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XB-ART-41482
Dev Neurobiol September 15, 2010; 70 (11): 764-80.

Retinal patterning by Pax6-dependent cell adhesion molecules.

Rungger-Brändle E , Ripperger JA , Steiner K , Conti A , Stieger A , Soltanieh S , Rungger D .


Abstract
Long-standing evidence gained from Pax6 mutant embryos pointed to an involvement of Pax6-dependent cell adhesion molecules in patterning the central nervous system and, in particular, the retina. However, direct evidence for such pathways remained elusive. We here present direct evidence that knockdown of Pax6 expression by morpholino antisense molecules in Xenopus embryos and knockdown of maternal N-cadherin (mNcad), N-cadherin (Ncad) and neural cell adhesion molecule (NCAM) produce similar phenotypes. Eye formation is reduced and retinal lamination is heavily disorganized. In Pax6 knockdown embryos, the levels of mRNAs coding for these cell adhesion molecules are markedly reduced. Overexpression of Pax6 efficiently rescues the phenotype of Pax6 knockdown embryos and restores expression of these putative target genes. Rescue of Pax6-deficiency by the putative target gene mNcad moderately rescues eye formation. The promoters of the genes coding for cell adhesion molecules contain several putative Pax6 binding sites, as determined by computer analysis. Chromatin immunoprecipitation shows that, in embryonic heads, Pax6 binds to promoter regions containing such predicted binding sites. Thus, several cell adhesion molecules are direct target genes of Pax6 and cooperate in retinal patterning.

PubMed ID: 20556827
Article link: Dev Neurobiol

Genes referenced: acta4 clock ncam1 pax6 rpe snrpb utp25 vim
Antibodies: Pax6 Ab3
Morpholinos: cdh2 MO1 cdh4 MO1 ncam1 MO1 pax6 MO1


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