Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development
Kunwar AJ, Rickmann M, Backofen B, Browski SM, Rosenbusch J, Schoening S, Fleischmann T, Krieglstein K, Fischer von Mollard G (2011)
Proceedings of the National Academy of Sciences 108(6): 2575-2580.
Zeitschriftenaufsatz
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Autor*in
Kunwar, Ajaya J.;
Rickmann, Michael;
Backofen, Bianca;
Browski, Sascha M.UniBi;
Rosenbusch, Joachim;
Schoening, Susanne;
Fleischmann, Thomas;
Krieglstein, Kerstin;
Fischer von Mollard, GabrieleUniBi
Einrichtung
Abstract / Bemerkung
Fusion between membranes is mediated by specific SNARE complexes. Here we report that fibroblasts survive the absence of the trans-Golgi network/early endosomal SNARE vti1a and the late endosomal SNARE vti1b with intact organelle morphology and minor trafficking defects. Because vti1a and vti1b are the only members of their SNARE subclass and the yeast homolog Vti1p is essential for cell survival, these data suggest that more distantly related SNAREs acquired the ability to function in endosomal traffic during evolution. However, absence of vti1a and vti1b resulted in perinatal lethality. Major axon tracts were missing, reduced in size, or misrouted in Vti1a(-/-) Vti1b(-/-) embryos. Progressive neurodegeneration was observed in most Vti1a(-/-) Vti1b(-/-) peripheral ganglia. Neurons were reduced by more than 95% in Vti1a(-/-) Vti1b(-/-) dorsal root and geniculate ganglia at embryonic day 18.5. These data suggest that special demands for endosomal membrane traffic could not be met in Vti1a(-/-) Vti1b(-/-) neurons. Vti1a(-/-) and Vti1b(-/-) single deficient mice were viable without these neuronal defects, indicating that they can substitute for each other in these processes.
Stichworte
endosome;
neurite outgrowth;
neuronal survival
Erscheinungsjahr
2011
Zeitschriftentitel
Proceedings of the National Academy of Sciences
Band
108
Ausgabe
6
Seite(n)
2575-2580
ISSN
0027-8424
eISSN
1091-6490
Page URI
https://pub.uni-bielefeld.de/record/2093998
Zitieren
Kunwar AJ, Rickmann M, Backofen B, et al. Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development. Proceedings of the National Academy of Sciences. 2011;108(6):2575-2580.
Kunwar, A. J., Rickmann, M., Backofen, B., Browski, S. M., Rosenbusch, J., Schoening, S., Fleischmann, T., et al. (2011). Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development. Proceedings of the National Academy of Sciences, 108(6), 2575-2580. https://doi.org/10.1073/pnas.1013891108
Kunwar, Ajaya J., Rickmann, Michael, Backofen, Bianca, Browski, Sascha M., Rosenbusch, Joachim, Schoening, Susanne, Fleischmann, Thomas, Krieglstein, Kerstin, and Fischer von Mollard, Gabriele. 2011. “Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development”. Proceedings of the National Academy of Sciences 108 (6): 2575-2580.
Kunwar, A. J., Rickmann, M., Backofen, B., Browski, S. M., Rosenbusch, J., Schoening, S., Fleischmann, T., Krieglstein, K., and Fischer von Mollard, G. (2011). Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development. Proceedings of the National Academy of Sciences 108, 2575-2580.
Kunwar, A.J., et al., 2011. Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development. Proceedings of the National Academy of Sciences, 108(6), p 2575-2580.
A.J. Kunwar, et al., “Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development”, Proceedings of the National Academy of Sciences, vol. 108, 2011, pp. 2575-2580.
Kunwar, A.J., Rickmann, M., Backofen, B., Browski, S.M., Rosenbusch, J., Schoening, S., Fleischmann, T., Krieglstein, K., Fischer von Mollard, G.: Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development. Proceedings of the National Academy of Sciences. 108, 2575-2580 (2011).
Kunwar, Ajaya J., Rickmann, Michael, Backofen, Bianca, Browski, Sascha M., Rosenbusch, Joachim, Schoening, Susanne, Fleischmann, Thomas, Krieglstein, Kerstin, and Fischer von Mollard, Gabriele. “Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development”. Proceedings of the National Academy of Sciences 108.6 (2011): 2575-2580.
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Zweifel LS, Kuruvilla R, Ginty DD., Nat. Rev. Neurosci. 6(8), 2005
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A role for synaptotagmin VII-regulated exocytosis of lysosomes in neurite outgrowth from primary sympathetic neurons.
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Jahn R, Scheller RH., Nat. Rev. Mol. Cell Biol. 7(9), 2006
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Lindwall C, Fothergill T, Richards LJ., Curr. Opin. Neurobiol. 17(1), 2007
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Syntaxin 16 and syntaxin 5 are required for efficient retrograde transport of several exogenous and endogenous cargo proteins.
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An elaborate classification of SNARE proteins sheds light on the conservation of the eukaryotic endomembrane system.
Kloepper TH, Kienle CN, Fasshauer D., Mol. Biol. Cell 18(9), 2007
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The retromer complex influences Wnt secretion by recycling wntless from endosomes to the trans-Golgi network.
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A syntaxin 10-SNARE complex distinguishes two distinct transport routes from endosomes to the trans-Golgi in human cells.
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New insights into the mechanisms of macroautophagy in mammalian cells.
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Roles of endosomal trafficking in neurite outgrowth and guidance.
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Combinational soluble N-ethylmaleimide-sensitive factor attachment protein receptor proteins VAMP8 and Vti1b mediate fusion of antimicrobial and canonical autophagosomes with lysosomes.
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Rapaport D, Lugassy Y, Sprecher E, Horowitz M., PLoS ONE 5(3), 2010
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Integrin signaling switches the cytoskeletal and exocytic machinery that drives neuritogenesis.
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