Lack of protein-tyrosine sulfation disrupts photoreceptor outer segment morphogenesis, retinal function and retinal anatomy
Version of Record online: 12 OCT 2010
© 2010 The Authors. European Journal of Neuroscience © 2010 Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 32, Issue 9, pages 1461–1472, November 2010
How to Cite
Sherry, D. M., Murray, A. R., Kanan, Y., Arbogast, K. L., Hamilton, R. A., Fliesler, S. J., Burns, M. E., Moore, K. L. and Al-Ubaidi, M. R. (2010), Lack of protein-tyrosine sulfation disrupts photoreceptor outer segment morphogenesis, retinal function and retinal anatomy. European Journal of Neuroscience, 32: 1461–1472. doi: 10.1111/j.1460-9568.2010.07431.x
- Issue online: 2 NOV 2010
- Version of Record online: 12 OCT 2010
- Received 11 February 2010, revised 27 July 2010, accepted 28 July 2010
Fig. S1. Representative electroretinographic traces for wt and Tpst DKO retinas.
Fig. S2. Immunoblot (Western) analysis of cone opsins and synpatotagmin 2.
Fig. S3. Bipolar cell populations and placement are unaffected by the absence of tyrosine sulfation.
Fig. S4. Amacrine cell populations and placement are normal in the absence of tyrosine sulfation, but plexes of some amacrine cells are reduced.
Fig. S5. Horizontal, ganglion and Müller glial cells are normal in the absence of tyrosine sulfation.
Table S1. Primary antibodies, antisera and lectins used to label retinal cells and synapses.
Table S2. Effects of Tpst1 and Tpst2 double knockout on cell-specific morphology and synaptic protein expression.
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