Conclusion

Together, the data indicate that the snoRNA HBII-52 contributes to alternative splicing regulation of the 5-HT2C receptor. The exact molecular mechanism of the regulation is currently unveiled. The HBII-52 snoRNA is processed into smaller snoRNA fragments (Kishore et al. 2010) that most likely directly influence the 5-HT2C receptor pre-mRNA. Finally, it is likely HBII-52 controls other pre-mRNAs, and it is therefore expected that the 5-HT2C receptor mRNA is not the only deregulated RNA in PWS. However, since mouse models of the 5-HT2C receptor mutants recapitulate some aspects of PWS, we expect that the dysregulation of the receptor plays a decisive role in this disease.

Acknowledgments The laboratory is supported by the Deutsche Forschungsgemeinschaft (DFG), the European Union (EURASNET), and the NIH.

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