Abstract
Pax3, a member of the paired-class homeodomain family of transcription factors, plays an important role in embryonic development of neurepithelium and mesenchyme-derived tissues in the mouse and is an early marker for myogenic differentiation. In the present work we identify an alternative splicing event for endogenous Pax3 in primary mouse myoblasts. The resulting splice variant arises through the utilization of a previously unreported splice donor consensus sequence present at the junction between exons 7 and 8 in the Pax3 sequence. The use of this splice donor site in conjunction with the splice acceptor site present between intron 8 and exon 9 results in the deletion of exon 8 and removes a majority of the Pax3 transcriptional activation domain. Consistent with this fact, we demonstrate that the alternatively spliced form of Pax3 is transcriptionally inactive and that the presence of this isoform can effectively inhibit the activity of the full-length protein.
Published Version
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