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First published online June 20, 2006
doi: 10.1242/10.1242/jcs.03053

Journal of Cell Science 119, 2635-2641 (2006)
Published by The Company of Biologists 2006
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The connection between splicing and cancer

Anabella Srebrow and Alberto R. Kornblihtt*

Laboratorio de Fisiología y Biología Molecular, Departamento de Fisiología, Biología Molecular y Celular, IFIBYNE-CONICET, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pabellón 2, (C1428EHA) Buenos Aires, Argentina


Figure 1
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  		Fig. 1. Cis-acting sequences that control splicing. (A) Consensus sequences for the 5' splice site (donor), branch site and 3' splice site (acceptor). (B) Arrangement of donor (D) and acceptor (A) sites in the architecture of a typical eukaryotic gene. Whereas internal exons are limited by acceptor and donor sites, the first exon is limited by the Cap site and a donor, and the last exon is limited by an acceptor and the poly(A) site. (C) Examples of sequences for strong and weak acceptor sites. Red indicates the 3' acceptor splice site; bold indicates deviations from the consensus sequence. (D) Schematic roles of exonic splicing enhancers (ESE), exonic splicing silencers (ESS), intronic splicing enhancers (ISE) and intronic splicing silencers (ISS) on the recognition of a weak acceptor by the splicing machinery; red indicates enhancing, blue indicates silencing. In A-D, exon sequences are boxed.

 

Figure 2
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  		Fig. 2. (A) Different modes of alternative splicing. (B) Alternative promoters provoke mRNA diversity but do not necessarily imply alternative splicing. There are two alternative promoters, P1 and P2. If promoter P2 is used, exons 2, 3 and 4 are constitutively included. If promoter P1 is used, exon 2 simply does not exist for the splicing machinery because, being a 5' terminal exon of the P1 transcription unit, it lacks an upstream 3' splice site. Therefore, the splicing machinery has no option but to join exon 1 directly to exon 3, generating a 1-3-4 mRNA.

 

Figure 3
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  		Fig. 3. Causes and consequences of splicing pattern alterations. For simplicity, only SR and hnRNP proteins are shown. However, other factors not belonging to any of these families could also be targets of these signaling pathways (e.g. Sam68).

 




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