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WormBase Tree Display for Variation: WBVar00088241

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Name Class

WBVar00088241EvidencePaper_evidenceWBPaper00005370
WBPaper00061133
NamePublic_namekm4
Other_nameR03G5.2.1:c.238-425_985-53del
HGVSgCHROMOSOME_X:g.7817901_7819984del
Sequence_detailsSMapS_parentSequenceR03G5
Flanking_sequencesttcattttcatccatacactagaataagtgctatgctagatttgcgaaaaattgcaaaaa
Mapping_targetR03G5
Type_of_mutationDeletion
SeqStatusSequenced
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
Strain (34)
Component_of_genotypeWBGenotype00000159
LaboratoryKU
JN
StatusLive
AffectsGeneWBGene00004758
TranscriptR03G5.2.1VEP_consequencesplice_acceptor_variant,splice_donor_variant,coding_sequence_variant,intron_variant
VEP_impactHIGH
HGVScR03G5.2.1:c.238-425_985-53del
Intron_number4-7/8
Exon_number5-7/9
Interactor (75)
GeneticsInterpolated_map_positionX-1.13782
Mapping_dataIn_multi_point4653
DescriptionPhenotypeWBPhenotype:0000016Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Remark% of animals paralyzed after 60 min on 1mM aldicarb was significantly higher than % of N2 animals paralyzed.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00003650Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0007833PATO:0001549Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0000114Paper_evidenceWBPaper00035891
Curator_confirmedWBPerson2987
Remark"The p38 MAPK PMK-1 is activated by an upstream MAPKK called SEK-1 (16). Because SEK-1 might signal through MAPKs other than PMK-1, we also tested whether sek-1 was required for induction of irg-1. Of the infection response genes we tested, sek-1 mutants appeared to have similar effects on gene induction as pmk-1 mutants: a subset of genes were not fully induced by P. aeruginosa in sek-1 mutants, but most genes were still induced, including irg-1, irg-2, and irg-3 (Fig S1A). Therefore, sek-1 does not appear to be required for the pmk-1-independent-gene induction."Paper_evidenceWBPaper00035891
Curator_confirmedWBPerson2987
WBPhenotype:0000137Paper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
RemarkEndogenous T24B8.5 mRNA expression is diminished in sek-1(km4) mutantsPaper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
Variation_effectProbable_null_via_phenotypePaper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
WBPhenotype:0000142Paper_evidenceWBPaper00031666
Curator_confirmedWBPerson712
RemarkUpregulation of pnlp-29::GFP after infection with D. coniospora or after wounding was markedly decreased from that observed for wild type.Paper_evidenceWBPaper00031666
Curator_confirmedWBPerson712
Phenotype_assayTreatmentAnimals were infected with D. coniospora at the L4 stage and maintained on OP50 at 20C. Animals were wounded by microinjection needle pricking of the cuticle or by femtosecond laser busts.Paper_evidenceWBPaper00031666
Curator_confirmedWBPerson712
GenotypefrIs7Paper_evidenceWBPaper00031666
Curator_confirmedWBPerson712
WBPhenotype:0000180Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
RemarkThe intensity of GFP::SNB-1 axonal fluorescence was significantly lower than that observed in wild type.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0005190PATO:0000460Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Phenotype_assayGenotypejuIs1Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0000420Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Remark% of animals paralyzed after 60 min on 200mM levamisole was significantly higher than % of N2 animals paralyzed under same conditions.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00004019Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0000593Paper_evidenceWBPaper00024218
Curator_confirmedWBPerson2987
RemarkThe sek-1(km4) mutation caused a modest sensitivity to copper ion (Figure 7C)Paper_evidenceWBPaper00024218
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00002862Paper_evidenceWBPaper00024218
Curator_confirmedWBPerson2987
Phenotype_assayTreatmentStrains were placed on agar plates containing cadmium ions (up to a concentration of 100 micromolar) and their development was monitored for any signs of an altered response to these toxic compounds.Paper_evidenceWBPaper00024218
Curator_confirmedWBPerson2987
WBPhenotype:0000631Paper_evidenceWBPaper00032209
Curator_confirmedWBPerson712
RemarkAnimals showed arsenite-sensitive phenotypes.Paper_evidenceWBPaper00032209
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00004596Paper_evidenceWBPaper00032209
Curator_confirmedWBPerson712
Phenotype_assayTreatmentWell-fed young adults of each animal were transferred to normal plates containing 5 mM sodium arsenite. The percentage of animals surviving after incubation for 1 day were scored.Paper_evidenceWBPaper00032209
Curator_confirmedWBPerson712
WBPhenotype:0000655Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
