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Nucleic Acids Research Advance Access originally published online on November 2, 2007
Nucleic Acids Research 2007 35(22):7636-7650; doi:10.1093/nar/gkm931
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Nucleic Acids Research, 2007, Vol. 35, No. 22 7636-7650
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

RNA

Regulatory mechanisms for 3'-end alternative splicing and polyadenylation of the Glial Fibrillary Acidic Protein, GFAP, transcript

Jenny Blechingberg1, Søren Lykke-Andersen2, Torben Heick Jensen2, Arne Lund Jørgensen1 and Anders Lade Nielsen1,*

1Institute of Human Genetics, The Bartholin Building and 2Centre for mRNP Biogenesis and Metabolism, Department of Molecular Biology, University of Aarhus, DK-8000 Aarhus C, Denmark

*To whom correspondence should be addressed. Tel: +45 89421690; Fax: +45 86123173; Email: aln{at}humgen.au.dk

Received August 28, 2007. Revised October 10, 2007. Accepted October 11, 2007.

The glial fibrillary acidic protein, GFAP, forms the intermediate cytoskeleton in cells of the glial lineage. Besides the common GFAP{alpha} transcript, the GFAP{varepsilon} and GFAP{kappa} transcripts are generated by alternative mRNA 3'-end processing. Here we use a GFAP minigene to characterize molecular mechanisms participating in alternative GFAP expression. Usage of a polyadenylation signal within the alternatively spliced exon 7a is essential to generate the GFAP{kappa} and GFAP{kappa} transcripts. The GFAP{kappa} mRNA is distinct from GFAP{varepsilon} mRNA given that it also includes intron 7a. Polyadenylation at the exon 7a site is stimulated by the upstream splice site. Moreover, exon 7a splice enhancer motifs supported both exon 7a splicing and polyadenylation. SR proteins increased the usage of the exon 7a polyadenylation signal but not the exon 7a splicing, whereas the polypyrimidine tract binding (PTB) protein enhanced both exon 7a polyadenylation and exon 7a splicing. Finally, increasing transcription by the VP16 trans-activator did not affect the frequency of use of the exon 7a polyadenylation signal whereas the exon 7a splicing frequency was decreased. Our data suggest a model with the selection of the exon 7a polyadenylation site being the essential and primary event for regulating GFAP alternative processing.


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