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: WBVar00275520

expand all nodes | collapse all nodes | view schema

Name Class

WBVar00275520NamePublic_namezu193
Sequence_detailsSeqStatusPending_curation
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
StrainWBStrain00007281
WBStrain00007282
LaboratoryJJ
StatusLive
AffectsGeneWBGene00003397
Interactor (14)
DescriptionPhenotypeWBPhenotype:0000047Paper_evidenceWBPaper00038341
Curator_confirmedWBPerson712
RemarkCells internalize late at the 4E stage in 72% of embryos.Paper_evidenceWBPaper00038341
Curator_confirmedWBPerson712
WBPhenotype:0000050Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
PenetranceCompletePaper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
WBPhenotype:0000219Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
RemarkAnimals from strains from either the Sternberg lab or the Eisenmann lab exhibit an underinduction phenotype.Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
Variation_effectProbable_null_via_phenotypePaper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
WBPhenotype:0000436Paper_evidenceWBPaper00026736
Curator_confirmedWBPerson2021
RemarkWRM-1 fails to be retained in the E nucleusPaper_evidenceWBPaper00026736
Curator_confirmedWBPerson2021
EQ_annotationsAnatomy_termWBbt:0001975PATO:0000460Paper_evidenceWBPaper00026736
Curator_confirmedWBPerson2021
Life_stageWBls:0000071PATO:0000460Paper_evidenceWBPaper00026736
Curator_confirmedWBPerson2021
Phenotype_assayTreatmentmom-5 mutants carrying the WRM-1::GFP transgene were examined. Nuclear retention was assayed by subjecting the animals to imb-4 RNAiPaper_evidenceWBPaper00026736
Curator_confirmedWBPerson2021
GenotypeneIs2 [WRM-1::GFP]Paper_evidenceWBPaper00026736
Curator_confirmedWBPerson2021
WBPhenotype:0000472Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
RemarkTable 1Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
PenetranceLow5% penetrancePaper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
WBPhenotype:0000760Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
RemarkIn mom-5(zu193) mutants, the EMS cell exhibited spindle orientation defects, with significant dorsal/ventral or left/right orientation components, in contrast to the normally anterior/posterior orientation of the wild type EMS spindle (data not shown).Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
In EMS cells derived from isolated P1 blastomeres from mom-5(zu193) mutants, spindles exhibited orientation defects, with a wide range of orientation angles, showing nearly random orientations (Figure 2).Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
In EMS blastomeres isolated from mom-5(zu193) mutant embryos and placed in contact with isolated wild type P2 blastomeres, EMS spindles exhibited orientation defects suggesting that mom-5 is required in EMS for proper EMS spindle orientation (Figure 4A).Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
PenetranceIncomplete57% penetrancePaper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006876PATO:0000460Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
WBbt:0006873PATO:0000460Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
Life_stageWBls:0000008PATO:0000460Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
WBls:0000071PATO:0000460Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
WBls:0000003PATO:0000460Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
Phenotype_assayTreatmentAuthors isolated the smaller, posterior-most blastomere in a two-cell-stage embryo, called P1, and allowed it to divide into its daughters, P2 and EMS. The orientation of the mitotic spindle in EMS was then measured relative to the plane of contact between EMS and P2.Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
For genetically mosaic partial embryos, wild-type and mutant early EMS and P2 blastomeres were concurrently isolated. EMS and P2 were recombined early in the EMS cell cycle allowing the cells to be in contact for at least 9 min before EMS cytokinesis.Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
WBPhenotype:0001495Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
RemarkE daughter cells of some (2/12) mom-5(zu193) mutant embryos divide earlier (compared to MS daughters) than in wild type embryosPaper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
PenetranceIncompletePaper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006733PATO:0000460Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
WBbt:0006612PATO:0000460Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
WBPhenotype:0001635Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
RemarkE blastomeres produced pharyngeal cells (aberrantly) instead of endoderm in 2/15 (13%) mom-5(zu193) mutantsPaper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0004804PATO:0000460Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
WBPhenotype:0001637Paper_evidenceWBPaper00005375
Curator_confirmedWBPerson2987
Remark4% of mom-5(zu193) embryos lacked an intestine (Table 1)Paper_evidenceWBPaper00005375
Curator_confirmedWBPerson2987
PenetranceLow4Paper_evidenceWBPaper00005375
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0005772PATO:0000460Paper_evidenceWBPaper00005375
Curator_confirmedWBPerson2987
Phenotype_not_observedWBPhenotype:0000218Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
RemarkAnimals from strains from either the Sternberg lab or the Eisenmann lab do not exhibit a significant level of overinduction although a very low level (2%) of the animals from the Eisenmann strain exhibit an overinduced phenotype; 0% of the animals from the Sternberg strain exhibit OI.Paper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
Variation_effectProbable_null_via_phenotypePaper_evidenceWBPaper00031110
Curator_confirmedWBPerson712
WBPhenotype:0000760Paper_evidenceWBPaper00002871
WBPaper00003645
Curator_confirmedWBPerson2987
RemarkThe ABar cells of pop-1(zu193) embryos exhibit normal spindle orientation, with the ABar spindle perpendicular to the ABpr spindle.Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
In EMS blastomeres isolated from wild type embryos and placed in contact with isolated mom-5(zu193) mutant P2 blastomeres, EMS spindles exhibited wild type orientation suggesting that mom-5 is dispensable in P2 for proper EMS spindle orientation (Figure 4A).Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006411PATO:0000460Paper_evidenceWBPaper00002871
Curator_confirmedWBPerson2987
WBbt:0006876PATO:0000460Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
WBbt:0006873PATO:0000460Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
Life_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
Phenotype_assayTreatmentFor genetically mosaic partial embryos, wild-type and mutant early EMS and P2 blastomeres were concurrently isolated. EMS and P2 were recombined early in the EMS cell cycle allowing the cells to be in contact for at least 9 min before EMS cytokinesis.Paper_evidenceWBPaper00003645
Curator_confirmedWBPerson2987
WBPhenotype:0000883Paper_evidenceWBPaper00035405
Curator_confirmedWBPerson2021
RemarkNerve ring development is normalPaper_evidenceWBPaper00035405
Curator_confirmedWBPerson2021
WBPhenotype:0001133Paper_evidenceWBPaper00005375
Curator_confirmedWBPerson2987
Remarkmom-5(zu193) animals exhibited no embryos with aberrant L-R division of EMS (Table 1)Paper_evidenceWBPaper00005375
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0006876PATO:0000460Paper_evidenceWBPaper00005375
Curator_confirmedWBPerson2987
WBPhenotype:0001224Paper_evidenceWBPaper00060654
Curator_confirmedWBPerson712
RemarkThere are six Wnt receptors encoded in the C. elegans genome: four Frizzled receptors (LIN-17, CFZ-2, MIG-1 and MOM-5,), one Ror receptor (CAM-1) and one Ryk receptor (LIN-18) (Sawa and Korswagen, 2013). We analyzed the effect of loss-of-function mutations for each receptor and found that loss 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
ReferenceWBPaper00038341
WBPaper00005375
WBPaper00002871
WBPaper00026736
WBPaper00003645
WBPaper00031110
WBPaper00035405
WBPaper00060654
MethodAllele