FB2024_03 , released June 25, 2024
Allele: Dmel\Lkb1X5
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General Information
Symbol
Dmel\Lkb1X5
Species
D. melanogaster
Name
FlyBase ID
FBal0213122
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Imprecise excision of lkb1EP-1 results in a specific deletion of the lkb1 locus (76208-77847th nucleotides of AE003701).

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

Imprecise excision deletion of nucleotides 76208-77847 (GB:AE003701).

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Lkb1X5 somatic clones in the follicular epithelium exhibit multilayering in about a third of cases, which is not observed in controls.

lkb1X5 mutant eye disc clones do not show an increase in apoptosis following fasting compared to wild type controls.

Mutant embryos derived from homozygous female germ-line clones contain cells with an excessive DNA content in the nucleus and have epithelial polarity defects.

Mutant larvae have mitotic and epithelial polarity defects.

lkb1X5 mutants die before the mid-pupal stage.

During nerve cord condensation (embryonic stage 16), significantly fewer apoptotic cells are observed, both in the ventral nerve cord and embryonic head of lkb1X5 mutants.

Homozygous lkb1X5 mutant larvae exhibit dramatically enlarged brain hemispheres and ventral ganglion, compared to wild-type.

A small portion (~10%) of lkb1X5 homozygotes exhibit various dorsal-open phenotypes in hatched or unhatched first-instar larvae.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference

lkb1[+]/Lkb1X5 is a non-suppressor of increased cell death phenotype of Scer\GAL4GMR.PF, egrUAS.cLa

Phenotype Manifest In
NOT Enhanced by
Statement
Reference

Lkb1X5 has follicle cell | somatic clone phenotype, non-enhanceable by Vps155

Suppressed by
Enhancer of
Statement
Reference

Lkb1X5 is an enhancer of eye disc | somatic clone | nutrition conditional phenotype of Axn127

Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference

Vps155, Lkb1X5 double mutant somatic clones in the follicular epithelium exhibit multilayering at a frequency similar to that of Lkb1X5 single clones rather than the high frequency observed in Vps155 single clones. The mis-localization of cell polarity markers presented by Vps155 homozygous follicle cell clones is also suppressed by Lkb1X5 homozygosity in the clones.

The moderate overgrowth of eye-antennal discs bearing clones expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C.PI is suppressed by Lkb1X5 homozygosity in the clones.

The severe eye-antennal disc tumor phenotype and delayed pupation resulting from larval eye-antennal disc clones both homozygous for Vps155 and expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C.PI are both suppressed by additional Lkb1X5 homozygosity in the clones.

Scer\GAL4e22c Sln6.Scer\UAS.T:Hsap\MYC-mediated apoptosis upon butyrate treatment is considerably suppressed in a lkb1X5 mutant background.

The epithelial polarity defects and genomic instability seen in lkb1X5 larvae are suppressed by expression of SNF1ATD.Scer\UAS under the control of Scer\GAL4hs.PB.

The epithelial polarity defects and genomic polyploidy defects seen in lkb1X5 larvae are suppressed by sqhE20.E21.

Ectopic activation of JNK signaling by overexpression of hepAct.Scer\UAS (under the control of Scer\GAL4hs.PB) completely rescues the 'big brain' phenotype of lkb1X5 mutants and restores embryonic apoptosis.

Trans-heterozygotic combinations between lkb1X5 and bsk1 or bsk2 induces significant dorsal open phenotypes in unhatched first instar larvae.

Dosage reduction of lkb1X5 does not affect Scer\GAL4GMR.PF; egrScer\UAS.cla induced apoptosis.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Transgenic expression of lkb1Scer\UAS.cLa using a Scer\GAL4hs.PB driver successfully rescues the lethality of lkb1X5 mutants.

Ectopic expression of lkb1Scer\UAS.cLa under the control of Scer\GAL4hs.PB successfully suppresses the 'big brain' phenotype observed in lkb1X5 mutants.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (10)