Journal
EMBO JOURNAL
Volume 29, Issue 11, Pages 1817-1829Publisher
WILEY
DOI: 10.1038/emboj.2010.70
Keywords
fission yeast; pyrimidine tract; SMN; snRNP; splicing
Categories
Funding
- CNRS
- GIS 'Institut des Maladies Rares'
- AFM
- ANR [ANR-06-MRAR-004-01]
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Spinal muscular atrophy results from deletions or mutations in the survival of motor neuron (SMN1) gene. The SMN protein has an essential role in the biogenesis of spliceosomal snRNPs, but the link between a defect in this process and specific splicing inhibition of pre-mRNAs has not been established. In this study, we report the construction of a temperature-degron (td) allele of the Schizosaccharomyces pombe SMN protein and show that its depletion at 37 degrees C affects splicing and formation of U1, U2, U4 and U5 snRNPs, but not of U6 and U3 ribonucleoproteins. The function of the tdSMN allele in snRNP assembly is already perturbed at 25 degrees C, suggesting a deleterious effect of the tag at this temperature. Using a genome-wide approach, we report that introns react unequally to lower levels of snRNPs in tdSMN cells and that increasing the length of the polypyrimidine tract can improve the splicing efficiency of some, but not all, affected introns. Altogether, our results suggest that the defects observed in tdSMN fission yeast cells mimic splicing deficits observed in SMN-deficient metazoan cells. The EMBO Journal (2010) 29, 1817-1829. doi:10.1038/emboj.2010.70; Published online 16 April 2010
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