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NOGO-A/RTN4A and NOGO-B/RTN4B Are Simultaneously Expressed in Epithelial, Fibroblast and Neuronal Cells and Maintain ER Morphology

Overview
Journal Sci Rep
Specialty Science
Date 2016 Oct 28
PMID 27786289
Citations 19
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Abstract

Reticulons (RTNs) are a large family of membrane associated proteins with various functions. NOGO-A/RTN4A has a well-known function in limiting neurite outgrowth and restricting the plasticity of the mammalian central nervous system. On the other hand, Reticulon 4 proteins were shown to be involved in forming and maintaining endoplasmic reticulum (ER) tubules. Using comparative transcriptome analysis and qPCR, we show here that NOGO-B/RTN4B and NOGO-A/RTN4A are simultaneously expressed in cultured epithelial, fibroblast and neuronal cells. Electron tomography combined with immunolabelling reveal that both isoforms localize preferably to curved membranes on ER tubules and sheet edges. Morphological analysis of cells with manipulated levels of NOGO-B/RTN4B revealed that it is required for maintenance of normal ER shape; over-expression changes the sheet/tubule balance strongly towards tubules and causes the deformation of the cell shape while depletion of the protein induces formation of large peripheral ER sheets.

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References
1.
Puhka M, Vihinen H, Joensuu M, Jokitalo E . Endoplasmic reticulum remains continuous and undergoes sheet-to-tubule transformation during cell division in mammalian cells. J Cell Biol. 2007; 179(5):895-909. PMC: 2099207. DOI: 10.1083/jcb.200705112. View

2.
He W, Shi Q, Hu X, Yan R . The membrane topology of RTN3 and its effect on binding of RTN3 to BACE1. J Biol Chem. 2007; 282(40):29144-51. DOI: 10.1074/jbc.M704181200. View

3.
Rismanchi N, Soderblom C, Stadler J, Zhu P, Blackstone C . Atlastin GTPases are required for Golgi apparatus and ER morphogenesis. Hum Mol Genet. 2008; 17(11):1591-604. PMC: 2902292. DOI: 10.1093/hmg/ddn046. View

4.
Kano F, Kondo H, Yamamoto A, Kaneko Y, Uchiyama K, Hosokawa N . NSF/SNAPs and p97/p47/VCIP135 are sequentially required for cell cycle-dependent reformation of the ER network. Genes Cells. 2005; 10(10):989-99. DOI: 10.1111/j.1365-2443.2005.00894.x. View

5.
Borgese N, Francolini M, Snapp E . Endoplasmic reticulum architecture: structures in flux. Curr Opin Cell Biol. 2006; 18(4):358-64. PMC: 4264046. DOI: 10.1016/j.ceb.2006.06.008. View