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General Information
Symbol
Dmel\bnl00857
Species
D. melanogaster
Name
FlyBase ID
FBal0057745
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
bnlP1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P{PZ} insertion is in the first intron.

Insertion components
P{PZ}bnl00857
Product class / Tool use(s)
Encoded product / tool
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

More than 60% of heterozygous bnl00857 mutant embryos show occasional missing or stalled branches with the ganglionic branches most affected.

bnl00857 mutant clones generated using the eyFLP method exhibit a glossy eye phenotype.

bnl00857 mutant eye clones lose their ability to constrict their apical surfaces at the morphogenetic furrow. They also lose normal contacts between cells and form aberrant-shaped clusters.

bnl00857 mutant eye clones produce defects in retinal basal glial (RBG) cell migration from second instar larval stage. The RBG cells migrate ectopically to anterior regions of the eye beyond the morphogenetic furrow, a phenotype that is not seen in wild type flies. RBG proliferation and survival are not affected. bnl00857 clones generated specifically in the glia do not show RBG migration defects.

40% of tracheal ganglionic branches fail to reach the central nervous system in heterozygous embryos.

Somatic clones of bnl00857 in the third instar wing disc columnar epithelium cause a decrease in the numbers and migration of air sac tracheoblasts.

The filopodia-like cell extensions that are seen in tracheal cells at stage 12 are missing in mutant embryos. The mutant embryos lack an interconnected dorsal trunk and instead show a segmental array of isolated metameric tracheal units with a lollipop-like structure in place of the dorsal trunk.

Stage 13 homozygous embryos show little tracheal branch outgrowth.

Heterozygous and hemizygous embryos show sporadic defects in primary tracheal branch outgrowth. This is manifest most significantly by the ganglionic tracheal branches, 9% of which fail to reach the central nervous system.

The number of terminal tracheal branches (GB, LG and LH) are reduced by 30%-50% in heterozygous bnl00857 larvae.

Almost every tracheal metamere appears as an unbranched, elongate sac of tracheal cells. Tracheal cells invaginate and form tracheal sacs but the branches fail to grow out. A few primary branches form that are rudimentary. Scer\GAL4C49 mediated expression of bnlScer\UAS.cSa allows branch formation and growth. Formation of muscles and the peripheral nervous system are unaffected. There are specific defects in the nervous system.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference

bnl00857 has cell migration defective phenotype, suppressible by ptc[+]/ptcD130

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
Statement
Reference

bnl[+]/bnl00857 is an enhancer of dorsal group branch precursor phenotype of Rac1J11, Rac2Δ/Rac2[+]

bnl[+]/bnl00857 is an enhancer of tracheal branch primordium phenotype of Rac1J11, Rac2Δ/Rac2[+]

bnl[+]/bnl00857 is an enhancer of dorsal trunk primordium phenotype of Rac1J11, Rac2Δ/Rac2[+]

Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

A ptcD130 heterozygous mutant background suppresses the tracheal ganglionic branch migration defects seen in bnl00857 mutants.

sr155/bnl00857 double mutants exhibit impaired ganglionic branch migration.

The increase in the number of tracheal branches that terminate on ventrolateral body wall muscle 12 caused by expression of agoΔF.Scer\UAS under the control of Scer\GAL4tey-5053A is suppressed if the flies are also heterozygous for bnl00857.

bnl00857 dominantly suppresses the increase in number of terminal branches per lateral LH cell seen in ago1/agoΔ3-7 larvae.

bnl00857/+ leads to a significant reduction in the penetrance of Scer\GAL4btl.PS VhldsRNA.Scer\UAS tracheal phenotypes.

Pak6; bnl00857 double heterozygotes have a range of tracheal phenotypes not seen in single heterozygotes for either of these alleles: The mildest phenotype is a misrouting of the dorsal branches toward the anteroposterior direction; more severely effected embryos also exhibit truncations of the dorsal trunk.

The bnl00857/+ tracheal branch outgrowth defects are partially suppressed by grhs2140/grhs2140; 78% of the tracheal ganglionic branches reach the central nervous system in the double mutant embryos.

Expression of Cdc42V12.Scer\UAS under the control of Scer\GAL4btl.PS in a bnl00857 background show occasional (4.4%) fusions of the adjacent lollipop-like dorsal trunk structures (bnl00857 single mutants show no fusion of the adjacent metameric tracheal units).

stumps09904b, bnl00857 double heterozygotes show a dramatic increase in tracheal outgrowth defects, with nearly four times as many stalled ganglionic branches as the bnl00857 heterozygote alone. The double heterozygotes also displayed increased dorsal branch outgrowth defects compared to bnl00857 heterozygotes as well as rare dorsal trunk outgrowth defects never seen in bnl00857 heterozygotes.

btlLG18 bnl00857 double mutants exhibit a tracheal phenotype similar to either mutant alone. btlLG19/btl+ bnl00857/bnl+ double heterozygote exhibits enhanced bnl00857 phenotype, defects in tracheal outgrowth. A constitutively activated form of the btl receptor (btl::tort4021b.hs.sev) can partially ameliorate the effect of absence of bnl; modest restoration of branching in bnl00857 embryos.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Complements: l(3)0134401344. Complements: l(3)0505005050. Complements: sr06915b. Complements: sr06948b.

P{PZ} insertion carries an internal deletion than removes most of the Tn\kanR and Ecol\ori region. Δ2-3 mediated transposition yields a homozygous viable revertant that restores tracheal branching and other revertants with intermediate tracheal phenotype. This confirms the P{PZ} element causes the bnl phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (35)