WormBase Tree Display for Variation: WBVar00142887
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WBVar00142887 | Name | Public_name | dx31 | ||||||
---|---|---|---|---|---|---|---|---|---|
Sequence_details | SeqStatus | Pending_curation | |||||||
Variation_type | Allele | ||||||||
Origin | Species | Caenorhabditis elegans | |||||||
Strain | WBStrain00005346 | ||||||||
WBStrain00005659 | |||||||||
WBStrain00005660 | |||||||||
WBStrain00008609 | |||||||||
WBStrain00029412 | |||||||||
WBStrain00029413 | |||||||||
WBStrain00029414 | |||||||||
WBStrain00029420 | |||||||||
WBStrain00029421 | |||||||||
WBStrain00029424 | |||||||||
WBStrain00029425 | |||||||||
WBStrain00040665 | |||||||||
Laboratory | EJ | ||||||||
Status | Live | ||||||||
Affects | Gene | WBGene00006868 | |||||||
Interactor | WBInteraction000502399 | ||||||||
WBInteraction000504065 | |||||||||
WBInteraction000517208 | |||||||||
WBInteraction000517209 | |||||||||
WBInteraction000518898 | |||||||||
WBInteraction000518901 | |||||||||
WBInteraction000519471 | |||||||||
WBInteraction000535985 | |||||||||
WBInteraction000535986 | |||||||||
WBInteraction000535988 | |||||||||
WBInteraction000535993 | |||||||||
WBInteraction000535994 | |||||||||
Description | Phenotype | WBPhenotype:0000050 | Paper_evidence | WBPaper00031951 | |||||
WBPaper00040551 | |||||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPerson2987 | |||||||||
Remark | N=805 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
"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_evidence | WBPaper00040551 | |||||||
Curator_confirmed | WBPerson2987 | ||||||||
Penetrance | Incomplete | 40 | Paper_evidence | WBPaper00040551 | |||||
Curator_confirmed | WBPerson2987 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
EQ_annotations | Life_stage | WBls:0000013 | PATO:0000460 | Paper_evidence | WBPaper00031951 | ||||
Curator_confirmed | WBPerson712 | ||||||||
WBls:0000003 | PATO:0000460 | Paper_evidence | WBPaper00031951 | ||||||
WBPaper00040551 | |||||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPerson2987 | |||||||||
Phenotype_assay | Treatment | Animals were reared on NA22 bacteria instead of OP50. | Paper_evidence | WBPaper00031951 | |||||
Curator_confirmed | WBPerson712 | ||||||||
Temperature | 20 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0000054 | Paper_evidence | WBPaper00031951 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | N=805 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
EQ_annotations | Life_stage | WBls:0000023 | PATO:0000460 | Paper_evidence | WBPaper00031951 | ||||
Curator_confirmed | WBPerson712 | ||||||||
Phenotype_assay | Treatment | Animals were reared on NA22 bacteria instead of OP50. | Paper_evidence | WBPaper00031951 | |||||
Curator_confirmed | WBPerson712 | ||||||||
Temperature | 20 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0000061 | Paper_evidence | WBPaper00035407 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | Animals have significantly longer life spans than control | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Genotype | fem-1(hc17) | Paper_evidence | WBPaper00035407 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000106 | Paper_evidence | WBPaper00027739 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | vab-1(null) hermaphrodites exhibit an expanded pattern of MAPK activation in which MAPKYT staining extends to distal oocytes | Paper_evidence | WBPaper00027739 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00027739 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
EQ_annotations | Anatomy_term | WBbt:0006797 | PATO:0000460 | Paper_evidence | WBPaper00027739 | ||||
Curator_confirmed | WBPerson2021 | ||||||||
