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Nucleic Acids Research, 2001, Vol. 29, No. 17 3557-3565
© 2001 Oxford University Press

5'- and 3'-terminal nucleotides in the FGFR2 ISAR splicing element core have overlapping roles in exon IIIb activation and exon IIIc repression

Richard B. Jones1,2, Russ P. Carstens3, Yongde Luo2 and Wallace L. McKeehan1,2,*

1Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX, USA, 2Center for Cancer Biology and Nutrition, Institute of Biosciences and Technology, Texas A&M University System Health Science Center, 2121 West Holcombe Boulevard, Houston, TX 77030-3303, USA and 3Renal-Electrolyte and Hypertension Division, 700 Clinical Research Building, 415 Curie Boulevard, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6144, USA

The cell type-specific, mutually-exclusive alternative splicing of the fibroblast growth factor receptor 2 (FGFR2) pre-mRNA is tightly regulated. A sequence termed ISAR (intronic splicing activator and repressor) has been implicated as an important cis regulatory element in both activation of exon IIIb and repression of exon IIIc splicing in epithelial cells. In order to better understand how this single sequence could have dual roles, we transfected minigenes containing a series of 2-bp mutations in the 18 3'-most nucleotides of ISAR that we refer to as the ISAR core. Transfection of cells with dual-exon (IIIb and IIIc) minigenes revealed that mutation of terminal sequences of the core led to decreased exon IIIb inclusion and increased exon IIIc inclusion. Transfection of cells with single-exon IIIb minigenes and single-exon IIIc minigenes revealed that mutation of terminal sequences of the ISAR core led to decreased exon IIIb inclusion and increased exon IIIc inclusion, respectively. Nucleotides of the ISAR core responsible for exon IIIb activation appear to overlap very closely with those required for exon IIIc repression. We describe a model in which ISAR and a 5' intronic sequence known as IAS2 form a stem structure required for simultaneous exon IIIb activation and exon IIIc repression.

* To whom correspondence should be addressed at: Institute of Biosciences and Technology, 2121 West Holcombe Boulevard, Houston, TX 77030-3303, USA. Tel: +1 713 677 7522; Fax: +1 713 677 7512; Email: wmckeeha{at}ibt.tamu.edu Present address:Richard B. Jones, Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA


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