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WormBase Tree Display for Variation: WBVar00142887

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Name Class

WBVar00142887NamePublic_namedx31
Sequence_detailsSeqStatusPending_curation
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
StrainWBStrain00005346
WBStrain00005659
WBStrain00005660
WBStrain00008609
WBStrain00029412
WBStrain00029413
WBStrain00029414
WBStrain00029420
WBStrain00029421
WBStrain00029424
WBStrain00029425
WBStrain00040665
LaboratoryEJ
StatusLive
AffectsGeneWBGene00006868
InteractorWBInteraction000502399
WBInteraction000504065
WBInteraction000517208
WBInteraction000517209
WBInteraction000518898
WBInteraction000518901
WBInteraction000519471
WBInteraction000535985
WBInteraction000535986
WBInteraction000535988
WBInteraction000535993
WBInteraction000535994
DescriptionPhenotypeWBPhenotype:0000050Paper_evidenceWBPaper00031951
WBPaper00040551
Curator_confirmedWBPerson712
WBPerson2987
RemarkN=805Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
"Many vab-1 null mutant [vab-1(0)] embryos fail to close the open ventral pocket before embryo elongation begins [8,13] . The residual hole in the mutant epidermis provides a conduit for the extrusion of internal blast cells from the embryo, thereby causing lethality (Figure S2A)... Despite more severe (Figures S3A-S3D) and eight times more penetrant midline alignment defects in the mab-20 null (Figure 5; Figures S3A-S3D; Table S2), the penetrance of lethality among mab-20(0) embryos is significantly lower than for vab-1(0) embryos (Figure 5C). These data suggest that the P cell alignment defects per se do not contribute significantly to vab-1(0) mutant lethality; instead, the lethality results from a more severe effect on pocket closure, including failure of P cells to migrate sufficiently to the midline before embryo elongation occurs or failure to form a proper midline seal."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
PenetranceIncomplete40Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Variation_effectNullPaper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
EQ_annotationsLife_stageWBls:0000013PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBls:0000003PATO:0000460Paper_evidenceWBPaper00031951
WBPaper00040551
Curator_confirmedWBPerson712
WBPerson2987
Phenotype_assayTreatmentAnimals were reared on NA22 bacteria instead of OP50.Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Temperature20Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBPhenotype:0000054Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
RemarkN=805Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Variation_effectNullPaper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
EQ_annotationsLife_stageWBls:0000023PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Phenotype_assayTreatmentAnimals were reared on NA22 bacteria instead of OP50.Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Temperature20Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBPhenotype:0000061Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
RemarkAnimals have significantly longer life spans than controlPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Phenotype_assayGenotypefem-1(hc17)Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0000106Paper_evidenceWBPaper00027739
Curator_confirmedWBPerson2021
Remarkvab-1(null) hermaphrodites exhibit an expanded pattern of MAPK activation in which MAPKYT staining extends to distal oocytesPaper_evidenceWBPaper00027739
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00027739
Curator_confirmedWBPerson2021
EQ_annotationsAnatomy_termWBbt:0006797PATO:0000460Paper_evidenceWBPaper00027739
Curator_confirmedWBPerson2021
Life_stageWBls:0000057PATO:0000460Paper_evidenceWBPaper00027739
Curator_confirmedWBPerson2021
Phenotype_assayTreatmentAntibody staining to the diphosphorylated activated form of MAPK (MAPK-YT)Paper_evidenceWBPaper00027739
Curator_confirmedWBPerson2021
WBPhenotype:0000119Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
RemarkIncreased DAF-18 expression is observed in oocytes of vab-1(dx31) mutants. vab-1(dx31) embryo lysates showed increased DAF-18/PTEN expression compared to wild-type levelsPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Phenotype_assayTreatmentWestern blots and Immunohistochemistry with DAF-18 antibodyPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0000125Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Remarkvab-1 mutants display increased activated MAPK expression compared to controlPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Phenotype_assayTreatmentStaining with activated MAPK antibodyPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0000128Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
RemarkIncreased dauer sensitivity was also observed in vab-1(dx31) animals at 27C, where vab-1(dx31) animals formed significantly more dauers than N2 wild-typePaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0000181Paper_evidenceWBPaper00031671
