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Vol. 12, No. 12, pp. 1894-1906, June 15, 1998
1 Laboratory of Mammalian Development, Medical Research
Council (MRC) National Institute for Medical Research, The
Ridgeway, London NW7 1AA, UK;
2 MRC Human Genetics Unit,
Western General Hospital, Edinburgh EH4 2XU, UK;
3 Molecular
Medicine Centre, Western General Hospital, Edinburgh EH4 2XU, UK
Heparan sulfate proteoglycans have been implicated in the
presentation of a number of secreted signaling molecules to their signal-transducing receptors. We have characterized a gene trap mutation in the gene encoding a heparan sulfate biosynthetic enzyme, heparan sulfate 2-sulfotransferase (HS2ST). Transgenic mice were generated from embryonic stem cells harboring this insertion. lacZ reporter gene activity in heterozygous embryos
demonstrates that the gene is expressed differentially during
embryogenesis, presumably directing dynamic changes in heparan sulfate
structure. Moreover, mice homozygous for the Hs2st gene trap
allele die in the neonatal period, exhibiting bilateral renal agenesis
and defects of the eye and the skeleton. Analysis of kidney development
in Hs2st mutants reveals that the gene is not required for two
early events
ureteric bud outgrowth from the Wolffian duct and initial induction of Pax-2 expression in the metanephric mesenchyme. It is
required, however, for mesenchymal condensation around the ureteric bud
and initiation of branching morphogenesis. Because 2-O-sulfation has been shown to influence the functional
interactions of ligands with heparan sulfate in vitro, we discuss the
possibility that the Hs2st mutant phenotype is a consequence of
compromised interactions between growth factors and their
signal-transducing receptors. These data provide the first genetic
evidence that the regulated synthesis of differentially glycosylated
proteoglycans can affect morphogenesis during vertebrate development.
[Key Words: Gene trap; heparan sulfate proteoglycan; sulfotransferase; kidney; induction]
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