Fig. 5

Concurrent depletion of RARαb1 and Cyp26a1 results in phenotypes resembling RA treatment.

(A–D) Control sibling, RARαb1 deficient, Cyp26a1 deficient, and RARαb1+Cyp26a1 deficient embryos. A suboptimal dose of the cyp26a1 MOs was used that did not cause ostensible defects for these experiments. In D, arrow indicates loss of the MHB and line indicates shortened tail. Images are lateral views with dorsal right and anterior up. (E–H) ISH for eng2a, which marks the MHB. 100% of (E) control sibling (n = 11), (F) RARαb1 deficient (n = 7), and (G) Cyp26a1 deficient (n = 7) had eng2a expression. 85% of (H) RARαb1+Cyp26a1 deficient embryos (n = 7) had a complete absence of eng2a expression (arrow in H). Equivalent results were obtained using pax2a, which also marks the MHB (data not shown). (I–L) Hearts from control sibling, RARαb1 deficient, Cyp26a1 deficient, and RARαb1+Cyp26a1 deficient Tg(-5.1myl7:DsRed-NLS)^f2 embryos. Images are frontal views. Red indicates ventricle. Green indicates atrium. (M–P) ISH for egfp in Tg(β-actin:GDBD-RLBD)^cch1;Tg(UAS:EGFP) embryos. Lateral views with dorsal right and anterior up. (Q) Mean CM number at 48 hpf and (R) qPCR for egfp expression at 15 s in control sibling, RARαb1 deficient, Cyp26a1 deficient, and RARαb1+Cyp26a1 deficient embryos. Double asterisks in Q indicate a statistically significant difference relative to control and RARαb1 deficient embryos. Pound sign in Q indicates a statistically significant difference relative to RARαb1 deficient embryos.