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WormBase Tree Display for Variation: WBVar00145253

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Name Class

WBVar00145253NamePublic_nameev574
Sequence_detailsSeqStatusPending_curation
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
LaboratoryNW
StatusLive
AffectsGeneWBGene00003111
InteractorWBInteraction000535986
WBInteraction000535987
WBInteraction000535990
WBInteraction000535994
WBInteraction000535995
WBInteraction000556037
DescriptionPhenotypeWBPhenotype:0000050Paper_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)... 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)."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
PenetranceIncomplete19Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsLife_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBPhenotype:0000384Paper_evidenceWBPaper00049274
Curator_confirmedWBPerson850
RemarkSDQL axon guidance is defectivePaper_evidenceWBPaper00049274
Curator_confirmedWBPerson850
WBPhenotype:0000594Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"Two of five mab-20(0) embryos exhibited a detectable skewing of the P cell leading edges from the D/V body wall axis as they migrate toward the midline (Figure 1D, 370' inset), not observed in the wild-type (n = 20). In contrast to vab-1 mutants, none of the mab-20 embryos showed a significant delay in either the onset or the rate of P cell migration (n = 5). For this reason we suggest that P cell misalignment in mab-20 and plx-2 mutants is caused by a defect in P cell polarity or guidance, or abnormal adhesions of P cell leading tips, but not by a defect in P cell progression toward the midline."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0008115PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Life_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBPhenotype:0001227Paper_evidenceWBPaper00027335
Curator_confirmedWBPerson48
RemarkRay commissure: R1.Paper_evidenceWBPaper00027335
Curator_confirmedWBPerson48
PenetranceIncompletePaper_evidenceWBPaper00027335
Curator_confirmedWBPerson48
Range66Paper_evidenceWBPaper00027335
Curator_confirmedWBPerson48
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:0002403Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"The penetrance of mab-20 and plx-2 null mutant P cell midline alignment defects are 86% and 8%, respectively (Figure 5A; Table S2). mab-20(0) and plx-2(0) embryos do not have obvious open pocket defects, yet mab-20(0) embryos extrude internal cells from the ventral side [6] suggesting that severe P cell alignment defects weaken the midline, causing it to rupture when circumferential constrictive forces of embryo elongation occur." see also Figure S3CPaper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
PenetranceHigh86Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0008115PATO:0001654Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Life_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
WBPhenotype:0002404Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Remark"All plexin band cells (i.e, bridge plus scaffold cells) are present in roughly normal positions in the vab-1 plx-2 double null mutant embryos. However, time-lapse analysis shows that double mutant embryos unexpectedly have narrow gaps between sister plexin band cells (hereafter referred to as sister cell gaps) that are not present in the vab-1 null or the wild-type (see Figure 2D, 340') in addition to the gaps between nonsister plexin band cells that are found in 97% of vab-1 null embryos. The gaps between sister plexin band cells in the vab-1 plx-2 double null are not as severe as in the mab-20; vab-1 double null because the former have some aggregates of sister cells that are absent in the latter (data not shown). These results suggest that PLX-2 and MAB-20 have redundant functions with VAB-1 in forming or maintaining adhesions between sister plexin band cells, just as they have redundant functions with VAB-1 in preventing embryonic lethality."Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
EQ_annotationsLife_stageWBls:0000003PATO:0000460Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Phenotype_assayGenotypevab-1(dx31)Paper_evidenceWBPaper00040551
Curator_confirmedWBPerson2987
Phenotype_not_observedWBPhenotype:0001652Paper_evidenceWBPaper00032446
Curator_confirmedWBPerson2021
ReferenceWBPaper00040551
WBPaper00032446
WBPaper00027335
WBPaper00018347
WBPaper00018341
WBPaper00049274
MethodAllele