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. 2012 Apr 15;139(8):1457–1466. doi: 10.1242/dev.069005

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© 2012.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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Fig. 3. — CHES-1-like represses Ndg expression in the FCMs by acting through either the Fkh2 or Fkh3 sites. Lateral views of stage 11 embryos with FCMs marked by the expression of Lmd (red) at low (A-D) and high (A′-D″′) magnification. (A-A″′) GFP expression driven by the wild-type Ndg enhancer (green) is limited to somatic FCs that do not express the FCM marker Lmd. (B-C″′) Mutating either Fkh2 and Fkh3 sites simultaneously (B-B″′) or all three Fkh sites together (C-C″′) results in the de-repression of reporter expression into Lmd-expressing FCMs (arrows) that are adjacent to the normal Ndg-positive FCs. (D-D″′) Similarly, in embryos homozygous for the CHES-1-like null mutation, reporter expression from the wild-type Ndg enhancer is also de-repressed into adjacent FCMs (arrows).