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WormBase Tree Display for Variation: WBVar00054467

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Name Class

WBVar00054467NamePublic_namect78
Sequence_detailsSeqStatusPending_curation
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
StrainWBStrain00003961
LaboratoryBW
StatusLive
AffectsGeneWBGene00000435
InteractorWBInteraction000536128
WBInteraction000536129
WBInteraction000536130
WBInteraction000536131
WBInteraction000536132
WBInteraction000536133
WBInteraction000536134
WBInteraction000536136
WBInteraction000536138
WBInteraction000536139
GeneticsMapping_dataIn_multi_point1499
1500
1501
1502
In_pos_neg_data4233
4234
DescriptionPhenotypeWBPhenotype:0000232Person_evidenceWBPerson261
Curator_confirmedWBPerson712
Remarkdefective CAN migrationsPerson_evidenceWBPerson261
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0006827PATO:0000460Person_evidenceWBPerson261
Curator_confirmedWBPerson712
WBPhenotype:0000594Person_evidenceWBPerson261
Curator_confirmedWBPerson712
Remarkmigrations of cells other than CAN defective at low penetrancePerson_evidenceWBPerson261
Curator_confirmedWBPerson712
PenetranceLowPerson_evidenceWBPerson261
Curator_confirmedWBPerson712
WBPhenotype:0000816Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Remark"To investigate the role of CEH-10 in ALA neuron development, we first examined whether the ALA neuron was present in ceh-10(rf) and ceh-10 null mutant animals. In wild type, the ALA neuron is identifiable by its position in the dorsal head ganglion alongside the RID neuron, which is not the sister cell of ALA but also expresses CEH-10. By DIC optics the ALA and RID nuclei can be seen in a region flanked by hypodermal nuclei, along the dorsal midline (Fig 5A)... In ceh-10(ct78) reduction-of-function mutant animals, these neurons can be found in their wild-type positions in 75% of cases, and in the remaining animals a single cell can be found where the ALA and RID normally reside (Fig 5A,B). Our examination of ALA-specific reporters below reveals that approximately 90% of ceh-10(rf) animals possess an ALA neuron, and we infer that in the majority of cases in which only one of these neurons is detectable, it is the RID that is missing."Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0003955PATO:0000460Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
WBbt:0003938PATO:0000460Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
WBPhenotype:0001224Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Remark"We then scored the extent of ALA axon migration and found that the ceh-10(rf) animals showed a ceh-17-like truncation of the ALA axons, albeit less severe (Fig 6B,C). While the ceh-17(lf) axon migration phenotype is similar when scored in either L1 or L2 stage animals, we found that a greater fraction of ceh-10(rf) ALA axons reach the tail by the L2 stage than at L1. This was surprising, as wild-type ALA axons complete their migration before hatching (Pujol et_al, 2000)."Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0003955PATO:0000460Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Phenotype_assayGenotypeunc-53:GFPPaper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
WBPhenotype:0001278Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Remark"To examine the state of ALA differentiation in animals with reduced CEH-10 function, we examined the expression of panneuronal and ALA-specific reporter genes in ceh-10(ct78) mutant animals. We observed wild-type expression of the pan-neuronal reporters unc-119:YFP and rab-3:GFP in both the ALA and RID neurons (not shown). However, expression of the ALA-specific reporters flp-7:GFP and plc-3:YFP are impaired, and more at the L1 stage than at L4 (Fig 5C,D). Thus the ceh-10(rf) mutation impairs ALA-specific gene expression, but this defect is ameliorated as development proceeds."Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0003955PATO:0000460Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Phenotype_assayGenotypeflp-7:GFPPaper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
plc-3:YFPPaper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
WBPhenotype:0001524Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Remark"Another transcription factor expressed in ALA is the Q50 Prd-like protein CEH-10/Chx10, which has roles in the specification of the AIY, RMED, RID and CAN neurons (Forrester et_al, 1998). CAN function is required for viability, and animals lacking CEH-10 activity die as first-stage larvae (Forrester et_al, 1998). To examine CEH-10 in ALA function throughout development, we used a viable reduction-of-function mutation, ceh-10(ct78). We found the ceh-10(rf) mutation conferred partial EGF-resistance (Table 3), consistent with a role for CEH-10 in ALA function."Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0003955PATO:0000460Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Phenotype_assayGenotypehs:LIN-3Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Phenotype_not_observedWBPhenotype:0000306Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Remark"To examine the state of ALA differentiation in animals with reduced CEH-10 function, we examined the expression of panneuronal and ALA-specific reporter genes in ceh-10(ct78) mutant animals. We observed wild-type expression of the pan-neuronal reporters unc-119:YFP and rab-3:GFP in both the ALA and RID neurons (not shown)."Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
"We also examined whether ceh-10(ct78) impairs the expression of ceh-17:GFP or ceh-14:GFP reporter genes in ALA, and found no difference from wild type, either at the L1 stage (Fig 5E) or later in development (not shown)."Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
"To determine whether CEH-10 and CEH-14 also play roles in ALA axon migration, we examined unc-53:GFP (pNP21; N. Pujol), which labels several neurons including ALA and the DA neurons of the ventral cord that extend commissural axons, marking body length (Stringham et al., 2002). In wild-type animals this reporter labels the ALA axons during the L1-L2 stages. We first examined unc-53:GFP in ALA in ceh-17(null) and ceh-10(rf) L1-L2 animals and found that expression of the reporter was not detectably impaired (Fig 6A)."Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
EQ_annotationsAnatomy_termWBbt:0003955PATO:0000460Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
WBbt:0003938PATO:0000460Paper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
Phenotype_assayGenotypeunc-119:YFPPaper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
rab-3:GFPPaper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
ceh-17::GFPPaper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
ceh-14::GFPPaper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
unc-53:GFPPaper_evidenceWBPaper00036308
Curator_confirmedWBPerson2987
WBPhenotype:0001652Paper_evidenceWBPaper00032446
Curator_confirmedWBPerson2021
ReferenceWBPaper00032446
WBPaper00013909
WBPaper00036308
WBPaper00016589
MethodAllele