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Glycobiology, 2002, Vol. 12, No. 12 785-792
© 2002 Oxford University Press

A complete {alpha}1,3-galactosyltransferase gene is present in the human genome and partially transcribed

Marion Lantéri2, Valérie Giordanengo2, Frédérique Vidal3, Patrick Gaudray4 and Jean-Claude Lefebvre1,2

2 INSERM U526, IFR50, Faculté de Médecine, 06107 Nice Cedex 2, France; 3 INSERM U470, Centre de Biochimie, Parc Valrose, 06108 Nice Cedex 2, France; and 4 CNRS-UNSA-UMR 6549, IFR50, Faculté de Médecine, 06107 Nice Cedex 2, France

The synthesis of Gal{alpha}1-3Gal-terminated oligosaccharides ({alpha}-Gal) epitopes has been interrupted during the course of evolution, starting with Old World primates. Partial sequences similar to the {alpha}1,3-galactosyltransferase ({alpha}1,3GalT) gene, which governs the synthesis of {alpha}-Gal epitopes, have been detected in the human genome and were found to correspond to pseudogenes. We completed the sequence of the human {alpha}1,3GalT pseudogene present on chromosome 9 and found it to be organized like the murine {alpha}1,3GalT gene. In human cell lines and several normal and tumor tissues we detected truncated transcripts corresponding to this pseudogene. Considering these mRNAs, translation of an open reading frame containing the first four translated exons but missing the two catalytic exons could predict a truncated {alpha}1,3GalT polypeptide that should be enzymatically inactive. We show that transcription of human {alpha}1,3GalT is prematurely terminated at the level of a strong transcriptional stop signal in the middle of intron VII. We were able to reproduce this effect in vitro by subcloning the implicated DNA region upstream from a reporter cDNA. The premature transcriptional arrest of human {alpha}1,3-GalT gene leads to an ectopic splicing event and to the connection of a short intronic sequence downstream from translated exons. Finally, we show that these truncated transcripts are overexpressed in cell lines with modifications of O-glycans.

1 To whom correspondence should be addressed; E-mail: lefebvre@unice.fr


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