Publication date: 20 December 2016
Source:Cell Reports, Volume 17, Issue 12
Author(s): Shilu Amin, Roel Neijts, Salvatore Simmini, Carina van Rooijen, Sander C. Tan, Lennart Kester, Alexander van Oudenaarden, Menno P. Creyghton, Jacqueline Deschamps
In vertebrate embryos, anterior tissues are generated early, followed by the other axial structures that emerge sequentially from a posterior growth zone. The genetic network driving posterior axial elongation in mice, and its disturbance in mutants with posterior truncation, is not yet fully understood. Here, we show that the combined expression of Cdx2 and T Brachyury is essential to establish the core signature of posterior axial progenitors. Cdx2 and T Brachyury are required for extension of a similar trunk portion of the axis. Simultaneous loss of function of these two genes disrupts axial elongation to a much greater extent than each single mutation alone. We identify and validate common targets for Cdx2 and T Brachyury in vivo, including Wnt and Fgf pathway components active in the axial progenitor niche. Our data demonstrate that integration of the Cdx/Hox and T Brachyury transcriptional networks controls differential axial growth during vertebrate trunk elongation.
Graphical abstract
Teaser
Vertebrate embryos elongate their body from a posterior growth zone containing tissue progenitors. Amin et al. find that two different transcription factors required for body elongation directly bind and activate the same growth-stimulating genes. The authors demonstrate the importance of these activation events for differential control of axial growth.http://ift.tt/2iipiH8
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