Fig. 6.

Expression of the FERM protein mosaic eyes (moe) in podocytes and cell-junction defects associated with moe loss of function. moe mRNA is highly expressed in 96 hpf wild-type podocytes (A) and not adjacent endothelial cells of the glomerular capillary (*) or the dorsal aorta (da). Homozygous moe mutants at 80 hpf show a dorsally bent body axis and pericardial edema (arrowhead in panel C) compared to sibling heterozygotes (B). Glomerular capillary formation in wild-type moe heterozygotes (D) and moe homozygotes (E) is similar, indicating that moe is not required for early glomerular morphogenesis. (F) In contrast to wild-type podocytes (see Fig. 1), moe mutant podocytes aberrantly extend cell processes from their apical surface (arrows; “microvillar” projections). Bowman’s space is also filled with an electron-dense precipitate (*) suggesting protein leakage. On moe podocyte foot processes that are adherent to the basement membrane (G), slit-diaphragms are not commonly observed (arrows denote missing slit-diaphragms); wild-type embryos commonly display slit-diaphragms (H) between similar types of foot processes (arrows). Podocyte cell processes in moe −/− embryos that project into Bowman’s space often show doublet cross-strands between nearby cell projections (arrows).