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. 2014 Mar 27;12:25. doi: 10.1186/1741-7007-12-25

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Copyright © 2014 Li et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Model of Isl1 function in mouse developing pyloric muscle. Bapx1 is lost in Barx1-null stomachs, Barx1 functions upstream of Bapx1, and loss of Bapx1 down-regulates Sox9 expression. We therefore suggest that Barx1 regulates Sox9 through Bapx1. Loss of Six2 reduces Nkx2.5, Gremlin, and Sox9 expression, and loss of Nkx2.5 also leads to loss of Sox9 expression. In addition, Sox9 is absent after deletion of Gata3. Our results demonstrate that Isl1 directly regulates Gata3, which suggests that Sox9 is regulated by Isl1 via Gata3. Dotted lines indicate that Nkx2.5 and Gremlin are down-regulated in Isl1^MCM/Del stomachs, but specific regulatory mechanisms still remain unclear.