Differential developmental deficits in retinal function in the absence of either protein tyrosine sulfotransferase-1 or -2

• Published in: PloS one Vol. 7; no. 6; p. e39702
• Main Authors: Sherry, David M, Kanan, Yogita, Hamilton, Robert, Hoffhines, Adam, Arbogast, Kelsey L, Fliesler, Steven J, Naash, Muna I, Moore, Kevin L, Al-Ubaidi, Muayyad R
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 22.06.2012; Public Library of Science (PLoS)
• Subjects: Animals; Biology; Electroretinography; Enzymes; Health sciences; Immunoblotting; Localization; Medicine; Mice; Mice, Knockout; Microscopy, Electron; Nervous system; Neurosciences; Phenols (Class of compounds); Photoreceptors; Plasma; Proteins; Retina; Retina - enzymology; Retina - growth & development; Retina - physiology; Rodents; Structure-function relationships; Studies; Sulfation; Sulfotransferase; Sulfotransferases - genetics; Sulfotransferases - metabolism; Tetanus; Tyrosine; New York; United States > US; Oklahoma
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0039702

To investigate the role(s) of protein-tyrosine sulfation in the retina and to determine the differential role(s) of tyrosylprotein sulfotransferases (TPST) 1 and 2 in vision, retinal function and structure were examined in mice lacking TPST-1 or TPST-2. Despite the normal histologic retinal appearance in both Tpst1(-/-) and Tpst2(-/-) mice, retinal function was compromised during early development. However, Tpst1(-/-) retinas became electrophysiologically normal by postnatal day 90 while Tpst2(-/-) mice did not functionally normalize with age. Ultrastructurally, the absence of TPST-1 or TPST-2 caused minor reductions in neuronal plexus. These results demonstrate the functional importance of protein-tyrosine sulfation for proper development of the retina and suggest that the different phenotypes resulting from elimination of either TPST-1 or -2 may reflect differential expression patterns or levels of the enzymes. Furthermore, single knock-out mice of either TPST-1 or -2 did not phenocopy mice with double-knockout of both TPSTs, suggesting that the functions of the TPSTs are at least partially redundant, which points to the functional importance of these enzymes in the retina.