Curator_confirmedWBPerson2021
Remarkvab-1 mutants exhibit minor defects in the development of the dorsal processes of the NSM neurons: 7% short dorsal process, 1% missing dorsal process and no sub-ventral defectsPaper_evidenceWBPaper00031671
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00031671
Curator_confirmedWBPerson2021
EQ_annotationsAnatomy_termWBbt:0003666PATO:0000460Paper_evidenceWBPaper00031671
Curator_confirmedWBPerson2021
Phenotype_assayGenotypezdIs13 [ tph-1p::GFP]Paper_evidenceWBPaper00031671
Curator_confirmedWBPerson2021
WBPhenotype:0000195Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
RemarkAnimals showed weak defects in DTC migration along the ventral body wall muscle between the hyp7 hypodermal syncytium (phase 1) and slightly more defects during the migration along the dorsal body wall muscle (phase 3), but not while crossing hyp7 (phase 2), as visualized by lag-2::GFP expression.Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
PenetranceIncompletePaper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Variation_effectNullPaper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0006865PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Life_stageWBls:0000035PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBls:0000038PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBls:0000041PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
GO_termGO:0016477PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Phenotype_assayTreatmentAnimals were reared on NA22 bacteria instead of OP50.Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Temperature20Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBPhenotype:0000357Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Remarkvab-1(dx31) animals laid significantly more unfertilized oocytes than wild-type animalsPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0000384Paper_evidenceWBPaper00049274
Curator_confirmedWBPerson850
RemarkSDQL axon guidance is defectivePaper_evidenceWBPaper00049274
Curator_confirmedWBPerson850
WBPhenotype:0000436Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
RemarkThe frequency of DAF-18 nuclear expression in oocytes is increased in vab-1 mutants compared to control animalsPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Phenotype_assayTreatmentImmunohistochemistry with DAF-18 antibodyPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0000438Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"Although the absence of these protrusions is the likely cause of ventral pocket defects in vab-1 null embryos, 97% of these also have gaps between nonsister plexin band cells beyond 340' post-first cleavage (PFC) of the zygote (Figure 1C, 340'; Figure 2C; Figure S2) when these gaps are usually closed in wild-type embryos (Figure 1B, 340'; Figure 2B). These gaps could, in principle, also be causal for embryonic lethality, however, in most null and kinase dead embryos, these gaps are closed with a delay (i.e, after 340' PFC), possibly by small filopodia-like protrusions sometimes seen emanating from bridge and scaffold cells (Figure S2, 360' closed arrowhead) or by constriction of the entire midline region. This suggests that these gaps delay rather than block pocket closure."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsLife_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBPhenotype:0000594Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"As a consequence of the protrusion defects or gaps between nonsister cells, the presumptive pocket bridge cells are impeded in their migration over the scaffold cells to reach the midline. The entire group of unrearranged cells caused by this defect is referred to hereafter as the "obstructed bridge" even though in many embryos it appears to assemble with a delay just in advance of P9/10 cell migration (see below). An obstructed pocket bridge variably hindered progression of P9/10 cells toward the midline (Figures 2C and 2E). In some vab-1 mutant embryos, P9/10 cells progressed minimally toward the ventral midline. In these cases, blocks in P9/10 migration often occurred at borders between scaffold cells (Figure 2E). In other embryos there was substantial progression of P9/10 cells toward the midline, but this was slower than in wild-type embryos and involved movement of the entire leading edge of the presumptive bridge cells toward the midline just in advance of the P9/10 leading edge (see Discussion). Five of eight P9/10 cells in kinase dead embryos and only eight of 28 in null embryos reached the midline before embryo elongation began. There were also few, if any, kinase dead embryos in which a P9/10 cell failed to migrate at all or migrated minimally toward the midline (0 of 8 compared to 12 of 28 for null embryos). Among the types of mutant embryos observed, only those in which both P9/10 cells fail to migrate (5 of 14 null and 0 of 4 kinase dead) have a severe open pocket defect at the time embryo elongation begins, whereas others have a small open pocket defect (Figure 2E). These results suggest that the ability of P9/10 cells to migrate over an obstructed pocket bridge is efficient enough in vab-1 null embryos to account for their 60% embryonic viability but even more efficient in vab-1 kinase dead embryos accounting for their 94% viability."