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Cell surface sialylation and fucosylation are regulated by the cell recognition molecule L1 via PLCγ and cooperate to modulate embryonic stem cell survival and proliferation
Author(s) -
Li Ya-Li,
Wu Guang-Zhi,
Zeng Li,
Dawe Gavin S.,
Sun Li,
Loers Gabriele,
Tilling Thomas,
Cui Shu-sen,
Schachner Melitta,
Xiao Zhi-Cheng
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.01.013
Subject(s) - fucosylation , fucosyltransferase , embryonic stem cell , microbiology and biotechnology , stem cell , cell growth , cell , downregulation and upregulation , biology , chemistry , biochemistry , fucose , gene , glycoprotein
Cell surface glycosylation patterns are markers of cell type and status. However, the mechanisms regulating surface glycosylation patterns remain unknown. Using a panel of carbohydrate markers, we have shown that cell surface sialylation and fucosylation are upregulated in L1‐transfected embryonic stem cells (L1‐ESCs). Consistently, the mRNA levels of sialyltransferase ST6Gal1 and ST3Gal4, and fucosyltransferase FUT9 were significantly increased in L1‐transfected ESCs. Activation of L1 signaling promoted cell survival and inhibited cell proliferation. ShRNAs knocking down FUT9, ST6Gal1 and ST3Gal4 blocked these effects. A phospholipase Cγ (PLCγ) inhibitor and shRNA reduced ST6Gal1, ST3Gal4 and FUT9 mRNA levels in the L1‐ESCs. Thus, embryonic stem cell surface sialylation and fucosylation are regulated via PLCγ by L1, with which they cooperate to modulate cell survival and proliferation.