Abstract
Heterochromatin formation at fission yeast centromeres is directed by RNA interference (RNAi). Noncoding transcripts derived from centromeric repeats are processed into small interfering RNAs (siRNAs) that direct the RNA-induced transcriptional silencing (RITS) effector complex to engage centromere transcripts, resulting in recruitment of the histone H3 lysine 9 methyltransferase Clr4, and hence silencing. We have found that defects in specific splicing factors, but not splicing itself, affect the generation of centromeric siRNAs and consequently centromeric heterochromatin integrity. Moreover, splicing factors physically associate with Cid12, a component of the RNAi machinery, and with centromeric chromatin, consistent with a direct role in RNAi. We propose that spliceosomal complexes provide a platform for siRNA generation and hence facilitate effective centromere repeat silencing.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphatases / genetics
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Adenosine Triphosphatases / metabolism
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Centromere / genetics*
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Centromere / metabolism
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Genes, Fungal
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Heterochromatin / metabolism
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Histones / metabolism
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Methylation
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Mutation
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Phosphoproteins / genetics
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Phosphoproteins / metabolism
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RNA Interference*
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RNA Splicing*
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RNA, Small Interfering / metabolism*
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Ribonucleoprotein, U2 Small Nuclear / genetics
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Ribonucleoprotein, U2 Small Nuclear / metabolism
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Schizosaccharomyces / genetics*
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Schizosaccharomyces / metabolism
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Schizosaccharomyces pombe Proteins / genetics
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Schizosaccharomyces pombe Proteins / metabolism*
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Spliceosomes / metabolism
Substances
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Heterochromatin
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Histones
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Phosphoproteins
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Prp12 protein, S pombe
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RNA, Small Interfering
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Ribonucleoprotein, U2 Small Nuclear
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Schizosaccharomyces pombe Proteins
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prp10 protein, S pombe
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Adenosine Triphosphatases
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PRP5 protein, S pombe