RemarkRates of endogenous IPSCs were significantly different from wild type.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0001012Paper_evidenceWBPaper00038304
Curator_confirmedWBPerson2987
Remark"Mutation in sek-1 , which encodes for a MAPK kinase essential for PMK-1 activation , also suppressed the enhanced resistance of octr-1 ( ok371 ) animals ( fig . S6 ) ."Paper_evidenceWBPaper00038304
Curator_confirmedWBPerson2987
WBPhenotype:0001013Paper_evidenceWBPaper00005370
WBPaper00035315
WBPaper00041562
WBPaper00045829
WBPaper00061439
Curator_confirmedWBPerson712
WBPerson2021
WBPerson6515
WBPerson2987
WBPerson49407
RemarkAnimals were hyper-susceptible to PA14 killing.Paper_evidenceWBPaper00005370
Curator_confirmedWBPerson712
The sek-1(km4) mutant exhibits enhanced susceptibility to killing by PA14 relative to wildtypePaper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
Figure 4bPaper_evidenceWBPaper00045829
Curator_confirmedWBPerson2987
Variation_effectProbable_null_via_phenotypePaper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
EQ_annotationsGO_termGO:0045087PATO:0000460Paper_evidenceWBPaper00045829
Curator_confirmedWBPerson2987
Phenotype_assayTreatmentApproximately 25 L4-stage worms were placed on each of three agar plates with PA14 lawns under standard slow killing (SK) assay conditions. Survival was assayed after 30 hours.Paper_evidenceWBPaper00005370
Curator_confirmedWBPerson712
WBPhenotype:0001073Paper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
RemarkEgg laying response to food is defectivePaper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
Variation_effectProbable_null_via_phenotypePaper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
WBPhenotype:0001173Paper_evidenceWBPaper00040855
Curator_confirmedWBPerson557
RemarkAdult males possess an inappropriately surviving linker cell in 28 percent of animals.Paper_evidenceWBPaper00040855
Curator_confirmedWBPerson557
PenetranceIncomplete28 percentPaper_evidenceWBPaper00040855
Curator_confirmedWBPerson557
WBPhenotype:0001278Paper_evidenceWBPaper00039783
Curator_confirmedWBPerson712
Remarkgcs-1 promoter induction was markedly reduced in these mutants.Paper_evidenceWBPaper00039783
Curator_confirmedWBPerson712
Phenotype_assayGenotype[gcs-1::GFP]Paper_evidenceWBPaper00039783
Curator_confirmedWBPerson712
WBPhenotype:0001319Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
RemarkRates of endogenous IPSCs were decreased compared to wild type.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0001351Paper_evidenceWBPaper00032209
WBPaper00039783
WBPaper00035583
Curator_confirmedWBPerson712
WBPerson2987
RemarkWestern blot analysis using an anti-phospho p38 antibody showed that animals lack the phosphorylated, activated form of p38 MAPK.Paper_evidenceWBPaper00032209
Curator_confirmedWBPerson712
Cycloheximide-induced elevation in phospho-p38 levels were markedly reduced in these mutants.Paper_evidenceWBPaper00039783
Curator_confirmedWBPerson712
Western blot analysis using an anti-phospho-p38 antibody that specifically recognizes the phosphorylated, activated form of p38 MAPK revealed that the sek-1(km4) mutant was defective in the phosphorylation of PMK-1 (Figure 2C, lane 1).Paper_evidenceWBPaper00035583
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004352Paper_evidenceWBPaper00039783
Curator_confirmedWBPerson712
WBPhenotype:0001381Paper_evidenceWBPaper00037959
Curator_confirmedWBPerson712
RemarkThe survival rate of animals with a mutation in sek-1 was higher than that of their wild-type counterparts.Paper_evidenceWBPaper00037959
Curator_confirmedWBPerson712
WBPhenotype:0001621Paper_evidenceWBPaper00032399
Curator_confirmedWBPerson712
RemarkAnimals exhibited reduced survival when exposed to oxidative-stress causing arsenite, compared to N2 animals.Paper_evidenceWBPaper00032399
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00004596Paper_evidenceWBPaper00032399
Curator_confirmedWBPerson712
Phenotype_assayTreatmentAnimals were treated with 10mM Arsenite.Paper_evidenceWBPaper00032399
Curator_confirmedWBPerson712
WBPhenotype:0001687Paper_evidenceWBPaper00056945
Curator_confirmedWBPerson712
Remarksek-1(km4) animals showed positive staining of L2-L4 stages. mAb M37 stains only the L1 stage in wild type C. elegans under normal growth conditions.Paper_evidenceWBPaper00056945
Curator_confirmedWBPerson712
ImageWBPicture0000014905Paper_evidenceWBPaper00056945
Curator_confirmedWBPerson712
WBPhenotype:0001857Paper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
RemarkNo induction of Ptph-1::GFP expression by PA14 in the sek-1(km4) mutant backgroundPaper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
Variation_effectProbable_null_via_phenotypePaper_evidenceWBPaper00035315
Curator_confirmedWBPerson2021
WBPhenotype:0002058Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
