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WormBase Tree Display for Variation: WBVar00091989

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Name Class

WBVar00091989NamePublic_nameok705
HGVSgCHROMOSOME_IV:g.17378126_17379461delinsGATATGTCCCGTATTGATAAGGTGACTTCCATAAAATAAGATCGAAGA
Sequence_detailsSMapS_parentSequenceC30H6
Flanking_sequencesggaagtcaccttatcaatacgggacatatcacagctcccggtagctgggaaattgatcaa
Mapping_targetC30H6
Type_of_mutationInsertionGATATGTCCCGTATTGATAAGGTGACTTCCATAAAATAAGATCGAAGA
Deletion
PCR_productok705_external
ok705_internal
SeqStatusSequenced
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
StrainWBStrain00031580
LaboratoryRB
PersonWBPerson46
KO_consortium_allele
StatusLive
AffectsGeneWBGene00007826
WBGene00001811
TranscriptC30H6.6.1VEP_consequencesplice_acceptor_variant,splice_donor_variant,coding_sequence_variant,3_prime_UTR_variant,intron_variant
VEP_impactHIGH
cDNA_position1057-?
CDS_position1048-?
Protein_position350-?
Intron_number7-9/10
Exon_number7-11/11
C30H6.9.1VEP_consequencecoding_sequence_variant,3_prime_UTR_variant
VEP_impactMODIFIER
cDNA_position546-?
CDS_position545-?
Protein_position182-?
Exon_number5-6/6
Interactor (23)
IsolationMutagenUV/TMP
DescriptionPhenotype (14)
Phenotype_not_observedWBPhenotype:0000306Paper_evidenceWBPaper00041370
WBPaper00045028
Curator_confirmedWBPerson2987
Remark"... hsp-60pr::gfp induction caused by mitochondrial stresses that arrest worm development, such as treatment with EtBr (100 mg/ml) or spg-7(RNAi), did not require haf-1 (fig S8). Additionally, UPRmt activation caused by conditions that directly inhibited mitochondrial import, such as treatment with tomm-40(RNAi) (fig S8A), tim-23(RNAi), cco-1(RNAi), or paraquat (9), also did not require haf-1 (Fig 3A). "Paper_evidenceWBPaper00041370
Curator_confirmedWBPerson2987
haf-1(ok705) did not affect expression of hsp-6p::GFP in response to cco-1 RNAiPaper_evidenceWBPaper00045028
Curator_confirmedWBPerson2987
haf-1(ok705) did not affect expression of hsp-6p::GFP in response to phb-2 RNAiPaper_evidenceWBPaper00045028
Curator_confirmedWBPerson2987
Phenotype_assayTreatmenthsp-6p::gfp induction was measured 3 days from hatch at 20 degrees CelsiusPaper_evidenceWBPaper00045028
Curator_confirmedWBPerson2987
Temperature20Paper_evidenceWBPaper00045028
Curator_confirmedWBPerson2987
Genotypehsp-60p::gfpPaper_evidenceWBPaper00041370
Curator_confirmedWBPerson2987
zcIs13 [hsp-6p::GFP]; cco-1(RNAi)Paper_evidenceWBPaper00045028
Curator_confirmedWBPerson2987
zcIs13 [hsp-6p::GFP]; phb-2(RNAi)Paper_evidenceWBPaper00045028
Curator_confirmedWBPerson2987
WBPhenotype:0000523Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Remark"By contrast, haf-1-deleted worms were indistinguishable from WT in their survival under reductive stress imposed by dithiothreitol (DTT), which promotes ER stress and activates the UPRER (Figure S2B)."Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004908Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
EQ_annotationsGO_termGO:0042221PATO:0000460Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Phenotype_assayTreatmentAnimals were exposed to 5 millimolar dithiothreitol (DTT) and assayed for survival over several daysPaper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
WBPhenotype:0000679Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Remark"the haf-1 deletion did not affect the nuclear distribution of DVE-1::GFP (Figure 6A), indicating that DVE-1 is not downstream of HAF-1 in UPRmt signaling and suggesting the existence of other UPRmt transcription factor(s) that had been missed in the original RNAi screen for genes that activate the UPRmt."Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
WBPhenotype:0001208Paper_evidenceWBPaper00027644
Curator_confirmedWBPerson557
RemarkAnimals were not resistant to RNAi as assayed on either pop-1 RNAi or unc-22 RNAi.Paper_evidenceWBPaper00027644
Curator_confirmedWBPerson557
Phenotype_assayTreatmentAnimals reared on both pop-1 and unc-22 feeding plates at 15, 20, 25, and 26C.Paper_evidenceWBPaper00027644
Curator_confirmedWBPerson557
WBPhenotype:0001258Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Remark"Whereas the positive control, eri-1(mg366), markedly sensitized worms to dpy-13(RNAi), haf-1 deletion had no effect on the sensitivity of worms to the RNAi feeding procedure (Figure S1E)."Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
WBPhenotype:0001719Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Remark"Specificity for the UPRmt was revealed by the observation that induction of the UPRER was unaffected by haf-1 deletion (Figure 1D)."Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
EQ_annotationsGO_termGO:0030968PATO:0000460Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
WBPhenotype:0002141Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Remark"By contrast, when exposed to the ER stress-inducing agent DTT, only minor differences in oxygen consumption were noted between WT and haf-1 mutant worms (Figure S2C)."Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004908Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
EQ_annotationsGO_termGO:0072592PATO:0000460Paper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
Phenotype_assayTreatmentAnimals were exposed to 5 millimolar dithiothreitol (DTT) and assayed for oxygen consumptionPaper_evidenceWBPaper00035985
Curator_confirmedWBPerson2987
ReferenceWBPaper00041212
WBPaper00041370
WBPaper00027644
WBPaper00035985
WBPaper00043917
WBPaper00045028
WBPaper00049307
RemarkSequenced by the C. elegans Gene Knockout ConsortiumPaper_evidenceWBPaper00041807
MethodKO_consortium_allele