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WormBase Tree Display for Variation: WBVar00091833

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Name Class

WBVar00091833NamePublic_nameok546
Other_nameK10B4.6a.1:c.161+156_414del
HGVSgCHROMOSOME_II:g.132477_133261del
Sequence_detailsSMapS_parentSequenceK10B4
Flanking_sequencestgagtgatcgtttttcgagtagtcacaacctgagaaattttcaagaagatttatcatgaa
Mapping_targetK10B4
Type_of_mutationDeletion
PCR_productOK546_external
OK546_internal
SeqStatusSequenced
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
Strain (21)
LaboratoryRB
PersonWBPerson46
KO_consortium_allele
StatusLive
AffectsGeneWBGene00000857
TranscriptK10B4.6a.1VEP_consequencesplice_acceptor_variant,splice_donor_variant,coding_sequence_variant,intron_variant
VEP_impactHIGH
HGVScK10B4.6a.1:c.161+156_414del
cDNA_position?-435
CDS_position?-414
Protein_position?-138
Intron_number2-4/10
Exon_number3-5/11
Interactor (45)
IsolationMutagenUV/TMP
DescriptionPhenotypeWBPhenotype:0000219Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
Remark13% of animals were underinduced (worms with fewer than 22 vulval cells or fewer than three VPCs induced).Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
WBPhenotype:0000239Paper_evidenceWBPaper00039829
Curator_confirmedWBPerson712
RemarkHeterozygous mutants displayed a reduction in P3.p and P4.p division frequencies compared to N2.Paper_evidenceWBPaper00039829
Curator_confirmedWBPerson712
Haplo_insufficientPaper_evidenceWBPaper00039829
Curator_confirmedWBPerson712
WBPhenotype:0000384Paper_evidenceWBPaper00027140
Curator_confirmedWBPerson3779
EQ_annotationsGO_termGO:0007411PATO:0000460Paper_evidenceWBPaper00027140
Curator_confirmedWBPerson3779
WBPhenotype:0000469Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Remark"... because each deletion removes a large portion of the gene, each is likely to eliminate gene function... Mutations in cwn-1, cwn-2, and egl-20 disrupted the migrations of QR descendant cells, as well as others, raising the possibility that they could function through CFZ-2 (Table 1; Desai et al., 1988; Forrester et al., 2004; Harris et al., 1996)... We focused on cwn-1, cwn-2, and egl-20 because they produced defects in QR descendant cell migration (Fig. 4, Table 1), a cfz-2 phenotype."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
PenetranceIncomplete73Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0004991PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0003832PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
GO_termGO:0016477PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"A QR cell descendant was scored as defective if its nucleus was posterior to the V2.a nucleus. Because they occupy positions near each other, the data for SDQR and AVM were combined. The position of AQR, a third QR descendant, was not included because it migrates to a location near other nuclei with similar morphology."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBPhenotype:0000470Paper_evidenceWBPaper00027140
Curator_confirmedWBPerson3779
EQ_annotationsAnatomy_termWBbt:0006830PATO:0000460Paper_evidenceWBPaper00027140
Curator_confirmedWBPerson3779
GO_termGO:0001764PATO:0000460Paper_evidenceWBPaper00027140
Curator_confirmedWBPerson3779
WBPhenotype:0000471Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Remark"We found that both cwn-1 and cwn-2 mutations not only affected migrations of subsets of neurons (Table 1), but also resulted in defects in axon development and guidance (Table 2)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
PenetranceLow8Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0005406PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
GO_termGO:0016477PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"An ALM was scored as anteriorly misplaced (Ant.) if its nucleus was anterior to the V2 nucleus and posteriorly misplaced (Post.) if posterior to the V3 nucleus."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBPhenotype:0000594Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Remark"We found that both cwn-1 and cwn-2 mutations not only affected migrations of subsets of neurons (Table 1), but also resulted in defects in axon development and guidance (Table 2)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
PenetranceIncomplete18Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006826PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
GO_termGO:0016477PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"A BDU was scored as defective if its nucleus was posterior to the V1 nucleus."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBPhenotype:0001761Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Remark"We found that both cwn-1 and cwn-2 mutations not only affected migrations of subsets of neurons (Table 1), but also resulted in defects in axon development and guidance (Table 2)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
PenetranceIncomplete33Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006830PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
GO_termGO:0007409PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"Axon morphology was examined by indirect immunofluorescence using anti-serotonin antibody (HSN and CP) or two independent GFP-expressing reporter transgenes, ceh-23::gfp and kal-1::gfp (CAN)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBPhenotype:0002490Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Remark"We found that both cwn-1 and cwn-2 mutations not only affected migrations of subsets of neurons (Table 1), but also resulted in defects in axon development and guidance (Table 2)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
