Several studies on small homogenous populations suggested that fragile
-X syndrome originated from a limited number of founder chromosomes. T
he Israeli Jewish population could serve as an adequate model for trac
ing a founder effect due to the unique ethnic makeup and traditional l
ifestyle. Furthermore, a common haplotype for Jewish Tunisian fragile
X patients was recently reported, To test for a similar occurrence in
the Jewish Ashkenazi population, we performed haplotype analysis of 23
fragile-X patients and 28 normal chromosomes, all Jewish Ashkenazi, u
sing microsatellite markers within and flanking the FMR-1 gene: FRAXAC
1, FRAXAC2, and DXS548, The combined triple-marker analysis identified
a wide range of diverse haplotypes in patients and controls, with no
distinct haplotype prevalent in the patient group. Our data suggest th
at no common ancestral X chromosome is associated with the fragile-X s
yndrome in the Israeli Jewish Ashkenazi patient population studied. Th
ese findings are in contrast to other reports on founder effect associ
ated with fragile-X syndrome in distinct European as well as Jewish Tu
nisian populations. On this basis, a more complex mechanism for the de
velopment of fragile-X syndrome in the Jewish Ashkenazi population sho
uld be considered.