FIGURE

Fig. 4

ID

ZDB-FIG-230829-22

Publication

George et al., 2022 - Zebrafish model of RERE syndrome recapitulates key ophthalmic defects that are rescued by small molecule inhibitor of shh signaling

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Fig. 4

Zebrafish rerea homozygous mutants exhibit disruption of retinal optic stalk boundary. Zebrafish larvae homozygous for rerea mutation exhibit disruption of retinal optic stalk boundary (A–C, D–F), which was further confirmed by isolation of eye cups (A, D, bottom panels) and detailed coronal histological sectioning (B, E) of 6 dpf larvae. Unfused margins of optic fissure can be observed (D bottom panel, red arrow). The presence of ectopic differentiated retinal layers (C, F) was confirmed by immunostaining with ZPR-1 (photoreceptors) and HuC/D (amacrine cells and ganglion cells).

Expression Data

Antibodies:	Ab5-elavl zpr-1
Fish:	AB/TL rerea^tb210/tb210 (AB/TL)
Anatomical Terms:	amacrine cell retinal ganglion cell layer retinal photoreceptor layer
Stage:	Day 6

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	rerea^tb210/tb210 (AB/TL)
Observed In:	diencephalon ventral region retinal neural layer
Stage:	Day 6

Phenotype Detail

Acknowledgments

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