Life_stage | WBls:0000057 | PATO:0000460 | Paper_evidence | WBPaper00027739 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Treatment | Antibody staining to the diphosphorylated activated form of MAPK (MAPK-YT) | Paper_evidence | WBPaper00027739 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000119 | Paper_evidence | WBPaper00035407 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | Increased 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 levels | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Treatment | Western blots and Immunohistochemistry with DAF-18 antibody | Paper_evidence | WBPaper00035407 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000125 | Paper_evidence | WBPaper00035407 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | vab-1 mutants display increased activated MAPK expression compared to control | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Treatment | Staining with activated MAPK antibody | Paper_evidence | WBPaper00035407 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000128 | Paper_evidence | WBPaper00035407 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | Increased dauer sensitivity was also observed in vab-1(dx31) animals at 27C, where vab-1(dx31) animals formed significantly more dauers than N2 wild-type | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000181 | Paper_evidence | WBPaper00031671 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | vab-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 defects | Paper_evidence | WBPaper00031671 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00031671 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
EQ_annotations | Anatomy_term | WBbt:0003666 | PATO:0000460 | Paper_evidence | WBPaper00031671 | ||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Genotype | zdIs13 [ tph-1p::GFP] | Paper_evidence | WBPaper00031671 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000195 | Paper_evidence | WBPaper00031951 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | Animals 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_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
Penetrance | Incomplete | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
EQ_annotations | Anatomy_term | WBbt:0006865 | PATO:0000460 | Paper_evidence | WBPaper00031951 | ||||
Curator_confirmed | WBPerson712 | ||||||||
Life_stage | WBls:0000035 | PATO:0000460 | Paper_evidence | WBPaper00031951 | |||||
Curator_confirmed | WBPerson712 | ||||||||
WBls:0000038 | PATO:0000460 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBls:0000041 | PATO:0000460 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
GO_term | GO:0016477 | PATO:0000460 | Paper_evidence | WBPaper00031951 | |||||
Curator_confirmed | WBPerson712 | ||||||||
Phenotype_assay | Treatment | Animals were reared on NA22 bacteria instead of OP50. | Paper_evidence | WBPaper00031951 | |||||
Curator_confirmed | WBPerson712 | ||||||||
Temperature | 20 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0000357 | Paper_evidence | WBPaper00035407 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | vab-1(dx31) animals laid significantly more unfertilized oocytes than wild-type animals | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000384 | Paper_evidence | WBPaper00049274 | |||||||
Curator_confirmed | WBPerson850 | ||||||||
Remark | SDQL axon guidance is defective | Paper_evidence | WBPaper00049274 | ||||||
Curator_confirmed | WBPerson850 | ||||||||
WBPhenotype:0000436 | Paper_evidence | WBPaper00035407 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | The frequency of DAF-18 nuclear expression in oocytes is increased in vab-1 mutants compared to control animals | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Treatment | Immunohistochemistry with DAF-18 antibody | Paper_evidence | WBPaper00035407 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000438 | Paper_evidence | WBPaper00040551 | |||||||
Curator_confirmed | WBPerson2987 | ||||||||
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_evidence | WBPaper00040551 | ||||||
Curator_confirmed | WBPerson2987 | ||||||||
EQ_annotations | Life_stage | WBls:0000003 | PATO:0000460 | Paper_evidence | WBPaper00040551 | ||||
Curator_confirmed | WBPerson2987 | ||||||||
WBPhenotype:0000594 | Paper_evidence | WBPaper00040551 | |||||||
Curator_confirmed | WBPerson2987 | ||||||||
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_evidence | WBPaper00040551 | ||||||
Curator_confirmed | WBPerson2987 | ||||||||
EQ_annotations | Anatomy_term | WBbt:0004412 | PATO:0000460 | Paper_evidence | WBPaper00040551 | ||||
