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Dana F DeSantis, Qingxiang Zhou, Scott J Neal, Francesca Pignoni; β-catenin promotes non-neural cell fate in the developing Drosophila eye through canonical Wnt signaling. Invest. Ophthalmol. Vis. Sci. 2017;58(8):122.
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© ARVO (1962-2015); The Authors (2016-present)
The the eye disc of Drosophila, the peripodial epithelium (PE) is a support tissue, that, like the RPE of the vertebrate optic vesicle, supports development of the neural retina. We have identified Armadillo (Arm), the fly homolog of β-catenin, as a key regulator of fate in the eye disc epithelium. Here, we explore the role of Arm in suppressing retina fate and promoting PE fate.
The GAL4/UAS system was used to induce loss (UAS-RNAi) and gain (UAS-cDNA) of function in either the entire eye disc (ey-FLP, Act>IC>GAL4) or in the PE alone (odd-GAL4). Changes in fate within the eye disc were assessed by immunohistochemistry for retinal, neuronal, and PE markers, followed by confocal microscopy and statistical analysis for <100% penetrant phenotypes.
We show that, in the eye disc, loss of Arm function results in the transformation of PE into neural retina (4 independent transgenic RNAi lines), and, conversely, overexpression of constitutively active ArmAct is sufficient to suppress retinal fate. We confirm that Arm function is required in the presumptive PE by inducing tissue-specific loss-of-function. In addition, we find that loss of canonical Wnt-pathway components, including Wnt4 (4 RNAi lines), Hyx (3 RNAi lines), and Pygo (1 RNAi line), induces PE-to-retina transformation. Lastly, overexpression of the GSK3-β kinase homolog, Sgg, results in PE-to-retina transformation, whereas depletion of Sgg results in suppression of retinal fate. This is consistent with known regulation of β-catenin activity by phosphorylation.
In the Drosophila eye disc, as in the vertebrate optic vesicle, the binary choice between the neural retina and its support tissue is dependent on Arm/β-catenin. We show that this fate choice in the fly occurs via canonical Wnt signaling, which activates Arm in order to promote PE formation and suppress retinal fate.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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