Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/137225
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Type: | Journal article |
Title: | Nr6a1 controls Hox expression dynamics and is a master regulator of vertebrate trunk development |
Author: | Chang, Y.-C. Manent, J. Schroeder, J. Wong, S.F.L. Hauswirth, G.M. Shylo, N.A. Moore, E.L. Achilleos, A. Garside, V. Polo, J.M. Trainor, P. McGlinn, E. |
Citation: | Nature Communications, 2022; 13(1):1-19 |
Publisher: | Springer Nature |
Issue Date: | 2022 |
ISSN: | 2041-1723 2041-1723 |
Statement of Responsibility: | Yi-Cheng Chang, Jan Manent, Jan Schroeder, Siew Fen Lisa Wong, Gabriel M. Hauswirth, Natalia A. Shylo, Emma L. Moore, Annita Achilleos, Victoria Garside, Jose M. Polo, Paul Trainor, Edwina McGlinn |
Abstract: | The vertebrate main-body axis is laid down during embryonic stages in an anterior-to-posterior (head-to-tail) direction, driven and supplied by posteriorly located progenitors. Whilst posterior expansion and segmentation appears broadly uniform along the axis, there is developmental and evolutionary support for at least two discrete modules controlling processes within different axial regions: a trunk and a tail module. Here, we identify Nuclear receptor subfamily 6 group A member 1 (Nr6a1) as a master regulator of trunk development in the mouse. Specifically, Nr6a1 was found to control vertebral number and segmentation of the trunk region, autonomously from other axial regions. Moreover, Nr6a1 was essential for the timely progression of Hox signatures, and neural versus mesodermal cell fate choice, within axial progenitors. Collectively, Nr6a1 has an axially-restricted role in all major cellular and tissue-level events required for vertebral column formation, supporting the view that changes in Nr6a1 levels may underlie evolutionary changes in axial formulae. |
Keywords: | Spine Mesoderm Animals Vertebrates Mice Gene Expression Regulation, Developmental Body Patterning |
Rights: | © The Author(s) 2022. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/ licenses/by/4.0/. |
DOI: | 10.1038/s41467-022-35303-4 |
Grant ID: | http://purl.org/au-research/grants/arc/DP180102157 |
Published version: | http://dx.doi.org/10.1038/s41467-022-35303-4 |
Appears in Collections: | Molecular and Biomedical Science publications |
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