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Promoter choice influences alternative splicing and determines the balance of isoforms expressed from the mouse bcl-X gene.
J Biol Chem. 2001 Jun 15; 276(24):21062-9.JB

Abstract

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 (Grillot, D. A., M., G.-G., Ekhterae, D., Duan, L., Inohara, N., Ohta, S., Seldin, M. F., and Núñez, G. (1997) J. Immunol. 158, 4750-4757). 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 noncoding exons to a common acceptor site located in the first translated exon. Reverse transcriptase-polymerase chain reaction, primer extension, and RNase protection assays demonstrate a tissue-specific pattern of promoter usage. P1 and P2 are active in all tissues analyzed, whereas the other three promoter show tissue-specific activities. P3 is active in spleen, liver, and kidney, P4 is active in uterus and spleen, and P5 is active 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-X(L), whereas transcripts from P2 generate mRNAs for the isoforms Bcl-X(L), Bcl-X(S), and Bcl-X(gamma) and transcripts from P3 yield mainly mRNAs for the isoform Bcl-X(gamma). Our results suggest a key role of promoter choice in determining alternative splicing and, thus, the balance of Bcl-X isoforms.

Authors+Show Affiliations

Institut für Molekularbiologie und Tumorforschung (IMT), Marburg 35033, Germany.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11274164

Citation

Pecci, A, et al. "Promoter Choice Influences Alternative Splicing and Determines the Balance of Isoforms Expressed From the Mouse bcl-X Gene." The Journal of Biological Chemistry, vol. 276, no. 24, 2001, pp. 21062-9.
Pecci A, Viegas LR, Baranao JL, et al. Promoter choice influences alternative splicing and determines the balance of isoforms expressed from the mouse bcl-X gene. J Biol Chem. 2001;276(24):21062-9.
Pecci, A., Viegas, L. R., Baranao, J. L., & Beato, M. (2001). Promoter choice influences alternative splicing and determines the balance of isoforms expressed from the mouse bcl-X gene. The Journal of Biological Chemistry, 276(24), 21062-9.
Pecci A, et al. Promoter Choice Influences Alternative Splicing and Determines the Balance of Isoforms Expressed From the Mouse bcl-X Gene. J Biol Chem. 2001 Jun 15;276(24):21062-9. PubMed PMID: 11274164.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Promoter choice influences alternative splicing and determines the balance of isoforms expressed from the mouse bcl-X gene. AU - Pecci,A, AU - Viegas,L R, AU - Baranao,J L, AU - Beato,M, Y1 - 2001/03/26/ PY - 2001/3/29/pubmed PY - 2001/7/20/medline PY - 2001/3/29/entrez SP - 21062 EP - 9 JF - The Journal of biological chemistry JO - J Biol Chem VL - 276 IS - 24 N2 - 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 (Grillot, D. A., M., G.-G., Ekhterae, D., Duan, L., Inohara, N., Ohta, S., Seldin, M. F., and Núñez, G. (1997) J. Immunol. 158, 4750-4757). 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 noncoding exons to a common acceptor site located in the first translated exon. Reverse transcriptase-polymerase chain reaction, primer extension, and RNase protection assays demonstrate a tissue-specific pattern of promoter usage. P1 and P2 are active in all tissues analyzed, whereas the other three promoter show tissue-specific activities. P3 is active in spleen, liver, and kidney, P4 is active in uterus and spleen, and P5 is active 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-X(L), whereas transcripts from P2 generate mRNAs for the isoforms Bcl-X(L), Bcl-X(S), and Bcl-X(gamma) and transcripts from P3 yield mainly mRNAs for the isoform Bcl-X(gamma). Our results suggest a key role of promoter choice in determining alternative splicing and, thus, the balance of Bcl-X isoforms. SN - 0021-9258 UR - https://www.unboundmedicine.com/medline/citation/11274164/Promoter_choice_influences_alternative_splicing_and_determines_the_balance_of_isoforms_expressed_from_the_mouse_bcl_X_gene_ DB - PRIME DP - Unbound Medicine ER -