Abstract
The enrichment of specific intronic splicing enhancers upstream of weak PY tracts suggests a novel mechanism for intron recognition that compensates for a weakened canonical pre-mRNA splicing motif.
Highlights
While the current model of pre-mRNA splicing is based on the recognition of four canonical intronic motifs (5' splice site, branchpoint sequence, polypyrimidine (PY) tract and 3' splice site), it is becoming increasingly clear that splicing is regulated by both canonical and noncanonical splicing signals located in the RNA sequence of introns and exons that act to recruit the spliceosome and associated splicing factors
We present results showing that G-rich and C-rich motifs, similar to those predicted by our computational approach to be enriched upstream of weak PY tracts, are intronic splicing enhancer (ISE) important for the splicing of lecithin cholesterol acyltransferase (LCAT) intron 4, which has a weak PY tract
Visual inspection of human introns reveals that, the PY tract region is enriched in uridines in general, there is a great deal of sequence variation between introns
Summary
While the current model of pre-mRNA splicing is based on the recognition of four canonical intronic motifs (5' splice site, branchpoint sequence, polypyrimidine (PY) tract and 3' splice site), it is becoming increasingly clear that splicing is regulated by both canonical and noncanonical splicing signals located in the RNA sequence of introns and exons that act to recruit the spliceosome and associated splicing factors. Genome Biology 2008, Volume 9, Issue 6, Article R97 Murray et al R97.2 introns and exons. This is underlined by the observation that incorrect pre-mRNA splicing is a major contributor to human genetic diseases [4,5,6]. Is splicing a crucial step in the accurate transfer of genetic information from DNA to RNA to protein, it is a step that allows for regulation of gene expression as well as increased protein diversity through alternative splicing decisions [7]
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