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© 1994 Oxford University Press

OTHER

Absence of the XIST gene from late-replicating isodicentric X chromosomes in leukaemia

K. A. Rack+, J. Chelly1,+, R. J. Gibbons, S. Rider1, D. Benjamin2, R. G. Lafrenlère3, D. Oscier4, R. W. Hendriks2, I. W. Craig2, H. F. Willard3, A. P. Monaco1 and V. J. Buckle*

MRC Molecular Haematology Unit, Institute of Molecular Medicine, John Radcliffe Hospital Headington, Oxford OX3 9DU, Oxford, UK 1Imperial Cancer Research Fund, Institute of Molecular Medicine, John Radcliffe Hospital Headington, Oxford OX3 9DU, Oxford, UK 2Genetics Laboratory, Department of Biochemistry, Oxford University South Parks Road, Oxford, UK 3Department of Genetics, Case Western Reserve University, School of Medicine 10900 Euclid Avenue, Cleveland, OH 44106, USA 4Department of Haematology, Royal Bournemouth Hospital Castle Lane East, Bournemouth BH7 7DW, UK

+The first two authour have made equivalent contributions to the findings presented in this paper

Received February 1, 1994; Revised February 25, 1994; Accepted February 25, 1994

The mechanism of X-inactivation in man is thought to involve a specific cis-acting locus within the X-inactivation centre at Xq13 (1, 2). The XIST gene (X inactive specific transcript) at Xq13 is ubiquitously expressed only from the inactive X and as such may be involved In or influenced by the X-inactivation process (3, 4). We have localised the breakpoints on two acquired isodicentric X chromosomes associated with leukaemia to a 450 kilobase region of DNA within Xq13, which result in deletion of the XIST gene. We have demonstrated that these chromosomes remain inactive and that there is no evidence of XIST expression from the remaining intact X chromosomes. The data suggest that XIST is not required for the maintenance of X-inactivation on these somatically rearranged X chromosomes.


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