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. 2014 Feb 15;141(4):878–888. doi: 10.1242/dev.101709

Fig. 5.

Fig. 5.

Myb is an activator of the Ndg enhancer in the heart. (A-C′′) The posterior-most four CCs are marked by Tin expression (red), and the PCs are marked by Zfh1 expression (blue). (A-A′′) A β-galactosidase reporter (green) driven by the wild-type Ndg enhancer is expressed in only two Tin-expressing CCs per hemisegment (square brackets). (B-B′′) Mutations in the Myb binding sites result in partial but significant inactivation of reporter expression in these two CCs. (C-C′′) Reporter expression from the wild-type Ndg enhancer is also partially but significantly inactivated in these two CCs in embryos hemizygous for the MybMH30 null mutation. (D) Histogram showing the mean number of CCs with 95% confidence intervals expressing the reporter and the significance of partial inactivation as a result of either the Myb binding site mutations in the Ndg enhancer or the MybMH30 null mutation.