PenetranceIncomplete67Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Low8Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_term (11)
GO_termGO:0007409PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"Axon morphology was examined by indirect immunofluorescence using anti-serotonin antibody (HSN and CP) or two independent GFP-expressing reporter transgenes, ceh-23::gfp and kal-1::gfp (CAN)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_not_observedWBPhenotype:0000050Paper_evidenceWBPaper00025190
Curator_confirmedWBPerson712
WBPhenotype:0000104Paper_evidenceWBPaper00044679
Curator_confirmedWBPerson2987
RemarkThe cwn-1(ok546) mutation does not affect anteroposterior polarity in the AVG interneuronPaper_evidenceWBPaper00044679
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0003850PATO:0000460Paper_evidenceWBPaper00044679
Curator_confirmedWBPerson2987
WBPhenotype:0000218Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
RemarkNo significant number of overinduced animals (worms with greater than three VPCs induced) were detected.Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
WBPhenotype:0000232Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Remark"We found that both cwn-1 and cwn-2 mutations not only affected migrations of subsets of neurons (Table 1), but also resulted in defects in axon development and guidance (Table 2)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006827PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
GO_termGO:0016477PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"A CAN was scored as anteriorly misplaced (Ant.) if its nucleus was anterior to the V3 nucleus and posteriorly misplaced (Post.) if posterior to the V4 nucleus."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBPhenotype:0000469Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Remark"We found that both cwn-1 and cwn-2 mutations not only affected migrations of subsets of neurons (Table 1), but also resulted in defects in axon development and guidance (Table 2)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0004993PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004086PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
GO_termGO:0016477PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"A QL cell descendant was scored as misplaced anteriorly if its nucleus was anterior to V4.p. Because they occupy positions near each other, the data for SDQL and PVM were combined. The position of PQR, a third QL descendant, was not included because it migrates to a location near other nuclei with similar morphology."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBPhenotype:0000470Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Remark"We found that both cwn-1 and cwn-2 mutations not only affected migrations of subsets of neurons (Table 1), but also resulted in defects in axon development and guidance (Table 2)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006830PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
GO_termGO:0016477PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"An HSN was scored as defective if its nucleus was posterior to the V4 nucleus."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBPhenotype:0000471Paper_evidenceWBPaper00038522
Curator_confirmedWBPerson712
RemarkALM does not exhibit significant migration defects.Paper_evidenceWBPaper00038522
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0005406PATO:0000460Paper_evidenceWBPaper00038522
Curator_confirmedWBPerson712
WBPhenotype:0000633Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
RemarkTable 2Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Variation_effectPredicted_null_via_sequencePaper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0004903PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004901PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004899PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004897PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004895PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004893PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004891PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004889PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004888PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBbt:0004887PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
GO_termGO:0007409PATO:0000460Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"Axon morphology was examined by indirect immunofluorescence using anti-serotonin antibody (HSN and CP) or two independent GFP-expressing reporter transgenes, ceh-23::gfp and kal-1::gfp (CAN)."Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
WBPhenotype:0000883Paper_evidenceWBPaper00035405
Curator_confirmedWBPerson2021
RemarkNerve ring development is normalPaper_evidenceWBPaper00035405
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035405
Curator_confirmedWBPerson2021
WBPhenotype:0001408Paper_evidenceWBPaper00039829
Curator_confirmedWBPerson712
RemarkThe anterior LIN-39 level, as assayed through LIN-39::GFP protein fusion expression, was not altered at the early L2 stage.Paper_evidenceWBPaper00039829
Curator_confirmedWBPerson712
ReferenceWBPaper00038522
WBPaper00039829
WBPaper00010775
WBPaper00031110
WBPaper00035405
WBPaper00026706
WBPaper00027140
WBPaper00025190
WBPaper00026256
WBPaper00044679
RemarkLast updated on 29 Nov 2002
Sequenced by the C. elegans Gene Knockout ConsortiumPaper_evidenceWBPaper00041807
MethodKO_consortium_allele