FB2024_03 , released June 25, 2024
Allele: Dmel\btlLG19
Open Close
General Information
Symbol
Dmel\btlLG19
Species
D. melanogaster
Name
FlyBase ID
FBal0030667
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description
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 ( 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

btlLG19 mutant clones generated using the eyFLP method exhibit a glossy eye phenotype. btlLG19 mutant clusters often contain a reduced number and altered arrangement of cells. Defective actin organisation is seen in btlLG19 mutant cells.

In btlLG19 mutant embryos, invagination begins normally until the formation of the finger-like structure, but this structure does not extend further during stage 11.

btlLG19 embryos do not show tracheal branch integrity defects.

In btl95/btlLG19 embryos, migration of all primary tracheal branches is affected to varying degrees.

btlLG19/+ larvae have normal numbers S phase neuroblasts per brain lobe.

The filopodia-like cell extensions that are seen in tracheal cells at stage 12 are missing in mutant embryos.

In mutant embryos tracheal cells are confined to elongated sacs that sometimes have occasional extensions. The gap between the most dorsal muscle precursors and the more ventral ones are missing.

Homozygous clones in the eye are wild-type.

Tracheal cell migration is severely affected in homozygous embryos; virtually no branches form from the initial tracheal invaginations.

Tracheal cells invaginate and occupy a position similar to that of wild-type tracheal cells, although no tracheal branches are formed in homozygous embryos.

Tracheal cells are confined to elongated sacs with occasional short extensions in homozygous embryos.

Tracheae do not branch in homozygous embryos.

Clones in which all border cells are btl- show no defects in border cell migration, though mild delays or low frequency defects would not have been detected.

btlLG19/btlH82Δ3 heterozygotes exhibit the tracheal phenotype.

Tracheal pits form, but tracheal cells do not undergo significant migration, and remain clustered at the site of the tracheal pit. Posterior pair of midline glia cells begin to migrate anteriorly, but fail to reach posterior commisure. This phenotype only evident in midline glia cells, even though btl expressed in several midline cell types.

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

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4ey.PH rescues the glossy eye phenotype seen in btlLG19 mutant clones.

Tracheal invagination initiates in rho7M43 btlLG19 double mutants, but rotation of dorsal cells does not occur, as in rho7M43 single mutants. However, a finger-like structure is never formed, instead, the tracheal cells remain as a cavity.

Expression of Mkp3GS801 under the control of Scer\GAL4btl.PS in a btlLG19/+ background does not affect the penetrance of the Scer\GAL4btl.PS>Mkp3GS801 branch integrity phenotype but results in a significant increase in failure of branch formation.

In both btlLG19/+, put10460/+ and btlLG19/+, kni6/+ embryos, most primary tracheal branches fail to migrate.

trol13/trol13; btlLG19/+ larvae have reduced numbers S phase neuroblasts per brain lobe compared to trol13 homozygotes.

Expression of btl::tor4021.Scer\UAS under the control of Scer\GAL4btl.PS in btlLG19 mutant embryos partially rescues tracheal cell migration, and additional tracheal branching is seen, as in embryos expressing btl::tor4021.Scer\UAS under the control of Scer\GAL4btl.PS in a wild-type background. Expression of Ras85DV12.Scer\UAS under the control of Scer\GAL4btl.PS in btlLG19 mutant embryos partially rescues tracheal morphogenesis. Expression of phl::tor13D.hs.sev in btlLG19 mutant embryos partially rescues tracheal morphogenesis.

btlLG19/btl+ bnl00857/bnl+ double heterozygote exhibits enhanced bnl00857 phenotype, defects in tracheal outgrowth.

Dominantly enhances the border cell migration defect of slboe7b/slboe14a.

Multiple heat shocks of the constitutively active btl::tort4021b.hs.sev protein can partially rescue tracheal migration in homozygous embryos, a single early heat shock allows reduced correction of the mutant phenotype. Partial rescue can also be achieved by the constitutively active proteins tor13D.hs.sev, Ras85DQ13.hs, phl::tor13D.hs.sev, sev::tor13D.hs.sev, Egfr::tort4021E.hs.sev and htl::tort4021F.hs.sev.

Xenogenetic Interactions
Statement
Reference

Expression of Hvul\kringScer\UAS.T:Hsap\MYC under the control of Scer\GAL4btl.PS fails to rescue the tracheal defects of btlLG19 embryos.

Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Isolated on basis of lethality over Df(3L)fz-GF3b and Df(3L)fz-GS1a. Phenotype of homozygote indistinguishable from phenotype of heterozygote with Df(3L)fz-GF3b or Df(3L)fz-GS1a. The btl alleles form a phenotypic series with respect to the tracheal phenotype. In decreasing order of severity, btlLG18 = btlLG19 > btlH82Δ3 > btlH82Δ11 > btl6-81Δ1.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (30)