Curator_confirmed | WBPerson2987 | ||||||||
WBbt:0004411 | PATO:0000460 | Paper_evidence | WBPaper00040551 | ||||||
Curator_confirmed | WBPerson2987 | ||||||||
Life_stage | WBls:0000003 | PATO:0000460 | Paper_evidence | WBPaper00040551 | |||||
Curator_confirmed | WBPerson2987 | ||||||||
WBPhenotype:0000666 | Paper_evidence | WBPaper00035407 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | vab-1(dx31) animals have a significantly higher ovulation rate than wild-type | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0001140 | Paper_evidence | WBPaper00031951 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | Head neurons were positioned, sometimes, too anteriorly to the bulb, as visualized by a pan-neuronal transgenic reporter and DiI uptake. | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
EQ_annotations | Anatomy_term | WBbt:0006751 | PATO:0001921 | Paper_evidence | WBPaper00031951 | ||||
Curator_confirmed | WBPerson712 | ||||||||
WBbt:0005394 | PATO:0001921 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
Phenotype_assay | Treatment | Animals were reared on NA22 bacteria instead of OP50. Amphid sensory neurons were labeled with DiI. | Paper_evidence | WBPaper00031951 | |||||
Curator_confirmed | WBPerson712 | ||||||||
Temperature | 20 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0001172 | Paper_evidence | WBPaper00040629 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | Relative 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_evidence | WBPaper00040629 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0001224 | Paper_evidence | WBPaper00003665 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | 41% of animals showed wild-type ASI amphid neuron outgrowth. Mutants also showed lateral axon outgrowth (59%). | Paper_evidence | WBPaper00003665 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
Penetrance | Incomplete | 59% | Paper_evidence | WBPaper00003665 | |||||
Curator_confirmed | WBPerson712 | ||||||||
EQ_annotations | Anatomy_term | WBbt:0005666 | PATO:0000460 | Paper_evidence | WBPaper00003665 | ||||
Curator_confirmed | WBPerson712 | ||||||||
Phenotype_assay | Genotype | kyIs128[str-3::GFP] | Paper_evidence | WBPaper00003665 | |||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0001346 | Paper_evidence | WBPaper00040551 | |||||||
Curator_confirmed | WBPerson2987 | ||||||||
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_evidence | WBPaper00040551 | ||||||
Curator_confirmed | WBPerson2987 | ||||||||
EQ_annotations | Life_stage | WBls:0000003 | PATO:0000460 | Paper_evidence | WBPaper00040551 | ||||
Curator_confirmed | WBPerson2987 | ||||||||
WBPhenotype:0001409 | Paper_evidence | WBPaper00035407 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | DAF-18 expression is visible in neuronal tissues of vab-1 mutants, whereas wild-type neurons lack DAF-18 expression | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Treatment | Immunohistochemistry with DAF-18 antibody | Paper_evidence | WBPaper00035407 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0001566 | Paper_evidence | WBPaper00031951 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | Animals exhibited similar defects to vpr-1(tm1411), as assayed by 4D time-lapse DIC micrographs. | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
EQ_annotations | Life_stage | WBls:0000013 | PATO:0000460 | Paper_evidence | WBPaper00031951 | ||||
Curator_confirmed | WBPerson712 | ||||||||
GO_term | GO:0009790 | PATO:0000460 | Paper_evidence | WBPaper00031951 | |||||
Curator_confirmed | WBPerson712 | ||||||||
Phenotype_assay | Treatment | Animals were reared on NA22 bacteria instead of OP50. | Paper_evidence | WBPaper00031951 | |||||
Curator_confirmed | WBPerson712 | ||||||||
Temperature | 20 | Paper_evidence | WBPaper00031951 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0001761 | Paper_evidence | WBPaper00006471 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | Midline crossover defects of PVQL and PVQR axons, with either contralateral analog inappropriately crossing the midline | Paper_evidence | WBPaper00006471 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
