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Papers In Press, published online ahead of print March 26, 2001
I. M. T., University of Marburg, Marburg 35033
Corresponding Author: beato{at}imt.uni-marburg.de
Differential splicing from the bcl-X gene generates several isoforms with opposite effects on the apoptotic response. To explore the mechanism controlling the balance between the various isoforms we have characterized the 5´-region of the mouse bcl-X gene. We identified three new promoters in addition to the two previously described (1). These five promoters (P1-P5) would give rise to at least five mRNAs with different 5´-untranslated region all sharing the same translation initiation site. Except for the product of the most proximal promoter (P1), the other mRNAs are generated by alternative splicing of non-coding exons to a common acceptor site, located in the first translated exon. RT-PCR, primer extension and RNase protection assays demonstrate a tissue-specific pattern of promoter usage. P1 and P2 are active in all tissues analyzed, while the others three promoter show tissue-specific activities: P3 is active in spleen, liver and kidney; P4 in uterus and spleen; and P5 in spleen, liver, brain and thymus. We present evidence suggesting that promoter selection influences the outcome of the splice process. Transcripts from P1 generate mainly the mRNA for the long isoform Bcl-XL, whereas transcripts from P2 generate mRNAs for the isoforms Bcl-XL, Bcl-XS and Bcl-X
J. Biol. Chem, 10.1074/jbc.M008665200
Submitted on September 21, 2000
Revised on March 21, 2001
Accepted on March 26, 2001
Promoter choice influences alternative splicing and determines the balance of isoforms expressed from the mouse bcl-X gene
, and transcripts from P3 yield mainly mRNAs for the isoform Bcl-X. Our results suggest a key role of promoter choice in determining alternative splicing and, thus, the balance of Bcl-X isoforms.
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