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Regulation of Alternative Splicing
Author(s) -
Hertel Klemens,
Mueller William,
Busch Anke,
Erkelenz Steffen,
Schaal Heiner
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.201.2
Subject(s) - rna splicing , exonic splicing enhancer , exon , alternative splicing , genetics , minigene , splicing factor , enhancer , biology , sr protein , intron , computational biology , gene , rna , gene expression
The recognition splice sites is aided by cis‐acting splicing regulatory elements that either activate or repress splice site selection. Over the past years it has been established that members of the SR splicing factors activate splicing and that members of the hnRNP family repress exon recognition, leading to the commonly accepted designation of SR proteins splicing enhancers and hnRNP proteins splicing repressors. However, recent genome‐wide analyses called this strict designation into question We set out to determine whether dual and antagonistic functionality is a common feature of SR and hnRNP splicing regulators. Our results prove that indeed this is the case, but only in a strict position‐dependent manner. SR proteins activate splicing only from within exons, but repress exon recognition from intronic positions. For hnRNP splicing factors we show analogous opposing activities, but in a reversed position dependence. Both types of splicing regulatory proteins display highly position‐dependent activities that negatively or positively influence splice site choice. These results challenge current computational approaches to define the splicing code.