Developmental expression of beta-catenin in mouse retina.

Xiao Liu*, Vijay P. Sarthy, Cheryl M. Craft, Yoshihito Honda, Chizuka Ide

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Recent studies have shown that catenins play a pivotal role in neuronal signalling during vertebrate development. In order to study the significance of beta-catenin in the developing mouse retina, the localization of beta-catenin was examined by immunohistochemistry from embryonic day (E) 12 to adult mice. Immunoreactivity for beta-catenin was found in ganglion cells of the retina at E12, and extended to the inner and outer plexiform layer as well as the ganglion-cell layer with the strongest immunolabelling from E16 through to postnatal day (P) 5. The immunoreactivity of ganglion cells was distributed on the cell surface. Thereafter, the immunoreactivity gradually decreased, being limited to the inner plexiform layer and ganglion-cell layer, including the nerve-fiber layer in P10. By P16, the weak immunoreactivity was detected in the inner plexiform layer and ganglion-cell layer, and almost disappeared in the adult retina. No distinct immunoreactivity was found in the retinal pigment epithelium. The reverse transcription polymerase chain reaction showed that beta-catenin messenger ribonuclic acid was detected at E12, E16, P1 and P16, and thereafter markedly decreased, being weakest in the adult. These findings show that beta-catenin is expressed during development at the sites of synaptic connections of inner and outer plexiform layers, and on the ganglion cells and their fibers in the retina, suggesting that beta-catenin might play an important role in the synapse formation and ganglion-cell development during the morphogenesis of the retina.

Original languageEnglish (US)
Pages (from-to)182-188
Number of pages7
JournalAnatomical science international / Japanese Association of Anatomists
Issue number3
StatePublished - Sep 2002

ASJC Scopus subject areas

  • Anatomy


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