Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/61632
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dc.contributorSchool of Optometry-
dc.creatorHe, F-
dc.creatorAgosto, MA-
dc.creatorAnastassov, IA-
dc.creatorTse, DY-
dc.creatorWu, SM-
dc.creatorWensel, TG-
dc.date.accessioned2016-12-19T08:56:38Z-
dc.date.available2016-12-19T08:56:38Z-
dc.identifier.urihttp://hdl.handle.net/10397/61632-
dc.language.isoenen_US
dc.publisherNature Publishing Groupen_US
dc.rightsThis work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/en_US
dc.rightsThe following publication He, F. et al. Phosphatidylinositol-3-phosphate is light-regulated and essential for survival in retinal rods. Sci. Rep. 6, 26978 (2016) is available at https://dx.doi.org/10.1038/srep26978en_US
dc.titlePhosphatidylinositol-3-phosphate is light-regulated and essential for survival in retinal rodsen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.volume6-
dc.identifier.doi10.1038/srep26978-
dcterms.abstractPhosphoinositides play important roles in numerous intracellular membrane pathways. Little is known about the regulation or function of these lipids in rod photoreceptor cells, which have highly active membrane dynamics. Using new assays with femtomole sensitivity, we determined that whereas levels of phosphatidylinositol-3,4-bisphosphate and phosphatidylinositol-3,4,5-Trisphosphate were below detection limits, phosphatidylinositol-3-phosphate (PI(3)P) levels in rod inner/outer segments increased more than 30-fold after light exposure. This increase was blocked in a rod-specific knockout of the PI-3 kinase Vps34, resulting in failure of endosomal and autophagy-related membranes to fuse with lysosomes, and accumulation of abnormal membrane structures. At early ages, rods displayed normal morphology, rhodopsin trafficking, and light responses, but underwent progressive neurodegeneration with eventual loss of both rods and cones by twelve weeks. The degeneration is considerably faster than in rod knockouts of autophagy genes, indicating defects in endosome recycling or other PI(3)P-dependent membrane trafficking pathways are also essential for rod survival.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationScientific reports, 1 2016, v. 6, no. , p. 1-12-
dcterms.isPartOfScientific reports-
dcterms.issued2016-
dc.identifier.isiWOS:000377158600001-
dc.identifier.scopus2-s2.0-84973295078-
dc.identifier.pmid27245220-
dc.identifier.ros2016004914-
dc.identifier.eissn2045-2322-
dc.identifier.rosgroupid2016004787-
dc.description.ros2016-2017 > Academic research: refereed > Publication in refereed journal-
dc.description.validate201804_a bcma-
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_IR/PIRAen_US
dc.description.pubStatusPublisheden_US
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