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While our results confirm that deletions of chromo-some 7ql 1.23 are particularly frequent in sporadic WS, they suggest that the deletions vary in size, as they did not consistently involve lociD7S1870 and D7S489. In addition, heterozygosity for probes AFM199wflO and AFM295yg9 showed that the flanking loci D7S653 and D7S675 were not involved in the deletion in 10 of 27 probands (fig. 2). Yet deletions most probably extend far beyond the elastin gene, as already noted by Ewart et al.(1993). Moreover, as the failure of parental inheri-tance involved both the paternal (34%) and the maternal chromosome 7 (44%, difference nonsignificant), our re-sults argue against a role for genomic imprinting in the pathogenesis of Williams syndrome. The availability of microsatellite DNA markers, which detect de novo deletions in almost 80% of spo-radic WS, has several practical consequences. First, the PCR-based genotypic …