期刊
GLYCOBIOLOGY
卷 20, 期 7, 页码 872-882出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/glycob/cwq045
关键词
nucleotide sugars metabolism; trypanosomatids; UDP-galactose; UDP-glucose
资金
- impact-based institutional funding (Leistungsorientiere Mittelvergabe, LOM)
- Deutsche Forschungsgemeinschaft (DFG)
- National Institute of Diabetes and Digestive and Kidney Diseases [P30DK056341]
- National Institutes of Health [AI31078]
- United States Public Health Service [P41-RR00954, P60-DK20579, P30-DK56341]
The nucleotide sugar UDP-galactose (UDP-Gal) is essential for the biosynthesis of several abundant glycoconjugates forming the surface glycocalyx of the protozoan parasite Leishmania major. Current data suggest that UDP-Gal could arise de novo by epimerization of UDP-glucose (UDP-Glc) or by a salvage pathway involving phosphorylation of Gal and the action of UDP-glucose:alpha-d-galactose-1-phosphate uridylyltransferase as described by Leloir. Since both pathways require UDP-Glc, inactivation of the UDP-glucose pyrophosphorylase (UGP) catalyzing activation of glucose-1 phosphate to UDP-Glc was expected to deprive parasites of UDP-Gal required for Leishmania glycocalyx formation. Targeted deletion of the gene encoding UGP, however, only partially affected the synthesis of the Gal-rich phosphoglycans. Moreover, no alteration in the abundant Gal-containing glycoinositolphospholipids was found in the deletion mutant. Consistent with these findings, the virulence of the UGP-deficient mutant was only modestly affected. These data suggest that Leishmania elaborates a UDP-Glc independent salvage pathway for UDP-Gal biosynthesis.
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