Distribution of SR protein exonic splicing enhancer motifs in human protein-coding genes

被引:124
作者
Wang, JH [1 ]
Smith, PJ [1 ]
Krainer, AR [1 ]
Zhang, MQ [1 ]
机构
[1] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
关键词
D O I
10.1093/nar/gki810
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Exonic splicing enhancers (ESEs) are pre-mRNA cis-acting elements required for splice-site recognition. We previously developed a web-based program called ESEfinder that scores any sequence for the presence of ESE motifs recognized by the human SR proteins SF2/ASF, SRp40, SRp55 and SC35 (http://rulai.cshl.edu/tools/ESE/). Using ESEfinder, we have undertaken a large-scale analysis of ESE motif distribution in human protein-coding genes. Significantly higher frequencies of ESE motifs were observed in constitutive internal protein-coding exons, compared with both their flanking intronic regions and with pseudo exons. Statistical analysis of ESE motif frequency distributions revealed a complex relationship between splice-site strength and increased or decreased frequencies of particular SR protein motifs. Comparison of constitutively and alternatively spliced exons demonstrated slightly weaker splice-site scores, as well as significantly fewer ESE motifs, in the alternatively spliced group. Our results underline the importance of ESE-mediated SR protein function in the process of exon definition, in the context of both constitutive splicing and regulated alternative splicing.
引用
收藏
页码:5053 / 5062
页数:10
相关论文
共 58 条
[1]   Familial adenomatous polyposis:: Aberrant splicing due to missense or silent mutations in the APC gene [J].
Aretz, S ;
Uhlhaas, S ;
Sun, Y ;
Pagenstecher, C ;
Mangold, E ;
Caspari, R ;
Möslein, G ;
Schulmann, K ;
Propping, P ;
Friedl, W .
HUMAN MUTATION, 2004, 24 (05) :370-380
[2]   Characterization of disease-associated mutations affecting an exonic splicing enhancer and two cryptic splice sites in exon 13 of the cystic fibrosis transmembrane conductance regulator gene [J].
Aznarez, I ;
Chan, EM ;
Zielenski, J ;
Blencowe, BJ ;
Tsui, LC .
HUMAN MOLECULAR GENETICS, 2003, 12 (16) :2031-2040
[3]   ANALYSIS OF THE RNA-RECOGNITION MOTIF AND RS AND RGG DOMAINS - CONSERVATION IN METAZOAN PRE-MESSENGER-RNA SPLICING FACTORS [J].
BIRNEY, E ;
KUMAR, S ;
KRAINER, AR .
NUCLEIC ACIDS RESEARCH, 1993, 21 (25) :5803-5816
[4]   Mechanisms of alternative pre-messenger RNA splicing [J].
Black, DL .
ANNUAL REVIEW OF BIOCHEMISTRY, 2003, 72 :291-336
[5]   Exonic splicing enhancers: mechanism of action, diversity and role in human genetic diseases [J].
Blencowe, BJ .
TRENDS IN BIOCHEMICAL SCIENCES, 2000, 25 (03) :106-110
[6]   Functional selection of splicing enhancers that stimulate trans-splicing in vitro [J].
Boukis, LA ;
Bruzik, JP .
RNA, 2001, 7 (06) :793-805
[7]  
Bourgeois CF, 1999, MOL CELL BIOL, V19, P7347
[8]   A nonsense mutation in the fibrillin-1 gene of a Marfan syndrome patient induces NMD and disrupts an exonic splicing enhancer [J].
Caputi, M ;
Kendzior, RJ ;
Beemon, KL .
GENES & DEVELOPMENT, 2002, 16 (14) :1754-1759
[9]   Listening to silence and understanding nonsense: Exonic mutations that affect splicing [J].
Cartegni, L ;
Chew, SL ;
Krainer, AR .
NATURE REVIEWS GENETICS, 2002, 3 (04) :285-298
[10]   Disruption of an SF2/ASF-dependent exonic splicing enhancer in SMN2 causes spinal muscular atrophy in the absence of SMN1 [J].
Cartegni, L ;
Krainer, AR .
NATURE GENETICS, 2002, 30 (04) :377-384