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WormBase Tree Display for RNAi: WBRNAi00106278

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Name Class

WBRNAi00106278HomolHomol_homolC47E8:RNAi
Sequence_infoPCR_productsjj_C47E8.5
ExperimentGenotypeunc-45(e286)
TreatmentAge synchronized L1 unc-45(e286) mutant animals kept at permissive conditions (15°C) were treated with RNAi for different molecular chaperones and monitored for motility defects.
Delivered_byBacterial_feeding
InhibitsPredicted_geneC47E8.11Inferred_automaticallyRNAi_primary
C47E8.5Inferred_automaticallyRNAi_primary
GeneWBGene00044180Inferred_automaticallyRNAi_primary
WBGene00000915Inferred_automaticallyRNAi_primary
TranscriptC47E8.5.1Inferred_automaticallyRNAi_primary
C47E8.11.1Inferred_automaticallyRNAi_primary
C47E8.5.2Inferred_automaticallyRNAi_primary
SpeciesCaenorhabditis elegans
ReferenceWBPaper00046852
PhenotypeWBPhenotype:0000059Remark"RNAi knockdown of chaperones was next performed with unc-45(ts) mutant strains under permissive conditions. Age synchronized L1 unc-45(e286) mutant animals kept at permissive conditions (15C) were treated with RNAi for different molecular chaperones and monitored for motility defects. We first sought chaperones that cause unc-45(e286)-specific phenotypes at permissive conditions when depleted (Figure 2A). Of the 96 RNAi constructs tested, five genes induced loss of coordination and/or an egg-laying defect, resulting in reduced motility in more than 70% of the unc-45(e286) mutant animals. As noted above, down-regulation of unc-45 or unc-23 also induced a loss of coordination in wild-type animals (Table 1); these were discarded from the candidate gene list (Figure 2A). The remaining chaperones identified in the screen are CeHsp90 (daf-21), CeHop (sti-1) and CeAha1 (C01G10.8) (Figures 2B,C)." "RNAi treatment for CeHsp90, encoding a known myosin chaperone, resulted in a strong larval arrest phenotype in both wild-type and unc45(e286) animals but induced a strong motility defect only in unc-45(e286) animals (76.4 8.3%, as compared to 12.1 4% motile animals)."
WBPhenotype:0000644Remark"RNAi knockdown of chaperones was next performed with unc-45(ts) mutant strains under permissive conditions. Age synchronized L1 unc-45(e286) mutant animals kept at permissive conditions (15C) were treated with RNAi for different molecular chaperones and monitored for motility defects. We first sought chaperones that cause unc-45(e286)-specific phenotypes at permissive conditions when depleted (Figure 2A). Of the 96 RNAi constructs tested, five genes induced loss of coordination and/or an egg-laying defect, resulting in reduced motility in more than 70% of the unc-45(e286) mutant animals. As noted above, down-regulation of unc-45 or unc-23 also induced a loss of coordination in wild-type animals (Table 1); these were discarded from the candidate gene list (Figure 2A). The remaining chaperones identified in the screen are CeHsp90 (daf-21), CeHop (sti-1) and CeAha1 (C01G10.8) (Figures 2B,C)." "RNAi treatment for CeHsp90, encoding a known myosin chaperone, resulted in a strong larval arrest phenotype in both wild-type and unc45(e286) animals but induced a strong motility defect only in unc-45(e286) animals (76.4 8.3%, as compared to 12.1 4% motile animals)."
Remark(Figure 2) daf-21/CeHsp90 RNAi. Exact sequence used for RNAi not stated by authors, Ahringer laboratory clone used for curation. If Ahringer clone not available, Vidal laboratory clone used for curation.
MethodRNAi