Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration

BACKGROUND: Cell surface glycosylation patterns are markers of cell type and status. However, the mechanisms regulating surface glycosylation patterns remain unknown. METHODOLOGY/PRINCIPAL FINDINGS: Using a panel of carbohydrate surface markers, we have shown that cell surface sialylation and fucosy...

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Autores principales: Li, Ya-li, Wu, Guang-zhi, Dawe, Gavin S., Zeng, Li, Cui, Shu-sen, Loers, Gabriele, Tilling, Thomas, Sun, Li, Schachner, Melitta, Xiao, Zhi-Cheng
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2008
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2585790/
https://www.ncbi.nlm.nih.gov/pubmed/19048108
http://dx.doi.org/10.1371/journal.pone.0003841
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author Li, Ya-li
Wu, Guang-zhi
Dawe, Gavin S.
Zeng, Li
Cui, Shu-sen
Loers, Gabriele
Tilling, Thomas
Sun, Li
Schachner, Melitta
Xiao, Zhi-Cheng
author_facet Li, Ya-li
Wu, Guang-zhi
Dawe, Gavin S.
Zeng, Li
Cui, Shu-sen
Loers, Gabriele
Tilling, Thomas
Sun, Li
Schachner, Melitta
Xiao, Zhi-Cheng
author_sort Li, Ya-li
collection PubMed
description BACKGROUND: Cell surface glycosylation patterns are markers of cell type and status. However, the mechanisms regulating surface glycosylation patterns remain unknown. METHODOLOGY/PRINCIPAL FINDINGS: Using a panel of carbohydrate surface markers, we have shown that cell surface sialylation and fucosylation were downregulated in L1(−/y) neurons versus L1(+/y) neurons. Consistently, mRNA levels of sialyltransferase ST6Gal1, and fucosyltransferase FUT9 were significantly reduced in L1(−/y) neurons. Moreover, treatment of L1(+/y) neurons with L1 antibodies, triggering signal transduction downstream of L1, led to an increase in cell surface sialylation and fucosylation compared to rat IgG-treated cells. ShRNAs for both ST6Gal1 and FUT9 blocked L1 antibody-mediated enhancement of neurite outgrowth, cell survival and migration. A phospholipase Cγ (PLCγ) inhibitor and shRNA, as well as an Erk inhibitor, reduced ST6Gal1 and FUT9 mRNA levels and inhibited effects of L1 on neurite outgrowth and cell survival. CONCLUSIONS: Neuronal surface sialylation and fucosylation are regulated via PLCγ by L1, modulating neurite outgrowth, cell survival and migration.
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spelling pubmed-25857902008-12-02 Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration Li, Ya-li Wu, Guang-zhi Dawe, Gavin S. Zeng, Li Cui, Shu-sen Loers, Gabriele Tilling, Thomas Sun, Li Schachner, Melitta Xiao, Zhi-Cheng PLoS One Research Article BACKGROUND: Cell surface glycosylation patterns are markers of cell type and status. However, the mechanisms regulating surface glycosylation patterns remain unknown. METHODOLOGY/PRINCIPAL FINDINGS: Using a panel of carbohydrate surface markers, we have shown that cell surface sialylation and fucosylation were downregulated in L1(−/y) neurons versus L1(+/y) neurons. Consistently, mRNA levels of sialyltransferase ST6Gal1, and fucosyltransferase FUT9 were significantly reduced in L1(−/y) neurons. Moreover, treatment of L1(+/y) neurons with L1 antibodies, triggering signal transduction downstream of L1, led to an increase in cell surface sialylation and fucosylation compared to rat IgG-treated cells. ShRNAs for both ST6Gal1 and FUT9 blocked L1 antibody-mediated enhancement of neurite outgrowth, cell survival and migration. A phospholipase Cγ (PLCγ) inhibitor and shRNA, as well as an Erk inhibitor, reduced ST6Gal1 and FUT9 mRNA levels and inhibited effects of L1 on neurite outgrowth and cell survival. CONCLUSIONS: Neuronal surface sialylation and fucosylation are regulated via PLCγ by L1, modulating neurite outgrowth, cell survival and migration. Public Library of Science 2008-12-02 /pmc/articles/PMC2585790/ /pubmed/19048108 http://dx.doi.org/10.1371/journal.pone.0003841 Text en This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. https://creativecommons.org/publicdomain/zero/1.0/ This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
spellingShingle Research Article
Li, Ya-li
Wu, Guang-zhi
Dawe, Gavin S.
Zeng, Li
Cui, Shu-sen
Loers, Gabriele
Tilling, Thomas
Sun, Li
Schachner, Melitta
Xiao, Zhi-Cheng
Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration
title Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration
title_full Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration
title_fullStr Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration
title_full_unstemmed Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration
title_short Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration
title_sort cell surface sialylation and fucosylation are regulated by l1 via phospholipase cγ and cooperate to modulate neurite outgrowth, cell survival and migration
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2585790/
https://www.ncbi.nlm.nih.gov/pubmed/19048108
http://dx.doi.org/10.1371/journal.pone.0003841
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