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0004412PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBbt:0004411PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Life_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBPhenotype:0000666Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Remarkvab-1(dx31) animals have a significantly higher ovulation rate than wild-typePaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0001140Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
RemarkHead neurons were positioned, sometimes, too anteriorly to the bulb, as visualized by a pan-neuronal transgenic reporter and DiI uptake.Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Variation_effectNullPaper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0006751PATO:0001921Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBbt:0005394PATO:0001921Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Phenotype_assayTreatmentAnimals were reared on NA22 bacteria instead of OP50. Amphid sensory neurons were labeled with DiI.Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Temperature20Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBPhenotype:0001172Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
RemarkRelative to wild type, vab-1(dx31) mutants showed a reduction in cell deaths according to both methods. | Apoptosis in cohorts of vab-1(dx31) and N2 wild-type adults over a period of 3 days, demonstrated only a 7% increase in the proportion of cell deaths dependent upon vab-1, despite a 100% increase in total cell deaths.Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
WBPhenotype:0001224Paper_evidenceWBPaper00003665
Curator_confirmedWBPerson712
Remark41% of animals showed wild-type ASI amphid neuron outgrowth. Mutants also showed lateral axon outgrowth (59%).Paper_evidenceWBPaper00003665
Curator_confirmedWBPerson712
PenetranceIncomplete59%Paper_evidenceWBPaper00003665
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0005666PATO:0000460Paper_evidenceWBPaper00003665
Curator_confirmedWBPerson712
Phenotype_assayGenotypekyIs128[str-3::GFP]Paper_evidenceWBPaper00003665
Curator_confirmedWBPerson712
WBPhenotype:0001346Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"To further examine the roles of Eph receptor and semaphorin signaling in pocket closure, we followed dozens of carefully staged embryos of vab-1 null and kinase dead mutants and also analyzed null (n = 14) and kinase dead (n = 4) embryos by time-lapse photomicroscopy. The spatiotemporal pattern of plx-2 expression revealed that the pocket bridge and scaffold progenitors, their subsequent divisions, and adhesion between sister cells appeared unaffected in all vab-1 null and kinase dead embryos examined (Figures 1C and 2C; Figure S2). Reported gastrulation defects in vab-1(0) embryos [8] did not produce obvious disorganization of plexin band cells in any embryos we examined, possibly because embryos can correct or bypass these defects. However, we did find that none of the vab-1(0) or vab-1(k) mutant embryos was able to form or maintain the narrow bridge cell protrusions that normally extend over the anterior surface of the scaffold cells to pull the presumptive bridge cells to the midline. These protrusions were also never observed in the staged mutant embryos."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsLife_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBPhenotype:0001409Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
RemarkDAF-18 expression is visible in neuronal tissues of vab-1 mutants, whereas wild-type neurons lack DAF-18 expressionPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Phenotype_assayTreatmentImmunohistochemistry with DAF-18 antibodyPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0001566Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
RemarkAnimals exhibited similar defects to vpr-1(tm1411), as assayed by 4D time-lapse DIC micrographs.Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Variation_effectNullPaper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
EQ_annotationsLife_stageWBls:0000013PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
GO_termGO:0009790PATO:0000460Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Phenotype_assayTreatmentAnimals were reared on NA22 bacteria instead of OP50.Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
Temperature20Paper_evidenceWBPaper00031951
Curator_confirmedWBPerson712
