A conserved signal-responsive sequence mediates activation-induced alternative splicing of CD45.
Alternative splicing of nascent transcripts is a widespread mechanism for altering protein expression in response to extracellular stimuli. However, little is known about the sequences that mediate signal-induced alternative splicing, complicating efforts to identify genes whose splicing may be regulated in response to a particular stimuli. Here we define a sequence element that is both the primary determinant of CD45 variable exon exclusion following T cell stimulation by PMA and is sufficient to confer activation-induced skipping of a heterologous exon. Additionally, we show that this regulatory element has homology to sequences in other signal-regulated genes, suggesting that the alternative splicing of large families of genes may be regulated by common signaling pathways.
Rothrock
Caryn
C
Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Cannon
Brian
B
Hahm
Brandon
B
Lynch
Kristen W
KW
D017398:Alternative Splicing; D001483:Base Sequence; D002460:Cell Line; D016384:Consensus Sequence; D005091:Exons; D006801:Humans; D017493:Leukocyte Common Antigens / Q000235:genetics* / Q000378:metabolism*; D012045:Regulatory Sequences, Nucleic Acid; D016415:Sequence Alignment; D015398:Signal Transduction / Q000502:physiology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000502:physiology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D017493:Leukocyte Common Antigens; D013755:Tetradecanoylphorbol Acetate