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First published online 5 October 2005
doi: 10.1242/dev.02031
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Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Institut Clinique de la Souris (ICS), CNRS/INSERM/ULP, Collège de France, BP10142, 67404 Illkirch Cedex, CU de Strasbourg, France
Author for correspondence (e-mail:
norbert{at}igbmc.u-strasbg.fr)
Accepted 8 August 2005
Using genetic approaches in the mouse, we show that the primary target
tissue of retinoic acid (RA) action during eye morphogenesis is not the retina
nor the corneal ectoderm, which both express RA-synthesizing retinaldehyde
dehydrogenases (RALDH1 and RALDH3), but the neural crest cell-derived
periocular mesenchyme (POM), which is devoid of RALDH. In POM, the effects of
the paracrine RA signal are mediated by the nuclear RA receptors heterodimers
RXR
/RARß and RXR/RAR
. These heterodimers appear to
control: (1) the remodeling of the POM through activation of
Eya2-related apoptosis; (2) the expression of Foxc1 and
Pitx2, which play crucial roles in anterior eye segment development;
and (3) the growth of the ventral retina. We additionally show that RALDH1 and
RALDH3 are the only enzymes that are required for RA synthesis in the eye
region from E10.5 to E13.5, and that patterning of the dorsoventral axis of
the retina does not require RA.
Key words: Retinoic acid receptor, Retinaldehyde dehydrogenase, Periocular mesenchyme, Somatic mutagenesis, Axenfeld-Rieger's syndrome
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