a stage at which NMPs relocate from the epiblast to the tailbud and coinciding with the trunk-to-tail transition. Previous genetic ablation of Nr6a1 in mouse caused a severely truncated axis, supporting its role in NMP self-renewal. Furthermore, it has been shown that Nr6a1 plays a key role in controlling the differentiation of the embryonic stem (ES) cells induced by RA signalling by inhibiting the pluripotency factors. To elucidate the roles of Nr6a1 in anterior-posterior axial elongation and NMP proliferation, we have generated a series of novel tools, including Nr6a1-deficient ES cells and stably transduced Dox-inducible Nr6a1 gain-of-function ES cells. Together, these tools will allow us to dissect the role of this orphan nuclear receptor in cell behaviours of mouse in vitro derived NMPs, identify the direct downstream targets of Nr6a1 in this context, and reveal novel protein-interacting partners of Nr6a1.