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Methods to Discover Alternative Promoter Usage and Transcriptional Regulation of Murine Bcrp1
11:02

Methods to Discover Alternative Promoter Usage and Transcriptional Regulation of Murine Bcrp1

Published on: May 27, 2016

Alternative 5' exons in c-abl mRNA

Y Ben-Neriah, A Bernards, M Paskind

    Cell
    |February 28, 1986
    PubMed

    Insights

    The cellular abl proto-oncogene, a protein-tyrosine kinase, shows varied mRNA sizes due to alternative splicing. This splicing occurs at the same site involved in the Philadelphia chromosome translocation.

    Area of Science:

    • Molecular Biology
    • Oncogenesis
    • Gene Expression

    Background:

    • The cellular abl proto-oncogene encodes a protein-tyrosine kinase.
    • This gene is expressed in various cell types, typically as two or three distinct mRNA size variants.

    Purpose of the Study:

    • To investigate the structural diversity of mouse c-abl cDNAs.
    • To understand the mechanisms generating heterogeneity in c-abl mRNA.
    • To explore the relationship between c-abl splicing and oncogenic transformations.

    Main Methods:

    • Cloning of four types of mouse c-abl complementary DNAs (cDNAs) from 70Z/3 lymphoid cells.
    • Analysis of the 5' sequences of the cloned cDNAs to determine predicted N-terminal amino acid sequences.
    • Comparison of c-abl cDNA sequences with viral abl (v-abl) sequences.

    Main Results:

    • Four distinct mouse c-abl cDNAs were identified, each with unique 5' sequences encoding predicted N-terminal regions of 20-45 amino acids.
    • One cDNA shared a met-gly-gln N-terminal sequence with the gag N terminus of v-abl.
    • The observed 5' heterogeneity in c-abl cDNAs is attributed to the alternative addition of 5' exons to a common set of 3' exons.
    • Alternative splicing was found to occur at the identical site where BCR sequences attach to ABL sequences in the Philadelphia chromosome translocation.

    Conclusions:

    • The cellular abl proto-oncogene exhibits significant structural diversity at the mRNA level.
    • Alternative splicing is a key mechanism generating different forms of c-abl.
    • The splicing site involved in c-abl heterogeneity is conserved in the context of oncogenic translocations like the Philadelphia chromosome.

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