Fig. 6

Pronephron defects in osr1el593 mutants are partially suppressed by loss of npas4l function. Dorsal views, anterior to the left, of wild-type control (A,E), osr1el593 mutant (B,F), npas4ls5 mutant (C,G) and npas4ls5;osr1el593 double mutant (D,H) embryos at 26 hpf (A?D) and 13 som (E?H). In situ hybridization shows expression of wt1b in glomerular precursors (arrowhead), cdh17 throughout the pronephron tubules (arrow) (A?D), and etv2 in vessel progenitors (E?H). Compared with wild-type controls (A), pronephron glomerular expression is absent and tubule expression is thin and shortened anteriorly in osr1el593 mutants (B), expanded in npas4ls5 mutants (C); and relatively similar to wild-type in npas4ls5;osr1el593 double mutants (D; n = 8; 75% with normal tubules and wt1b glomeruli expression; 25% with normal tubules and absent wt1b glomeruli expression). In contrast, compared with wild-type controls (E), etv2 vessel progenitor expression is unaffected in osr1 mutants (F; expression was expanded in the midbody region (asterisks), as previously reported (Perens et al., 2021)), but is mostly absent in both npas4ls5 mutants (G) and npas4ls5;osr1el593 double mutants (H). n = 112 (A), 49 (B), 43 (C), 8 (D), 64 (E), 19 (F), 21 (G), 6 (H). Scale bars: 100 ?m.