Retinoic acid perturbs Otx gene expression in the ascidian pharynx

In vertebrate embryos, ectopic application of all-trans retinoic acid (RA) alters the expression of Otx genes in the developing midbrain. In conjuncti on with RA-induced misexpression of other regulatory genes this leads to a loss of anterior CNS. In the ascidian Herdmania curvata, RA primarily inhib its the development of the juvenile pharynx. An ascidian Otx gene, Hec-Otx, is expressed largely in this tissue, associated stomodeal structures and t he anterior endostyle of the juvenile. Treatment with 10(-6) M RA reduces H ec-Otx mRNA levels in the juvenile to about 12% of normal and is correlated closely with the loss of pharyngeal structures. During embryogenesis the e xpression of Hec-Otx becomes restricted to cell lineages fated to give rise to the anterior-most nervous system and the stomodeal component of the pri mordial pharynx. In hatched larvae Hec-Otx transcripts are detected only in the sensory (brain) vesicle. RA reduces Hec-Otx expression in the tailbud stomodeal pharynx primordium/anterior nervous system cell line but not in t he larval sensory vesicle, suggesting that RA regulation of Hec-Otx express ion is restricted to pharyngeal tissues throughout embryonic and postlarval development. RA does not affect expression of Hec-Pax2/5/8, which is norma lly expressed within the developing nervous system immediately posterior to Hec-Otx at the tailbud stage, lending support to the proposition that RA d oes not impact CNS axial patterning. These data combined with those from ot her chordates suggest that RA regulation of Otx expression in the anterior nerve cord and pharynx is a primitive chordate feature which has been maint ained predominantly in pharyngeal tissues in the ascidian.