| http://purl.uniprot.org/citations/18945809 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18945809 | http://www.w3.org/2000/01/rdf-schema#comment | "The maternal contribution of gene products enables embryos to initiate their developmental program in the absence of zygotic gene expression. In Caenorhabditis elegans, maternal CDC-25.1 levels are tightly regulated to promote early cell divisions, while stabilization of this phosphatase by gain-of-function mutations gives rise to intestinal-specific hyperplasia. To identify regulators of CDC-25.1 levels and/or function, we performed a modifier screen of the cdc-25.1(gf)-dependent hyperplasia. One of the isolated suppressor mutants possesses a donor splice site mutation in prp-8, a key splicing factor of the U5-specific snRNP. prp-8(rr40) produces aberrant prp-8 splice variants that generate C-terminal truncations at the expense of wild-type prp-8. Levels of maternal transcripts are reduced, including cdc-25.1, while zygotic transcripts appear unperturbed, suggesting a germ-line-specific role for this splicing factor in regulating the splicing, and consequently, the steady-state levels of maternal transcripts. Using a novel feeding RNAi strategy we found that only a subset of splicing factors suppress cdc-25.1(gf), suggesting that they too may play specific roles in germ-line spliceosome function. In humans, mutations in the corresponding hPrp8 C-terminal domain result in retinitis pigmentosa, a retinal-specific disorder. Intriguingly, despite affecting the general splicing apparatus, both human and C. elegans show tissue-specific defects resulting from mutations in this key splicing component. Our findings suggest that in addition to its important regulatory function in the C. elegans germ line, prp-8(rr40) may provide further insight into the etiology of this splicing-associated human disorder."xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://purl.org/dc/terms/identifier | "doi:10.1261/rna.1168408"xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://purl.uniprot.org/core/author | "Roy R."xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://purl.uniprot.org/core/author | "Drysdale J."xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://purl.uniprot.org/core/author | "Hebeisen M."xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18945809 | http://purl.uniprot.org/core/name | "RNA"xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://purl.uniprot.org/core/pages | "2618-2633"xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://purl.uniprot.org/core/title | "Suppressors of the cdc-25.1(gf)-associated intestinal hyperplasia reveal important maternal roles for prp-8 and a subset of splicing factors in C. elegans."xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://purl.uniprot.org/core/volume | "14"xsd:string |
| http://purl.uniprot.org/citations/18945809 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18945809 |
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| http://purl.uniprot.org/uniprot/#_A0A168H2N7-mappedCitation-18945809 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18945809 |
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| http://purl.uniprot.org/uniprot/#_E1B6V1-mappedCitation-18945809 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18945809 |
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| http://purl.uniprot.org/uniprot/#_P34659-mappedCitation-18945809 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18945809 |