J Cell Biol 2011,
PMID: 21518792
Lin, Jung-Chun; Tarn, Woan-Yuh
Alternative splicing contributes largely to cell differentiation and functional specification. We previously reported that the RNA-binding protein RBM4 antagonizes the activity of splicing factor PTB to modulate muscle cell-specific exon selection of α-tropomyosin. Here we show that down-regulation of PTB and its neuronal analogue nPTB during muscle cell differentiation may involve alternative splicing-coupled nonsense-mediated mRNA decay. RBM4 regulates PTB/nPTB expression by activating exon skipping of their transcripts during myogenesis. Moreover, RBM4 and PTB target a common set of transcripts that undergo muscle cell-specific alternative splicing. Overexpression of RBM4 invariably promoted expression of muscle cell-specific isoforms, which recapitulated in vivo alternative splicing changes during muscle differentiation, whereas PTB acted oppositely to RBM4 in expression of mRNA isoforms specific for late-stage differentiation. Therefore, RBM4 may synergize its effect on muscle cell-specific alternative splicing by down-regulating PTB expression and antagonizing the activity of PTB in exon selection, which highlights a hierarchical role for RBM4 in a splicing cascade that regulates myogenesis.
Document information provided by NCBI PubMed
Text Mining Data
PTB ⊣ mRNA decay: "
Here we show that down-regulation of
PTB and its neuronal analogue nPTB during muscle cell differentiation may
involve alternative splicing coupled nonsense mediated
mRNA decay
"
PTB/nPTB → RBM4: "
RBM4 regulates PTB/nPTB expression by activating exon skipping of their transcripts during myogenesis
"
PTB ⊣ RBM4: "
Therefore, RBM4 may synergize its effect on muscle cell-specific alternative splicing by down regulating PTB expression and antagonizing the activity of PTB in exon selection, which highlights a hierarchical role for RBM4 in a splicing cascade that regulates myogenesis
"
Manually curated Databases
No curated data.