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WormBase Tree Display for Variation: WBVar00145128

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Name Class

WBVar00145128EvidencePaper_evidenceWBPaper00004900
NamePublic_nameeh15
Other_nameF40E10.4.1:c.791_1548del
CE32412:p.Cys264SerfsTer16
HGVSgCHROMOSOME_X:g.14675922_14677866del
Sequence_detailsSMapS_parentSequenceC26G2
Flanking_sequencesgcgaaactgcggaaatttgtccactaccatctcctcttatctggaaacaatatctctacc
Mapping_targetC26G2
Type_of_mutationDeletion
SeqStatusSequenced
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
StrainWBStrain00005267
WBStrain00034914
LaboratoryHX
StatusLive
AffectsGeneWBGene00004854
TranscriptF40E10.4.1 (11)
Interactor (17)
GeneticsInterpolated_map_positionX19.7571
DescriptionPhenotypeWBPhenotype:0000181Paper_evidenceWBPaper00031671
Curator_confirmedWBPerson2021
RemarkThe slt-1 mutant caused the dorsal and sub-ventral NSM processes to be short in 16% and 22% of casesPaper_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:0000384Paper_evidenceWBPaper00036484
WBPaper00031828
WBPaper00040041
Curator_confirmedWBPerson712
RemarkAVM axons fail to grow ventrally.Paper_evidenceWBPaper00036484
Curator_confirmedWBPerson712
Loss of slt-1 function results in 40% failure of ALM ventral outgrowth.Paper_evidenceWBPaper00031828
Curator_confirmedWBPerson712
Animals exhibit AVM ventral axon guidance defects. These defects can be rescued by exogenous acetylcholine.Paper_evidenceWBPaper00040041
Curator_confirmedWBPerson712
PenetranceIncompletePaper_evidenceWBPaper00036484
Curator_confirmedWBPerson712
Affected_byMoleculeWBMol:00004765Paper_evidenceWBPaper00040041
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0003832PATO:0000460Paper_evidenceWBPaper00036484
WBPaper00031828
WBPaper00040041
Curator_confirmedWBPerson712
WBPhenotype:0000470Paper_evidenceWBPaper00038152
Curator_confirmedWBPerson712
RemarkWeak defects in HSN ventral migration.Paper_evidenceWBPaper00038152
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0006830PATO:0000460Paper_evidenceWBPaper00038152
Curator_confirmedWBPerson712
WBPhenotype:0001140Paper_evidenceWBPaper00050480
Curator_confirmedWBPerson712
Remarkslt-1 mutations had no effect on AQR and PQR migration on their ownPaper_evidenceWBPaper00050480
Curator_confirmedWBPerson712
EQ_annotationsAnatomy_termWBbt:0003927PATO:0000460Paper_evidenceWBPaper00050480
Curator_confirmedWBPerson712
WBbt:0004096PATO:0000460Paper_evidenceWBPaper00050480
Curator_confirmedWBPerson712
Phenotype_not_observedWBPhenotype:0001652Paper_evidenceWBPaper00032446
Curator_confirmedWBPerson2021
WBPhenotype:0001767Paper_evidenceWBPaper00032413
Curator_confirmedWBPerson2021
RemarkMutants lack significant defects in the sidedness of DA/DB motor axon projectionsPaper_evidenceWBPaper00032413
Curator_confirmedWBPerson2021
ReferenceWBPaper00038152
WBPaper00040041
WBPaper00031671
WBPaper00032446
WBPaper00032413
WBPaper00031828
WBPaper00036484
WBPaper00050480
RemarkThis deletion is coupled with a smaller deletion that deletes nucleotides 28197 to 28294 referring to the clone C26G2Paper_evidenceWBPaper00004900
MethodDeletion_allele