The developing eye is known to be rich in retinoic acid (RA), and pert
urbations in RA levels during formation of the optic primordia, as wel
l as RA receptor mutations, cause retinal malformations, especially in
ventral eye regions. To test the hypothesis that RA plays a role in t
he establishment of ventral retinal characteristics, we examined sever
al dorsal and ventral ocular markers in RA-treated zebrafish. The opti
c stalk represents the ventral-most region of the early eye field. Dur
ing normal development, the optic stalks constrict, decreasing in widt
h and are gradually replaced by the optic nerve. Systemic high RA leve
ls cause an expansion in the optic stalk with an increased cell conten
t and a patent lumen. In addition, the stalks do not constrict and per
sist into later stages of development indicating an enhancement of ear
ly ventral eye characteristics. Expression of the transcription factor
pax[b], normally confined to the ventral retina, expands into the dor
sal retina following RA treatment, whereas msh[c], normally expressed
in the dorsal retinal pole, disappears. Activity of an aldehyde dehydr
ogenase that normally occupies the dorsal third of the retina is reduc
ed or abolished following high systemic RA. When a localized RA source
, an RA-soaked bead, is placed next to the developing eye, a fissure r
esembling the choroid fissure appears in the eye facing the bead. Take
n together, these observations suggest that RA is involved in the dete
rmination of the ventral retina.