Figure 1.

αPS3 Integrin is required for apicalisation of cardioblasts. Slit is located in the heart lumen (arrow) in stage 17 wildtype embryos (A). The level of immuno-detected Slit (red) is much lower in scb2 mutants (D), and mys1 mutants (J) or if α or β Integrin levels are reduced by dsRNA knockdown (scbRNAi in G and mysRNAi in M, directed by dMEF2-GAL4). Residual Slit is not apicalised, and is found on lateral cell surfaces (arrowheads in insets of D and M). Most of the immunolabel for βPS1 Integrin is concentrated on the luminal surface in wildtype (red, B). Levels of βPS1 are reduced in scb mutants (E) and subsequent to scbRNAi expression (H), however, some luminal label remains. No βPS1 is detected in mys1 mutants (K), and trace levels of βPS1 remain after mysRNAi expression (N). Pericardin, synthesized by the pericardial cells (labeled with Zfh-1 antibody, blue in C, F, I, L, O) is restricted to the basal surface of the CBs in wildtype (red, C). Reduced Integrin function in scb and mys mutants (F, L), or subsequent to scbRNAi (I) or mysRNAi (O) expression results in Pericardin re-distribution around the entire pericardial cell perimeter (arrowheads, F, L, O), as well as between some CBs (arrowhead in I), and less at the basal surface of the CBs. Midline Pericardin marks medially displaced pericardial cells (asterisk in F, L). The CB nuclei here and subsequent fluorescence images are identified with antibody to dMEF2 (green), except where CB nuclei are labeled with β-galactosidase for the B2-3-20 enhancer trap in G, H, I, M, N, O (green). Anterior is to the left in all panels, and the arrow marks the dorsal midline. All images were generated at the same gain. The gain in the insets is adjusted to visualise low intensity immuno-label signals. Calibration: 10 microns

Vanderploeg et al. BMC Developmental Biology 2012 12:8   doi:10.1186/1471-213X-12-8
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