Fig. 4. Loss-of-DHCR7 affects cellular response toward Hh signaling in optic vesicle. (A-F) DHCR7 knockdown by MOs leads to eye defects. Four-cell stage Xenopus embryos were injected marginally in all four blastomeres with 5 ng of control MO (A,D), DHCR7 MOs (B,E) or DHCR7 MOs together with 125 pg of full-length DHCR7 rescue mRNA (C,F). Additional defects detected were in the heart and gut of the swimming tadpole stages (data not shown). (G-R) Loss of DHCR7 affects cellular response towards Hh signaling. Four-cell stage Xenopus embryos were injected with 20 ng of control MO (G,G',K,K',O,O'), 20ng of DHCR7 MOs alone (H,H',L,L',P,P'), 50 pg of Shh-N mRNA alone (I,I',M,M',Q,Q') or 20 ng of DHCR7 MOs with 50 pg of Shh-N mRNA (J,J',N,N',R,R'). Knockdown of DHCR7 reduces Pax6 expression (G-J), expands the expression of Pax2 expression (K-N) and upregulates Gli1 expression (O-R). (G'-R') Continuously treatment of embryos with cyclopamine (100 µM) from the blastula stage blocks Hh signaling (G-J,K-N,O-R). Circled areas mark optic vesicles.