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. 2016 Feb 2;9(2):119–129. doi: 10.1161/CIRCGENETICS.115.001254

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© 2016 The Authors.

Circulation: Cardiovascular Genetics is published on behalf of the American Heart Association, Inc., by Wolters Kluwer. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDervis License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 1. — Loss of pericardial nephrocytes and garland cells in dKlf15^NN mutants. A, Adult control (w¹¹¹⁸; A′) and dKlf15^NN mutant flies (A″) were dissected and the heart fixed and stained with phalloidin to visualize the heart’s actin cytoskeleton and antibodies to the pericardial nephrocyte marker Amnionless (CG11592). All pericardial nephrocytes fail to differentiate in the mutants, undergoing attrition during late larval development so that by adulthood there are none. B, Third instar larvae were dissected and the garland cells visualized after staining with Hoechst. In control flies (w¹¹¹⁸; B′) garland cells (GCs) are binucleate and situated at the interface between the proventriculus (PV) and esophagus (OE). In contrast, the garland cells fail to develop normally and are lost in the dKlf15^NN mutants (B″). Scale bar, 100 μm.