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Submitted on August 1, 2005
Accepted on November 30, 2005
The snoRNA HBII-52 Regulates Alternative Splicing of the Serotonin Receptor 2C
Shivendra Kishore 1 and Stefan Stamm 1*
1 Institut für Biochemie, Emil-Fisher-Zentrum, Friedrich-Alexander Universität Erlangen-Nürnberg, Fahrstraße 17, 91054 Erlangen, Germany.
* To whom correspondence should be addressed.
Stefan Stamm , E-mail: stefan{at}stamms-lab.net
The Prader-Willi syndrome is a congenital disease caused byloss of paternal gene expression from a maternally imprintedregion on chromosome 15. This region contains a small nucleolarRNA, HBII-52, that exhibits sequence complementarity to thealternatively spliced exonVb of the serotonin receptor 5-HT2CR.We found that HBII-52 regulates alternative splicing of 5-HT2CRby binding to a silencing element in exonVb. Prader-Willi syndromepatients do not express HBII-52. They have different 5-HT2CRmRNA isoforms than healthy individuals. Our results show thata snoRNA regulates processing of a mRNA expressed from a genelocated on a different chromosome and indicate that a defectin pre-mRNA processing contributes to the Prader-Willi syndrome.
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