WBPhenotype:0001761Paper_evidenceWBPaper00006471
Curator_confirmedWBPerson2021
RemarkMidline crossover defects of PVQL and PVQR axons, with either contralateral analog inappropriately crossing the midlinePaper_evidenceWBPaper00006471
Curator_confirmedWBPerson2021
EQ_annotationsAnatomy_termWBbt:0006976PATO:0000460Paper_evidenceWBPaper00006471
Curator_confirmedWBPerson2021
Phenotype_assayGenotypeoyIs14Paper_evidenceWBPaper00006471
Curator_confirmedWBPerson2021
WBPhenotype:0001908Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"Mutants of vab-1 and mab-20 are known to affect ventral pocket closure [6,8]. Many vab-1 null mutant [vab-1(0)] embryos fail to close the open ventral pocket before embryo elongation begins [8,13] . The residual hole in the mutant epidermis provides a conduit for the extrusion of internal blast cells from the embryo, thereby causing lethality (Figure S2A)."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsLife_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBPhenotype:0002045Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
RemarkMutants show decreased germ-cell corpse numbers.Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
WBPhenotype:0002403Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"Although approximately 40% of vab-1(0) mutant embryos die by expelling inner embryonic cells through an open pocket (Figure 5C; Figure S2; Table S2; see also [8]) or in principle through a weakened midline that breaks open (see below), the remaining embryos successfully complete ventral pocket closure and survive . Among these, only mild misalignments of contralateral P cells occur at the ventral midline (Figures S3A-S3D; Table S2)."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
PenetranceLow12Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0008115PATO:0001654Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Life_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBPhenotype:0002404Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"Although the absence of these protrusions is the likely cause of ventral pocket defects in vab-1 null embryos, 97% of these also have gaps between nonsister plexin band cells beyond 340' post-first cleavage (PFC) of the zygote (Figure 1C, 340'; Figure 2C; Figure S2) when these gaps are usually closed in wild-type embryos (Figure 1B, 340'; Figure 2B). These gaps could, in principle, also be causal for embryonic lethality, however, in most null and kinase dead embryos, these gaps are closed with a delay (i.e, after 340' PFC), possibly by small filopodia-like protrusions sometimes seen emanating from bridge and scaffold cells (Figure S2, 360' closed arrowhead) or by constriction of the entire midline region. This suggests that these gaps delay rather than block pocket closure."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsLife_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Phenotype_not_observedWBPhenotype:0000114Paper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Remarkdaf-18/pten transcript levels are not affected in a vab-1(dx31) mutant backgroundPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
Phenotype_assayTreatmentRT PCRPaper_evidenceWBPaper00035407
Curator_confirmedWBPerson2021
WBPhenotype:0000186Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
Remarkvab-1(dx31) mutants showed a slight increase in mature oocytes, although this was not significant.Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
WBPhenotype:0000424Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
RemarkTwo regions of MPK-1 (dpMPK-1) immunoreactivity were observed strong fluorescence in mature oocytes, and less intense but reproducible fluorescence preceding the gonad bend. In the apoptotic region a modest decrease in the mean fluorescence and the length of the signaling zone in vab-1 mutants was observed when compared with the N2 wild type, but these differences were not statistically significant.Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
WBPhenotype:0000684Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
RemarkLoss of vab-1 activity had no statistically significant impact on germ-cell numbers at any stage of development.Paper_evidenceWBPaper00040629
Curator_confirmedWBPerson712
WBPhenotype:0001660Paper_evidenceWBPaper00006052
Curator_confirmedWBPerson2021
RemarkNo disruption of ASE asymmetry (as seen with lim-6 reporters)Paper_evidenceWBPaper00006052
Curator_confirmedWBPerson2021
Variation_effectNullPaper_evidenceWBPaper00006052
Curator_confirmedWBPerson2021
Phenotype_assayGenotypeotIs114, otIs6Paper_evidenceWBPaper00006052
Curator_confirmedWBPerson2021
Disease_infoModifies_diseaseDOID:162
Modifies_disease_in_annotationWBDOannot00000548
ReferenceWBPaper00040629
WBPaper00040551
WBPaper00031671
WBPaper00006052
WBPaper00027739
WBPaper00025614
WBPaper00035407
WBPaper00018031
WBPaper00003665
WBPaper00011413
WBPaper00006471
WBPaper00031951
WBPaper00049274
WBPaper00065184
MethodAllele