Regulation of alternative splicing by snoRNAs

S. Kishore, S. Stamm

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


The SNURF-SNRPN locus located on chromosome 15 is maternally imprinted and generates a large transcript containing at least 148 exons. Loss of the paternal allele causes Prader-Willi syndrome (PWS). The 3′ end of the transcript harbors several evolutionarily conserved C/D box small nucleolar RNAs (snoRNAs) that are tissue-specifically expressed. With the exception of 47 copies of HBII-52 snoRNAs, none of the snoRNAs exhibit complementarity to known RNAs. Due to an 18-nucleotide sequence complementarity, HBII-52 can bind to the alternatively spliced exon Vb of the serotonin receptor 2C pre-mRNA, where it masks a splicing silencer, which results in alternative exon usage. This silencer can also be destroyed by RNA editing, which changes the amino acid sequence and appears to be independent of HBII-52. Lack of HBII-52 expression in individuals with PWS causes most likely a lack of the high-efficacy serotonin receptor, which could contribute to the disease. It is therefore possible that snoRNAs could act as versatile modulators of gene expression by modulating alternative splicing.

Original languageEnglish
Pages (from-to)329-334
Number of pages6
JournalCold Spring Harbor Symposia on Quantitative Biology
StatePublished - 2006

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics


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