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WormBase Tree Display for Variation: WBVar00091838

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Name Class

WBVar00091838NamePublic_nameok551
Other_nameF45E6.2.1:c.830_1684-64del
HGVSgCHROMOSOME_X:g.12482223_12484122del
Sequence_detailsSMapS_parentSequenceF45E6
Flanking_sequencesagaaggaagccgatgaacatatgaaaatgatgtgcagcttttagctagattcatatgtag
Mapping_targetF45E6
Type_of_mutationDeletion
PCR_productOK551_external
OK551_internal
SeqStatusSequenced
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
StrainWBStrain00031485
LaboratoryRB
PersonWBPerson46
KO_consortium_allele
StatusLive
AffectsGeneWBGene00000222
TranscriptF45E6.2.1VEP_consequencesplice_acceptor_variant,splice_donor_variant,coding_sequence_variant,intron_variant
VEP_impactHIGH
HGVScF45E6.2.1:c.830_1684-64del
cDNA_position830-?
CDS_position830-?
Protein_position277-?
Intron_number5-9/10
Exon_number5-9/11
InteractorWBInteraction000501560
WBInteraction000520460
WBInteraction000520496
WBInteraction000520567
WBInteraction000536401
WBInteraction000536416
WBInteraction000536419
WBInteraction000536435
WBInteraction000536444
IsolationMutagenUV/TMP
DescriptionPhenotypeWBPhenotype:0000136Paper_evidenceWBPaper00036076
Curator_confirmedWBPerson2987
Remark"To determine whether the transcription of rnf-121 is regulated by PEK-1 and the UPR pathway in C . elegans , we performed a real-time PCR analysis of the mutant strains pek-1 ( ok275 ) , ire-1 ( v33 ) , and atf-6 ( ok551 ) , as well as of wild-type worms , treated with the UPR inducers DTT , tunicamycin , and thapsigargin . Although the mRNA levels of hsp-4 were induced upon tunicamycin or DTT treatment and in pek-1 ( ok275 ) and atf-6 ( ok551 ) mutant backgrounds , and abolished in ire-1 ( v33 ) as shown previously ( Shen et al. , 2001 ) , the levels of rnf-121 mRNA were largely unaffected ( Figure 3B ) ."Paper_evidenceWBPaper00036076
Curator_confirmedWBPerson2987
WBPhenotype:0000137Paper_evidenceWBPaper00035294
Curator_confirmedWBPerson2987
Remark"In the control wild-type N2 worms, expression of ubiquilin and erasin transcripts increased after 6 h of tunicamycin treatment (Fig. 8). However, the induction of both genes was almost completely attenuated in ire-1(v33) mutant worms, and partially attenuated in the atf-6(ok551) and pek-1(ok275) mutants (Fig. 8). Together, these results indicate that in C. elegans, both ubiquilin and erasin genes are chiefly regulated by ire-1."Paper_evidenceWBPaper00035294
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004565Paper_evidenceWBPaper00035294
Curator_confirmedWBPerson2987
WBPhenotype:0000962Paper_evidenceWBPaper00045849
Curator_confirmedWBPerson712
RemarkA high level of hsp-4 expression is observed in a atf-6(ok551) mutant background.Paper_evidenceWBPaper00045849
Curator_confirmedWBPerson712
WBPhenotype:0001278Paper_evidenceWBPaper00041022
Curator_confirmedWBPerson2987
Remark"While several of the tested genes had an effect (results not shown), hsp-3 stood out for its strong effect, essentially totally blocking the induction of pnlp-29::GFP normally observed upon infection in adult worms (Fig. 2A). A similar abrogation of reporter gene expression was seen in an atf-6 mutant, but not in a pek-1 mutant background (Fig. S1)."Paper_evidenceWBPaper00041022
Curator_confirmedWBPerson2987
Phenotype_assayGenotypePnlp-29::GFPPaper_evidenceWBPaper00041022
Curator_confirmedWBPerson2987
WBPhenotype:0002058Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
RemarkIn the presence of low to moderate levels of the pore forming toxin (PFT) Cry5B, wild-type worms are slightly intoxicated compared to those found on control no-toxin plates, as evidenced by their smaller sizes and paler appearances. However, the mutant worms are more severely intoxicated than wild-type worms as they are relatively smaller and considerably paler compared to their corresponding no toxin controls. Compared to N2 and pek-1(ok275) animals, mutants were Hpo, i.e., more developmentally inhibited by Cry5B than wild-type animals.Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00005329Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
WBPhenotype:0002422Paper_evidenceWBPaper00036076
Curator_confirmedWBPerson2987
Remark"The ire-1 ( v33 ) and pek-1 ( ok275 ) mutant strains are more sensitive to tunicamycin than the wild-type ( Figure 3A , bars ; Shen et al . , 2001 ) , whereas atf-6 ( ok551 ) worms are less sensitive to tunicamycin ( Shen et al. , 2005 ) , and in our hands are more resistant than the wild type ( Figure 3A , bars ) ."Paper_evidenceWBPaper00036076
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004565Paper_evidenceWBPaper00036076
Curator_confirmedWBPerson2987
WBPhenotype:0002423Paper_evidenceWBPaper00037064
Curator_confirmedWBPerson2987
RemarkTunicamycin (Tm) preconditioning in wild type worms leads to increased tolerance to hypoxia. "... three loss-of-function mutant alleles of ire-1 (Fig. 3B), two alleles of atf-6 (Fig. 3D), and an allele of xbp-1 (Fig. 3F) all were defective for Tm preconditioning (Fig. 2D)."Paper_evidenceWBPaper00037064
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004565Paper_evidenceWBPaper00037064
Curator_confirmedWBPerson2987
Phenotype_not_observed (11)
Reference (12)
RemarkLast updated on 29 Nov 2002
Sequenced by the C. elegans Gene Knockout ConsortiumPaper_evidenceWBPaper00041807
MethodKO_consortium_allele