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© 1993 Oxford University Press

OTHER

Alternative splicing in the fragile X gene FMR1

Annemieke J.M.H. Verkerk, Esther de Graaff, Kristel De Boulle1, Evan E. Eichler2, David S. Konecki3, Edwin Reyniers1, Antonella Manca3, Annemarie Poustka3, Patrick J. Willems1, David L. Nelson2 and Ben A. Oostra*

Department of Clinical Genetics, Erasmus University, Dr Molewaterplein 50 3153 DR Rotterdam, The Netherlands 1Department of Medical Genetics, University of Antwerp UIA, 2610 Antwerp, Belgium 2Institute for Molecular Genetics, Baylor College of Medicine Houston, TX 77030, USA 3Deutsches Krebsforschungszentrum Heidelberg, Germany

* To whom correspondence should be addressed

Received December 10, 1992; Revised February 1, 1993; Accepted February 1, 1993

The FMR1 gene, associated with fragile X syndrome, has recently been cloned and the sequence of partial cDNA clones is known. We have determined additional cDNA sequences both at the 5' and 3' end. We have characterized the expressed gene by means of RT-PCR in various tissues and have found that alternative splicing takes place in the FMR1 gene, which does not seem to be tissue specific. When the different alternative splicing events are combined, 12 distinct mRNA products could result from FMR1 expression in each tested tissue. In all these transcripts the open reading frame is maintained until the same stop codon. At the 3' end alternative use of polyadenylation signals is found. The alternative splicing allows functional diversity of the FMR-1 gene. Whether all the possible proteins will be synthesized and whether they will be functionally active has to be determined.


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