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Nucleic Acids Research Advance Access originally published online on September 18, 2007
Nucleic Acids Research 2007 35(19):6414-6423; doi:10.1093/nar/gkm701
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Nucleic Acids Research, 2007, Vol. 35, No. 19 6414-6423
© 2007 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-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

RNA

Human ribosomal protein S13 regulates expression of its own gene at the splicing step by a feedback mechanism

Alexey A. Malygin1,2, Natalia M. Parakhnevitch1, Anton V. Ivanov1, Ian C. Eperon2 and Galina G. Karpova1,*

1Institute for Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, 630090, Russia and 2Biochemistry Department, University of Leicester, Leicester, UK

*To whom correspondence should be addressed. Tel: +7 383 335 6229; Fax: +7 383 333 3677; Email: karpova{at}niboch.nsc.ru

Received October 17, 2006. Revised August 22, 2007. Accepted August 22, 2007.

The expression of ribosomal protein (rp) genes is regulated at multiple levels. In yeast, two genes are autoregulated by feedback effects of the protein on pre-mRNA splicing. Here, we have investigated whether similar mechanisms occur in eukaryotes with more complicated and highly regulated splicing patterns. Comparisons of the sequences of ribosomal protein S13 gene (RPS13) among mammals and birds revealed that intron 1 is more conserved than the other introns. Transfection of HEK 293 cells with a minigene-expressing ribosomal protein S13 showed that the presence of intron 1 reduced expression by a factor of four. Ribosomal protein S13 was found to inhibit excision of intron 1 from rpS13 pre-mRNA fragment in vitro. This protein was shown to be able to specifically bind the fragment and to confer protection against ribonuclease cleavage at sequences near the 5' and 3' splice sites. The results suggest that overproduction of rpS13 in mammalian cells interferes with splicing of its own pre-mRNA by a feedback mechanism.


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