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Mol. Cell. Biol., Sep 1995, 4825-4834, Vol 15, No. 9
F Del Gatto and R Breathnach
Two alternative exons, BEK and K-SAM, code for part of the ligand binding
site of fibroblast growth factor receptor 2. Splicing of these exons is
mutually exclusive, and the choice between them is made in a
tissue-specific manner. We identify here pre-mRNA sequences involved in
controlling splicing of the K-SAM exon. The short K-SAM exon sequence
5'-TAGGGCAGGC-3' inhibits splicing of the exon. This inhibition can be
overcome by mutating either the exon's 5' or 3' splice site to make it
correspond more closely to the relevant consensus sequence. Two separate
sequence elements in the intron immediately downstream of the K-SAM exon,
one of which is a sequence rich in pyrimidines, are both needed for
efficient K-SAM exon splicing. This is no longer the case if either the
exon's 5' or 3' splice site is reinforced. Furthermore, if the exon
inhibitory sequence is removed, the intron sequences are not required for
splicing of the K-SAM exon in a cell line which normally splices this exon.
At least three elements are thus involved in controlling splicing of the
K-SAM exon: suboptimal 5' and 3' splice sites, an exon inhibitory sequence,
and intron activating sequences.
Copyright © 1995, American Society for Microbiology
Exon and intron sequences, respectively, repress and activate splicing of a fibroblast growth factor receptor 2 alternative exon
Institut National de la Sante et de la Recherche Medicale U211, Institut de Biologie-Centre Hospitalier Regional, Nantes, France.
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