RemarkIncreased splicing (activation) of xbp-1 in response to Cry5B does not occur in sek-1(km4) MAPKK mutant animals. Quantitatively, at the 3 h time point the spliced form of xbp-1 is induced 1.9 fold in animals with an intact p38 MAPK pathway and depressed 1.8 fold in sek-1(km4) MAPKK mutant animals relative to untreated controls. However, sek-1 is not absolutely required for splicing of xbp-1 since, in response to tunicamycin, splicing of xbp-1 is normal in sek-1(km4) mutant animals. Cry5B induction of mRNA Y41CA.11 was at lower levels than in wild-type animals.Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00005329Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
Phenotype_assayGenotypeglp-4;sek-1Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
WBPhenotype:0002059Paper_evidenceWBPaper00038321
WBPaper00032255
Curator_confirmedWBPerson712
RemarkMutant animals are significantly hypersensitive to Cry5B pore-forming toxins (PFTs) relative to wild type animals.Paper_evidenceWBPaper00038321
Curator_confirmedWBPerson712
Comparison of sek-1(km4) and xbp-1(zc12) mutant animals on Cry5B indicates sek-1(km4) animals are more severely intoxicated than xbp-1(zc12) animals at the same dose of Cry5B. This conclusion was quantitatively confirmed by performing LC50 experiments on N2 and sek-1(km4) animals. Whereas the LC50 of xbp-1(zc12) animals on Cry5B is 5.8 fold lower than N2, the LC50 of sek-1(km4) animals on Cry5B is 170 fold lower than N2.Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00005329Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
Phenotype_assayGenotypeglp-4;sek-1Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
Phenotype_not_observedWBPhenotype:0000359Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
RemarkIncreased splicing (activation) of xbp-1 in response to Cry5B does not occur in sek-1(km4) MAPKK mutant animals. Quantitatively, at the 3 h time point the spliced form of xbp-1 is induced 1.9 fold in animals with an intact p38 MAPK pathway and depressed 1.8 fold in sek-1(km4) MAPKK mutant animals relative to untreated controls. However, sek-1 is not absolutely required for splicing of xbp-1 since, in response to tunicamycin, splicing of xbp-1 is normal in sek-1(km4) mutant animals.Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00004565Paper_evidenceWBPaper00032255
Curator_confirmedWBPerson712
WBPhenotype:0000656Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
RemarkRate and amplitude of endogenous EPSCs were comparable to wild type.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0000847Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
RemarkThe density of GFP::SNB-1 puncta in GABAergic and cholinergic axons was not significantly different from wild type.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Phenotype_assayGenotypenuIs152 or juIs1Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0001171Paper_evidenceWBPaper00050656
Curator_confirmedWBPerson5092
RemarkFig. 2G. Mutant sek-1(km4) show similar lifespan compared to wild typePaper_evidenceWBPaper00050656
Curator_confirmedWBPerson5092
WBPhenotype:0001316Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
RemarkMuscimol activated currents were not significantly different than that observed for wild type.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Phenotype_assayGenotypePunc-129::GFP::SNB-1Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0001320Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
RemarkThe amplitudes of endogenous IPSCs were comparable to wild type.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0001685Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
RemarkPost-synaptic GABAAR::GFP puncta distribution was not significantly different from wild type.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Phenotype_assayGenotypeGFP-tagged GABAARPaper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0001725Paper_evidenceWBPaper00032031
Curator_confirmedWBPerson712
RemarkOsmotic-stress triggered upregulation of nlp-29 was not affected.Paper_evidenceWBPaper00032031
Curator_confirmedWBPerson712
Phenotype_assayTreatmentOsmotic stress was applied in liquid by incubating young adult worms in 300 mM NaCl for 6 h, with analysis occuring 24 hours later.Paper_evidenceWBPaper00032031
Curator_confirmedWBPerson712
GenotypefrIs7Paper_evidenceWBPaper00032031
Curator_confirmedWBPerson712
WBPhenotype:0002280Paper_evidenceWBPaper00046151
Curator_confirmedWBPerson557
Phenotype_assayTreatmentAnimals grown on 400 mmol/L NaCl.Paper_evidenceWBPaper00046151
Curator_confirmedWBPerson557
WBPhenotype:0002423Paper_evidenceWBPaper00049307
Curator_confirmedWBPerson2987
Remark"Multiple MAP kinase pathways were not required for Neuro-Nmnat1(gcIs30[Neuro-m-nonN-Nmnat1]) hypoxic survival." (Figure S3c)Paper_evidenceWBPaper00049307
Curator_confirmedWBPerson2987
EQ_annotationsGO_termGO:0001666PATO:0000460Paper_evidenceWBPaper00049307
Curator_confirmedWBPerson2987
Phenotype_assayGenotypegcIs30 [Neuro-m-nonN-Nmnat1]Paper_evidenceWBPaper00049307
Curator_confirmedWBPerson2987
Reference (30)
Remark
MethodDeletion_allele