FB2024_03 , released June 25, 2024
Allele: Dmel\kuze29-4
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General Information
Symbol
Dmel\kuze29-4
Species
D. melanogaster
Name
FlyBase ID
FBal0051471
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
kuzE29
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

2.4kb deletion near the 5' end of the gene, including DNA in the promoter region and the first and second exons.

Deletion of 2.4kb near the 5' end of kuz, including DNA in the promoter region and the first and second introns.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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 ( 1 )
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

In kuze29-4 homozygotes, the larval central brain exhibits ectopically proliferating neuroblasts (i.e. increased numbers in S-phase), compared to controls.

kuze29-4 embryos do not show blood-brain barrier or trachea barrier as, like in controls, dye injected into the body cavity does not diffuses into the ventral nerve cord of into the tracheal tubes; the trachea also presents a normal distribution of the septate junction protein, NrxIV.

kuze29-4 homozygous embryos do not show any obvious somatic musculature phenotype, as compared to controls.

kuze29-4/kuze29-4 mutant embryos show no change in overall neuroblast numbers, but show extra Ap neurons, and extra EL neurons, as compared with controls. These mutants also display increased proliferation of thoracic and abdominal neuroblast daughter cells at stage 14 and 15 (but not stage 12), but no significant difference in proliferation of thoracic or abdominal neuroblasts at stage 12, 14 or 15, as compared with controls.

kuze29-4/+ mutant embryos do not display a significant difference in the number of Ap neurons or EL neurons, as compared to controls.

Hemizygous embryos have an increased number of "Ap" neurons in the NB5-6T lineage.

Stage 16 kuze29-4 embryos exhibit thinning of the longitudinal connectives and thickening of the commissures compared to controls. FasII axons ectopically cross the midline.

kuze29-4 mutant embryos exhibit an approximately twofold excess of cardioblasts.

In kuze29-4 mutant embryos cardioblasts fail to adopt the final cell morphology. The characteristic bean-like shape of cardioblasts, that normally form the ostia at stage 16/17, is not recognizable. Also, the four tin-expressing cardioblasts, which usually have a flattened, cube-like morphology with a distinct polarisation, exhibit an abnormal morphology.

The neuromuscular innervation pattern appears normal in kuze29-4/kuzk01403 larvae.

Embryos that are maternally and zygotically homozygous kuze29-4 show hypertrophy of nervous system elements resulting in the lack of an organised CNS.

Mitotic clones reaching the wing margin result in notches on the wing blade. Clones in the notum result in clusters of supernumerary macrochaetes and microchaetes. Microchaetae clusters are abolished by expression of Nicd.hs at 7-9 hours APF.

A greater proportion of the embryo has developed as neural tissue that wild type, hypertrophy of the nervous system. Most embryos show no cuticle.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Enhancer of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference

kuz[+]/kuze29-4 is a non-enhancer of eye phenotype of Scer\GAL4hs.2sev, hbsVDRC.cUa

kuz[+]/kuze29-4 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, hbsVDRC.cUa

Suppressor of
NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

kuze29-4, Df(3R)BSC620 double homozygous embryos do not show any obvious somatic musculature phenotype, as compared to controls.

kuze29-4/kuze29-4, Df(3L)ED225/Df(3L)ED225 double mutant embryos display a similar degree of supernumerary Ap neurons, but an enhanced supernumerary EL neuron phenotype, as compared to kuze29-4/kuze29-4 single mutants. These double mutants also display increased proliferation of thoracic neuroblasts at stage 15 (but not stage 12 or 14), thoracic neuroblast daughter cells at stage 14 and 15 (but not stage 12), and abdominal neuroblasts and neuroblast daughter cells at stage 14 and 15 (but not stage 12), as compared with controls.

kuze29-4/+, dap7867/+ double mutant embryos display a significant increase in the number of Ap neurons and EL neurons, and show increased proliferation of neuroblast daughter cells, but not neuroblasts, as compared to controls.

kuze29-4/+, Df(3R)BSC751/+ double mutant embryos display a significant increase in the number of Ap neurons, as compared to controls.

Expression of dapScer\UAS.cUa under the control of Scer\GAL4elav.PU partially suppresses the increased Ap neuron number phenotype, and fully suppresses the increased EL neuron number phenotype, and suppresses the increased daughter cell proliferation of kuze29-4/kuze29-4 mutants.

kuze29-4/+ has no detectable effect on the eye-phenotype resulting from the expression of hbsVDRC.cUa under the control of Scer\GAL4hs.2sev.

kuze29-4 ; pros17 double mutant embryos show extensive overproliferation of the entire NB5-6T lineage, with an average of 69 cells. There is an increase in the number of "Ap" neurons generated in the NB5-6T lineage in the double mutant embryos compared to kuze29-4 single mutant embryos.

The wing vein phenotype resulting from the expression of uifasterisk.Scer\UAS under the control of Scer\GAL4A9 is enhanced by kuze29-4.

A kuze29-4 background enhances the FasII axon midline crossing phenotype seen in sli1, robo5 transheterozygous stage 16 embryos.

The addition of NScer\UAS.ΔLN.T:Ecol\lexA or NScer\UAS.ΔLNR.T:Ecol\lexA suppresses the neural hypertrophy seen in kuze29-4 embryos leading to an identifiable central nervous system.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (22)