Figure 1—figure supplement 5

Loss of Pten, an antagonist of phosphoinositide 3-kinase (PI3K) activity, causes cardiac fusion defects.

(A–I) Dorsal views, anterior to the top, of the myocardium labeled with myl7 at 22s. Neither ptena^−/− homozygous mutants (A), ptena^−/− homozygous; ptenb^−/+ heterozygous (B), nor ptena^−/−, ptenb^−/− double homozygous mutants (C), display cardiac fusion defects. However, maternal contribution of Pten has been reported to persist during development. Adding low concentrations of the Pten inhibitor VO-OHpic (VO-OH – 5, 10 μM) at bud stage to ptena^−/−, ptenb^−/− double homozygous mutants to inhibit maternal Pten activity did cause a significant increase in cardiac fusion defects (H, I), compared to DMSO (D, G) and low concentrations of VO-OH only (E, F). The number of embryos with cardiac fusion defects and total number analyzed are indicated. (J) Bar graph depicts the distribution of cardiac fusion defects (% of embryos analyzed) in wild-type or ptena^−/−, ptenb^−/− double homozygous mutants, treated with DMSO, or 5, 10 μM VO-OH. Blue – cardiac ring/normal; orange – fusion only at posterior end. Fisher’s exact test, letter change indicates p < 0.05. Scale bar, 40 μm. Raw data including quantification of all genotypes and full p-values included in the source file