Questions, Feedback & Help
Send us an email and we'll get back to you ASAP. Or you can read our Frequently Asked Questions.

WormBase Tree Display for Variation: WBVar00092168

expand all nodes | collapse all nodes | view schema

Name Class

WBVar00092168NamePublic_nameok895
Other_nameW01B6.1.1:c.229_917+78del
HGVSgCHROMOSOME_IV:g.10068357_10069261del
Sequence_detailsSMapS_parentSequenceW01B6
Flanking_sequencesccagctgtgagcatcggagcacaaaatgctcaatttttctttaaaaatgtaattttctaa
Mapping_targetW01B6
Type_of_mutationDeletion
PCR_productok895_external
ok895_internal
SeqStatusSequenced
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
Strain (21)
LaboratoryRB
PersonWBPerson46
KO_consortium_allele
StatusLive
AffectsGeneWBGene00000858
TranscriptW01B6.1.1VEP_consequencesplice_acceptor_variant,splice_donor_variant,coding_sequence_variant,intron_variant
VEP_impactHIGH
HGVScW01B6.1.1:c.229_917+78del
cDNA_position288-?
CDS_position229-?
Protein_position77-?
Intron_number3-6/7
Exon_number3-6/8
Interactor (20)
IsolationMutagenUV/TMP
DescriptionPhenotypeWBPhenotype: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
PenetranceIncomplete24Paper_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"... 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
PenetranceIncomplete47Paper_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: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
PenetranceIncomplete45Paper_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:0000625Paper_evidenceWBPaper00064204
Curator_confirmedWBPerson7196
WBPhenotype:0000633Paper_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
PenetranceIncomplete13Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
Low10Paper_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
WBPhenotype:0000883Paper_evidenceWBPaper00035405
Curator_confirmedWBPerson2021
Remarkcwn-2 mutants had anteriorly displaced nerve rings: the nerve ring circled the metacorpus of the pharynx instead of its usual location around the isthmus of the pharynxPaper_evidenceWBPaper00035405
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035405
Curator_confirmedWBPerson2021
WBPhenotype:0001224Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
RemarkLoss of cwn-2 caused a defective SMDD axonal phenotype, where axons do not extend along the dorsal sublateral cord, suggesting that the axons did not exit the nerve ring due to defects in axon outgrowth or guidance (Figure 1A-C). Expressing cwn-2 using this promoter partially rescues the defective axonal phenotype (Figure 1C).Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0004972PATO:0000460Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
WBbt:0004971PATO:0000460Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
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
PenetranceIncomplete31Paper_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
Phenotype_not_observedWBPhenotype:0000016Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Remark% animals paralyzed after 60 min on 1mM aldicarb was not higher than % N2 animals paralyzed.Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00003650Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0007833PATO:0000516Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
PATO:0000461Paper_evidenceWBPaper00031872
Curator_confirmedWBPerson712
WBPhenotype:0000104Paper_evidenceWBPaper00044679
Curator_confirmedWBPerson2987
RemarkThe cwn-2(ok895) 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:0000219Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
RemarkNo underinduced animals (worms with fewer than 22 vulval cells or fewer than three VPCs induced) were detected.Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
WBPhenotype:0000469Paper_evidenceWBPaper00038522
WBPaper00026706
Curator_confirmedWBPerson712
WBPerson2987
Remarkcwn-2 has no significant effect on QR.d positioning on its own.Paper_evidenceWBPaper00038522
Curator_confirmedWBPerson712
"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:0004054PATO:0000460Paper_evidenceWBPaper00038522
Curator_confirmedWBPerson712
WBbt: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
WBPaper00026706
Curator_confirmedWBPerson712
WBPerson2987
RemarkALM does not exhibit significant migration defects.Paper_evidenceWBPaper00038522
Curator_confirmedWBPerson712
"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:0005406PATO:0000460Paper_evidenceWBPaper00038522
WBPaper00026706
Curator_confirmedWBPerson712
WBPerson2987
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:0001681Paper_evidenceWBPaper00035553
Curator_confirmedWBPerson625
RemarkNo abnormal spindle orientation of BγPaper_evidenceWBPaper00035553
Curator_confirmedWBPerson625
EQ_annotationsAnatomy_termWBbt:0007830PATO:0000460Paper_evidenceWBPaper00035553
Curator_confirmedWBPerson625
GO_termGO:0000132PATO:0000460Paper_evidenceWBPaper00035553
Curator_confirmedWBPerson625
GO:0005819PATO:0000460Paper_evidenceWBPaper00035553
Curator_confirmedWBPerson625
WBPhenotype:0001761Paper_evidenceWBPaper00026706
Curator_confirmedWBPerson2987
RemarkTable 2Paper_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
RemarkTable 2Paper_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
ReferenceWBPaper00038522
WBPaper00031110
WBPaper00031872
WBPaper00035405
WBPaper00035553
WBPaper00026706
WBPaper00044679
WBPaper00060654
WBPaper00064204
RemarkSequenced by the C. elegans Gene Knockout ConsortiumPaper_evidenceWBPaper00041807
MethodKO_consortium_allele