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Nucleic Acids Research 2006 34(12):3421-3433; doi:10.1093/nar/gkl390
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Published online 19 July 2006

© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commerical use, distribution, and reproduction in any medium, provided the original work is properly cited.

Article

AUG sequences are required to sustain nonsense-codon-mediated suppression of splicing

Eyal Kamhi, Galit Yahalom, Gideon Kass, Yael Hacham, Ruth Sperling1 and Joseph Sperling*

Department of Organic Chemistry, The Weizmann Institute of Science Rehovot Israel 1 Department of Genetics, The Hebrew University Jerusalem, Israel

*To whom correspondence should be addressed. Tel: 972 8 934 2509; Fax: 972 8 934 4142; Email: j.sperling{at}weizmann.ac.il

Received April 14, 2006. Revised May 5, 2006. Accepted May 8, 2006.

More than 90% of human genes are rich in intronic latent 5' splice sites whose utilization in pre-mRNA splicing would introduce in-frame stop codons into the resultant mRNAs. We have therefore hypothesized that suppression of splicing (SOS) at latent 5' splice sites regulates alternative 5' splice site selection in a way that prevents the production of toxic nonsense mRNAs and verified this idea by showing that the removal of such in-frame stop codons is sufficient to activate latent splicing. Splicing control by SOS requires recognition of the mRNA reading frame, presumably recognizing the start codon sequence. Here we show that AUG sequences are indeed essential for SOS. Although protein translation does not seem to be required for SOS, the first AUG is shown here to be necessary but not sufficient. We further show that latent splicing can be elicited upon treatment with pactamycin—a drug known to block translation by its ability to recognize an RNA fold—but not by treatment with other drugs that inhibit translation through other mechanisms. The effect of pactamycin on SOS is dependent neither on steady-state translation nor on the pioneer round of translation. This effect is found for both transfected and endogenous genes, indicating that SOS is a natural mechanism.


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