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: WBVar00088286

expand all nodes | collapse all nodes | view schema

Name Class

WBVar00088286EvidencePaper_evidenceWBPaper00003851
NamePublic_nameks52
Other_nameC01G6.8c.1:c.1105_2112del
C01G6.8b.1:c.1504_2511del
CE32563:p.Thr528_Ala863delextTer?
C01G6.8c.2:c.1105_2112del
CE39126:p.Thr369_Ala704delextTer?
CE24774:p.Thr502_Ala837delextTer?
C01G6.8a.1:c.1582_2589del
HGVSgCHROMOSOME_II:g.9296655_9297713del
Sequence_details (5)
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
StrainWBStrain00007507
LaboratoryFK
StatusLive
AffectsGeneWBGene00000289
TranscriptC01G6.8c.1 (11)
C01G6.8b.1 (11)
C01G6.8c.2 (11)
C01G6.8a.1 (11)
InteractorWBInteraction000050666
WBInteraction000501680
GeneticsInterpolated_map_positionII1.10196
DescriptionPhenotypeWBPhenotype:0000232Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Remark"In cam-1 mutants, CAN neurons usually fail to migrate to their proper positions; they are misplaced anteriorly either near their starting points or along their migratory routes... In cam-1(ks52) mutants, CAN, ALM, BDU, and HSN migration are much less severely defective than in cam-1(gm122) or cam-1(sa692) mutants (Fig. 3, Table 1), confirming that the kinase domain is not required for proper embryonic cell migration."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
PenetranceIncomplete35Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006827PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Life_stageWBls:0000024PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"CAN was scored as defective if its nucleus was anterior to the V3 nucleus."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
WBPhenotype:0000469Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Remark"The final positions of QR descendants in cam-1(ks52) mutants were shifted slightly posterior to normal, suggesting that the kinase domain might play a minor role in QR migration." (Table 1, Figure 5)Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
PenetranceIncomplete18Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0004991PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
WBbt:0003832PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
WBbt:0004054PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Life_stageWBls:0000024PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"Because they occupy positions near each other, the data for SDQR and AVM were combined and are presented in QR column. SDQR and AVM were scored as defective if their nuclei were posterior to the V2.a nucleus."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
WBPhenotype:0000470Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Remark"In cam-1(ks52) mutants, CAN, ALM, BDU, and HSN migration are much less severely defective than in cam-1(gm122) or cam-1(sa692) mutants (Fig. 3, Table 1), confirming that the kinase domain is not required for proper embryonic cell migration."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
PenetranceIncomplete12Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006830PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Life_stageWBls:0000024PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"Because HSN sometimes was misplaced anteriorly and other times was misplaced posteriorly, we present the data for both phenotypes. HSN was scored as misplaced anteriorly if its nucleus was anterior to the P5/6 nucleus and misplaced posteriorly if its nucleus was posterior to the V4 nucleus."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
WBPhenotype:0000471Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Remark"In cam-1(ks52) mutants, CAN, ALM, BDU, and HSN migration are much less severely defective than in cam-1(gm122) or cam-1(sa692) mutants (Fig. 3, Table 1), confirming that the kinase domain is not required for proper embryonic cell migration."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
PenetranceLow7Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0005406PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Life_stageWBls:0000024PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"ALM was scored as defective if its nucleus was anterior to the V2 nucleus."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
WBPhenotype:0000594Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Remark"In cam-1(ks52) mutants, CAN, ALM, BDU, and HSN migration are much less severely defective than in cam-1(gm122) or cam-1(sa692) mutants (Fig. 3, Table 1), confirming that the kinase domain is not required for proper embryonic cell migration."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
PenetranceLow7Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006826PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Life_stageWBls:0000024PATO:0000460Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
Phenotype_assayTreatment"Because BDU sometimes was misplaced anteriorly and other times was misplaced posteriorly, we present the data for both phenotypes. BDU was scored as misplaced anteriorly if its nucleus was anterior to its normal position immediately anterior to V1 and misplaced posteriorly if its nucleus was posterior to the V1 nucleus."Paper_evidenceWBPaper00006269
Curator_confirmedWBPerson2987
WBPhenotype:0001224Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
RemarkLoss of cam-1, but not the other receptors, caused defective SMDD axonal development (Figure 1D).Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0004972PATO:0000460Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
WBbt:0004971PATO:0000460Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
WBPhenotype:0002212Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
Remark"Consistent with a previous report (Koga et al. 1999), we saw that cam-1/kin-8 mutants had a specific dye-filling defect in ASI neurons (Fig. 1C, E)."Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0005665PATO:0000460Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
WBbt:0005661PATO:0000460Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
WBbt:0005666PATO:0000460Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
WBbt:0005671PATO:0000460Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
WBbt:0005668PATO:0000460Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
WBbt:0005667PATO:0000460Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
WBPhenotype:0002535Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
RemarkConsistent with a previous report (Koga et al. 1999), we saw that cam-1/kin-8 mutants had a specific dye-filling defect in ASI neurons (Fig. 1C, E).Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0005666PATO:0000460Paper_evidenceWBPaper00061480
Curator_confirmedWBPerson712
Phenotype_not_observed (6)
ReferenceWBPaper00031110
WBPaper00006052
WBPaper00006269
WBPaper00035405
WBPaper00060654
WBPaper00061480
MethodDeletion_allele