<p>(<b>A–I</b>) Localization of Perlecan and Prc in stage 17 control embryos (A–C), compared to homozygous <i>loh<sup>MB05750</sup></i> (D–F) or homozygous <i>prc<sup>MB03017</sup></i> mutants (G–I). Prc but not Perlecan becomes mis-localized by the absence of Loh. (<b>J–O</b>) Localization of Loh in stage 17 control embryos (J–L) compared to homozygous <i>prc<sup>MB03017</sup></i> mutants (M–O). The localization of Loh to the ECM is not affected by the absence of Prc. Of note, the anti-Loh antiserum needs heat fixation leading to a different appearance of Prc in the stained control animals compared to chemical fixation as shown in A. (<b>P–R</b>) The luminal ECM of cardiomyocytes at embryonic stage 17 is not altered in either homozygous <i>loh<sup>MB05750</sup></i> or <i>prc<sup>MB03017</sup></i> mutants. The arrowheads indicate the thickness of the ECM. (<b>S</b>) Quantification of luminal basement membrane (BM) thickness in animals of the indicated genotypes. Mutants do not show significant alterations in ECM thickness. Error bars shown are standard deviation (s.d.) (<b>T–V</b>) TEM section of the adhesion area between cardiomyocytes (CC) and pericardial cells (PC). Lack of either <i>loh</i> or <i>prc</i> cause gaps between the cells. Scale bars are 250 nm.</p
