WormBase Tree Display for RNAi: WBRNAi00106387

WBRNAi00106387 Homol: Homol_homol: C09B8:RNAi
  Sequence_info: PCR_product: sjj_C09B8.6
  Experiment: Strain: WBStrain00000001
    Treatment: RNAi was introduced at the first larval stage of the C. elegans life cycle (L1) and its effects were examined after 5 days at 15 degrees Celsius (or after 3 days at 20 degrees Celsius), until animals grown on control RNAi reached adulthood (Table 1).
    Delivered_by: Bacterial_feeding
  Inhibits: Predicted_gene: C09B8.6b Inferred_automatically: RNAi_primary
      C09B8.6c Inferred_automatically: RNAi_primary
      C09B8.6a Inferred_automatically: RNAi_primary
    Gene: WBGene00002146 Inferred_automatically: RNAi_primary
      WBGene00002023 Inferred_automatically: RNAi_primary
    Transcript: C09B8.6c.2 Inferred_automatically: RNAi_primary
      C09B8.6b.1 Inferred_automatically: RNAi_primary
      C09B8.1a.1 Inferred_automatically: RNAi_primary
      C09B8.6c.1 Inferred_automatically: RNAi_primary
      C09B8.6a.1 Inferred_automatically: RNAi_primary
      C09B8.1b.1 Inferred_automatically: RNAi_primary
  Species: Caenorhabditis elegans
  Reference: WBPaper00046852
  Phenotype_not_observed: WBPhenotype:0000059 Remark: "... we first compiled a list of C-elegans chaperones (97 genes) (Table 1) and examined the effects of down-regulation of each chaperone in wild-type animals (Figure 2A). Down-regulation of genes encoding 10 chaperones (17 genes), including CTT, HSP-1 (Hsc70/HSPA8), HSP-4 (BIP), HSP-6 (Mortalin), and DAF-21 (Hsp90), resulted in severe organismal phenotypes, such as lethality, developmental arrest, or sterility (Table 1, Figure S2). In contrast, downregulation of genes encoding most chaperones examined had no apparent phenotypes (Table 1). Our data are in agreement with published RNAi screens for wild-type RNAi treatment (Table 1, data curated by wormbase). When knockout mutants or data from enhanced RNAi efficacy experiments, (for example via dsDNA [sic] injection into the gonads) were considered, more acute phenotypes were observed for some chaperones (Table 1, data curated by wormbase)." "As expected, down-regulation of only two chaperones, unc45 or unc-23, showed a marked movement defect. For example, based on their impact on muscular ultrastructure or their involvement in myopathies, molecular chaperones, such as TRIC (cct), alpha-B-crystallin/HSPB5 (hsp-25), and DNAJB6 (dnj-24), were suggested to play a key role in sarcomere assembly and maintenance (Ding and Candido, 2000; Vang et al., 2005; Kim et al., 2008; Willis et al., 2009; Willis and Patterson, 2010; Garrido et al., 2012; Haslbeck et al., 2012; Sarparanta et al., 2012). Although these chaperones are associated with the sarcomere (Leroux and Candido, 1997; Ding and Candido, 2000; Meissner et al., 2011), knockdown of their genes by feeding RNAi did not result in notable motility defects (Table 1)."
    WBPhenotype:0000643 Remark: "... we first compiled a list of C-elegans chaperones (97 genes) (Table 1) and examined the effects of down-regulation of each chaperone in wild-type animals (Figure 2A). Down-regulation of genes encoding 10 chaperones (17 genes), including CTT, HSP-1 (Hsc70/HSPA8), HSP-4 (BIP), HSP-6 (Mortalin), and DAF-21 (Hsp90), resulted in severe organismal phenotypes, such as lethality, developmental arrest, or sterility (Table 1, Figure S2). In contrast, downregulation of genes encoding most chaperones examined had no apparent phenotypes (Table 1). Our data are in agreement with published RNAi screens for wild-type RNAi treatment (Table 1, data curated by wormbase). When knockout mutants or data from enhanced RNAi efficacy experiments, (for example via dsDNA [sic] injection into the gonads) were considered, more acute phenotypes were observed for some chaperones (Table 1, data curated by wormbase)." "As expected, down-regulation of only two chaperones, unc45 or unc-23, showed a marked movement defect. For example, based on their impact on muscular ultrastructure or their involvement in myopathies, molecular chaperones, such as TRIC (cct), alpha-B-crystallin/HSPB5 (hsp-25), and DNAJB6 (dnj-24), were suggested to play a key role in sarcomere assembly and maintenance (Ding and Candido, 2000; Vang et al., 2005; Kim et al., 2008; Willis et al., 2009; Willis and Patterson, 2010; Garrido et al., 2012; Haslbeck et al., 2012; Sarparanta et al., 2012). Although these chaperones are associated with the sarcomere (Leroux and Candido, 1997; Ding and Candido, 2000; Meissner et al., 2011), knockdown of their genes by feeding RNAi did not result in notable motility defects (Table 1)."
    WBPhenotype:0000688 Remark: "... we first compiled a list of C-elegans chaperones (97 genes) (Table 1) and examined the effects of down-regulation of each chaperone in wild-type animals (Figure 2A). Down-regulation of genes encoding 10 chaperones (17 genes), including CTT, HSP-1 (Hsc70/HSPA8), HSP-4 (BIP), HSP-6 (Mortalin), and DAF-21 (Hsp90), resulted in severe organismal phenotypes, such as lethality, developmental arrest, or sterility (Table 1, Figure S2). In contrast, downregulation of genes encoding most chaperones examined had no apparent phenotypes (Table 1). Our data are in agreement with published RNAi screens for wild-type RNAi treatment (Table 1, data curated by wormbase). When knockout mutants or data from enhanced RNAi efficacy experiments, (for example via dsDNA [sic] injection into the gonads) were considered, more acute phenotypes were observed for some chaperones (Table 1, data curated by wormbase)." "As expected, down-regulation of only two chaperones, unc45 or unc-23, showed a marked movement defect. For example, based on their impact on muscular ultrastructure or their involvement in myopathies, molecular chaperones, such as TRIC (cct), alpha-B-crystallin/HSPB5 (hsp-25), and DNAJB6 (dnj-24), were suggested to play a key role in sarcomere assembly and maintenance (Ding and Candido, 2000; Vang et al., 2005; Kim et al., 2008; Willis et al., 2009; Willis and Patterson, 2010; Garrido et al., 2012; Haslbeck et al., 2012; Sarparanta et al., 2012). Although these chaperones are associated with the sarcomere (Leroux and Candido, 1997; Ding and Candido, 2000; Meissner et al., 2011), knockdown of their genes by feeding RNAi did not result in notable motility defects (Table 1)."
  Remark: (Table 1) hsp-25 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.
  Method: RNAi