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WormBase Tree Display for Variation: WBVar00092161

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Name Class

WBVar00092161NamePublic_nameok886
Other_nameY81G3A.3b.1:c.2444_3571del
CE47938:p.Cys815_Pro1191delinsSer
Y81G3A.3a.1:c.2444_3571del
CE47891:p.Cys815_Pro1191delinsSer
HGVSgCHROMOSOME_II:g.13086950_13088128del
Sequence_detailsSMapS_parentSequenceY81G3A
Flanking_sequencesaagtttggagaatcttttcggaagttttgtccggaatgaagtttactctgaaaatcgggc
Mapping_targetY81G3A
Type_of_mutationDeletion
PCR_productok886_external
ok886_internal
SeqStatusSequenced
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
StrainWBStrain00031690
LaboratoryRB
PersonWBPerson46
KO_consortium_allele
StatusLive
AffectsGeneWBGene00013591
TranscriptY81G3A.3b.1 (11)
Y81G3A.3a.1 (11)
InteractorWBInteraction000536842
IsolationMutagenUV/TMP
DescriptionPhenotypeWBPhenotype:0002423Paper_evidenceWBPaper00037064
Curator_confirmedWBPerson2987
Remark"HP (hypoxic preconditioning) consistently provided protection from subsequent harsh hypoxic exposure for wild-type animals (Fig. 4A and B)... However, unlike for TmP, gcn-2(ok871) completely blocked HP (Fig. 4C). gcn-2(ok886), an allele with a smaller deletion that removes less of the kinase and tRNA-binding domains (Fig. 3E), also failed to exhibit a significant increase in survival after HP, although there was a trend toward protection (Fig. 4C)."Paper_evidenceWBPaper00037064
Curator_confirmedWBPerson2987
Phenotype_not_observedWBPhenotype:0001349Paper_evidenceWBPaper00048983
Curator_confirmedWBPerson2987
Remark"To evaluate whether either GCN-2 or PEK-1 kinases are required for H2S-dependent phosphorylation of eIF2α, we introduced gcn-2(ok886) or pek-1(ok275) deletion alleles into sqrd-1(tm3378) mutant animals. When exposed to H2S, we observed robust phosphorylation of eIF2α in both pek-1; sqrd-1 and gcn-2; sqrd-1 double mutant animals (Fig. 3, A and B)."Paper_evidenceWBPaper00048983
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004296Paper_evidenceWBPaper00048983
Curator_confirmedWBPerson2987
ReferenceWBPaper00037064
WBPaper00048983
RemarkSequenced by the C. elegans Gene Knockout ConsortiumPaper_evidenceWBPaper00041807
MethodKO_consortium_allele