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Transcription factor AP-2delta regulates the expression of polysialyltransferase ST8SIA2 in chick retina
•AP-2δ is expressed in one-third of retinal ganglion cells.•ST8SIA2 is induced by AP-2δ overexpression in chick retina.•ST8SIA2 is direct target of AP-2δ based on ChIP and gel shift analysis.•Increases in PSA levels upon AP-2δ overexpression may be due to ST8SIA2 activation. The AP-2δ transcription...
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Published in: | FEBS letters 2014-03, Vol.588 (5), p.770-775 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •AP-2δ is expressed in one-third of retinal ganglion cells.•ST8SIA2 is induced by AP-2δ overexpression in chick retina.•ST8SIA2 is direct target of AP-2δ based on ChIP and gel shift analysis.•Increases in PSA levels upon AP-2δ overexpression may be due to ST8SIA2 activation.
The AP-2δ transcription factor is restricted to a subset of retinal ganglion cells. Overexpression of AP-2δ in chick retina results in induction of polysialylated neural cell adhesion molecule (PSA-NCAM) accompanied by misrouting and bundling of ganglion cell axons. Two polysialyltransferases, ST8SIA2 and ST8SIA4, are responsible for polysialylation of NCAM. Here, we investigate the mechanism driving the increase in PSA-NCAM observed upon AP-2δ overexpression. We show that ST8SIA2 is induced by AP-2δ overexpression in chick retina. We use chromatin immunoprecipitation and gel shift assays to demonstrate direct interaction between AP-2δ and the ST8SIA2 promoter. We propose that up-regulation of ST8SIA2 upon AP-2δ overexpression in retina increases ectopic polysialylation of NCAM which in turn causes premature bundling of axons and alters axonal response to guidance cues. |
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ISSN: | 0014-5793 1873-3468 |
DOI: | 10.1016/j.febslet.2014.01.024 |