EQ_annotations | Anatomy_term | WBbt:0006976 | PATO:0000460 | Paper_evidence | WBPaper00006471 | ||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Genotype | oyIs14 | Paper_evidence | WBPaper00006471 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0001908 | Paper_evidence | WBPaper00040551 | |||||||
Curator_confirmed | WBPerson2987 | ||||||||
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_evidence | WBPaper00040551 | ||||||
Curator_confirmed | WBPerson2987 | ||||||||
EQ_annotations | Life_stage | WBls:0000003 | PATO:0000460 | Paper_evidence | WBPaper00040551 | ||||
Curator_confirmed | WBPerson2987 | ||||||||
WBPhenotype:0002045 | Paper_evidence | WBPaper00040629 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | Mutants show decreased germ-cell corpse numbers. | Paper_evidence | WBPaper00040629 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0002403 | Paper_evidence | WBPaper00040551 | |||||||
Curator_confirmed | WBPerson2987 | ||||||||
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_evidence | WBPaper00040551 | ||||||
Curator_confirmed | WBPerson2987 | ||||||||
Penetrance | Low | 12 | Paper_evidence | WBPaper00040551 | |||||
Curator_confirmed | WBPerson2987 | ||||||||
EQ_annotations | Anatomy_term | WBbt:0008115 | PATO:0001654 | Paper_evidence | WBPaper00040551 | ||||
Curator_confirmed | WBPerson2987 | ||||||||
Life_stage | WBls:0000003 | PATO:0000460 | Paper_evidence | WBPaper00040551 | |||||
Curator_confirmed | WBPerson2987 | ||||||||
WBPhenotype:0002404 | Paper_evidence | WBPaper00040551 | |||||||
Curator_confirmed | WBPerson2987 | ||||||||
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_evidence | WBPaper00040551 | ||||||
Curator_confirmed | WBPerson2987 | ||||||||
EQ_annotations | Life_stage | WBls:0000003 | PATO:0000460 | Paper_evidence | WBPaper00040551 | ||||
Curator_confirmed | WBPerson2987 | ||||||||
Phenotype_not_observed | WBPhenotype:0000114 | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | daf-18/pten transcript levels are not affected in a vab-1(dx31) mutant background | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00035407 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Treatment | RT PCR | Paper_evidence | WBPaper00035407 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
WBPhenotype:0000186 | Paper_evidence | WBPaper00040629 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | vab-1(dx31) mutants showed a slight increase in mature oocytes, although this was not significant. | Paper_evidence | WBPaper00040629 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0000424 | Paper_evidence | WBPaper00040629 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | Two 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_evidence | WBPaper00040629 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0000684 | Paper_evidence | WBPaper00040629 | |||||||
Curator_confirmed | WBPerson712 | ||||||||
Remark | Loss of vab-1 activity had no statistically significant impact on germ-cell numbers at any stage of development. | Paper_evidence | WBPaper00040629 | ||||||
Curator_confirmed | WBPerson712 | ||||||||
WBPhenotype:0001660 | Paper_evidence | WBPaper00006052 | |||||||
Curator_confirmed | WBPerson2021 | ||||||||
Remark | No disruption of ASE asymmetry (as seen with lim-6 reporters) | Paper_evidence | WBPaper00006052 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Variation_effect | Null | Paper_evidence | WBPaper00006052 | ||||||
Curator_confirmed | WBPerson2021 | ||||||||
Phenotype_assay | Genotype | otIs114, otIs6 | Paper_evidence | WBPaper00006052 | |||||
Curator_confirmed | WBPerson2021 | ||||||||
Disease_info | Modifies_disease | DOID:162 | |||||||
Modifies_disease_in_annotation | WBDOannot00000548 | ||||||||
Reference | WBPaper00040629 | ||||||||
WBPaper00040551 | |||||||||
WBPaper00031671 | |||||||||
WBPaper00006052 | |||||||||
WBPaper00027739 | |||||||||
WBPaper00025614 | |||||||||
WBPaper00035407 | |||||||||
WBPaper00018031 | |||||||||
WBPaper00003665 | |||||||||
WBPaper00011413 | |||||||||
WBPaper00006471 | |||||||||
WBPaper00031951 | |||||||||
WBPaper00049274 | |||||||||
WBPaper00065184 | |||||||||
Method | Allele |