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© 1993 Oxford University Press

RESEARCH-ARTICLE

Paired STSs amplified from radiation hybrids, and from associated YACs, identify highly polymorphic loci flanking the ataxia telangiectasia locus on chromosome 11q22–23

Carmel M.McConville*, Philip J.Byrd, Helen J.Ambrose, Tanja Stankovic, Yael Ziv1, Anat Bar-Shira1, Lina Vanagaite1, Galit Rotman1, Yosef Shiloh1, Godfrey T.Gillett2, John H.Riley3 and A.Malcolm R.Taylor

Department of Cancer Studies, The Medical School, University of Birmingham Birmingham B15 2TJ, UK 1Department of Human Genetics, Sackler School of Medicine, Tel Aviv University Ramat Aviv 69978, Israel 2MRC Human Biochemical Genetics Unit, The Galton Laboratory, Wolfson House, University College London 4 Stephenson Way, London NW1 2HE 3Zeneca Pharmaceuticals Alderley Park, Macclesfield, Cheshire SK10 4GT UK

*To whom correspondence should be addressed

Received March 3, 1993; Revised April 30, 1993; Accepted April 30, 1993

The high resolution mapping of the ataxia telangiectasia (A-T) locus on chromosome 11q22–23 requires the generation of new polymorphic markers specifically within the segment of 11q22–23 to which the locus has been assigned. We have made use of a library of Alu-PCR clones, amplified from a radiation reduced somatic cell hybrid containing the relevant chromosome 11 segment, to generate sequence tagged sites (STS) within the 11q22–23 region and have used YAC clones to extend the loci identified by these STSs. The identification of paired polymorphisms (from Alu-PCR and the associated YAC derived clone), which are physically linked, but which show minimal linkage disequilibrium, provides a highly informative haplotype for use in genetic linkage analysis in A-T famllies. We describe the characterisation of 2 such polymorphic locl, D11S535 and D11S611, which map between existing flanking markers, and which provide additional information on the location of the major A-T locus.


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