Journal
JOURNAL OF CELL BIOLOGY
Volume 164, Issue 3, Pages 451-459Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200311112
Keywords
T-synthase; endothelial cell; galactosyltransferase; mucin; development
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Funding
- NCRR NIH HHS [RR 018758, RR 15577, P20 RR015577, P20 RR018758] Funding Source: Medline
- NHLBI NIH HHS [P50 HL054502, HL 54502] Funding Source: Medline
- NIAID NIH HHS [AI 48075, R01 AI048075] Funding Source: Medline
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The core 1 beta1-3-galactosyltransferase (T-synthase) transfers Gal from UDP-Gal to GalNAcalpha1-Ser/Thr (Tn antigen) to form the core 1 O-glycan Galbeta1-3GalNAcalpha1-Ser/Thr (T antigen). The T antigen is a precursor for extended and branched O-glycans of largely unknown function. We found that wild-type mice expressed the NeuAcalpha2-3Galbeta1-3GalNAcalpha1-Ser/Thr primarily in endothelial, hematopoietic, and epithelial cells during development. Gene-targeted mice lacking T-synthase instead expressed the nonsialylated Tn antigen in these cells and developed brain hemorrhage that was uniformly fatal by embryonic day 14. T-synthase-deficient brains formed a chaotic microvascular network with distorted capillary lumens and defective association of endothelial cells with pericytes and extracellular matrix. These data reveal an unexpected requirement for core 1-derived O-glycans during angiogenesis.
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