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General Information
Symbol
Dmel\lab14
Species
D. melanogaster
Name
FlyBase ID
FBal0011527
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
labvd1
Key Links
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Linked to:
BamHI-EcoRI restriction fragment
Comment:

lab14 is a small (<2kb) deletion which maps within a BamHI-EcoRI restriction fragment from Figure 1 of FBrf0049820.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology

Polytene chromosomes normal.

Nature of the lesion
Statement
Reference

Less than a 2kb deletion.

insertion

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

lab2/lab14 flies show a strong head phenotype; duplication and disarray of the postorbital bristles is seen. lab2/lab14 larvae lack midgut acidification at all temperatures. However, lab2/lab14 adults show no significant difference in midgut acidification compared to wild-type adults raised at the same temperature at 18, 25 or 31oC. Viability at 31oC is only 2-4%. The lab2/lab14 adults retain a full complement of copper cells at 31oC and the invaginated morphology of the copper cells is normal. Staining for Ank reveals that the characteristic ring-shaped profiles of the copper cells is still present, but the normal progression from large, thin rings in the anterior to smaller, thicker rings in the posterior is not seen.

Mutant embryonic brains lack the tritocerebral commissure and the longitudinal pathways between the supraesophageal and subesophageal ganglia are reduced or absent. The penetrance of the brain phenotype is 88.6%.

lab2/lab14 larvae are often defective in acidification of the midgut at both the permissive and restrictive temperatures.

The tritocerebral domain is not deleted in homozygous embryos, despite the severe axonal patterning defects seen in this domain.

Double mutant combinations with cnc- embryos show additive effects in the head skeleton. The dorsal pouch syndrome of Dfd14 embryos (labral structures are poorly involuted) is suppressed in the double mutant combination (closed oral aperture).

Nondefective in gonad assembly.

No salivary gland defects.

Expression of Ecol\lacZ driven by 5' labial promoter regions (construct P{HZ1.2}) is abolished in lab14 background.

The second midgut constriction is initiated by lab14 but the continuation of the constricting process is impeded.

Hemizygous animals die at the embryonic/first larval instar border. A variable cuticle phenotype is seen, with the severity of the defects correlating with the degree of failure of head involution. The frontal sac appears collapsed, and the pharynx occupies a more anterior position than normal. The salivary glands are missing.

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

lab14 has lethal phenotype, suppressible by Ggal\Hoxb1lab

Suppressor of
Statement
Reference
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

vvlScer\UAS.cCa; Scer\GAL4lab.PH partially suppresses the brain phenotype of lab14 homozygous embryos: longitudinal axon pathways in the tritocerebrum are restored but the tritocerebral commissure remains absent and axonal projection of the frontal connective remain abnormal.

Expression of pbScer\UAS.A under the control of Scer\GAL4lab.PH rescues the tritocerebral defects seen in lab14 embryonic brains. 41.7% of embryos show a complete rescue of the defects (taking into account that the phenotypic penetrance of the lab14 phenotype is 88.6%). Expression of DfdScer\UAS.cBa under the control of Scer\GAL4lab.PH rescues the tritocerebral defects seen in lab14 embryonic brains. 38.9% of embryos show a complete rescue of the defects (taking into account that the phenotypic penetrance of the lab14 phenotype is 88.6%). Expression of ScrScer\UAS.cMa under the control of Scer\GAL4lab.PH rescues the tritocerebral defects seen in lab14 embryonic brains. 36.4% of embryos show a complete rescue of the defects (taking into account that the phenotypic penetrance of the lab14 phenotype is 88.6%). Expression of AntpScer\UAS.cMb under the control of Scer\GAL4lab.PH rescues the tritocerebral defects seen in lab14 embryonic brains. 34.9% of embryos show a complete rescue of the defects (taking into account that the phenotypic penetrance of the lab14 phenotype is 88.6%). Expression of UbxScer\UAS.cMa under the control of Scer\GAL4lab.PH rescues the tritocerebral defects seen in lab14 embryonic brains. 32.6% of embryos show a complete rescue of the defects (taking into account that the phenotypic penetrance of the lab14 phenotype is 88.6%). Expression of abd-AScer\UAS.cGa under the control of Scer\GAL4lab.PH rescues the tritocerebral defects seen in lab14 embryonic brains. 28.4% of embryos show a complete rescue of the defects (taking into account that the phenotypic penetrance of the lab14 phenotype is 88.6%). Expression of Abd-BScer\UAS.cCa under the control of Scer\GAL4lab.PH does not rescue the tritocerebral defects seen in lab14 embryonic brains.

Xenogenetic Interactions
Statement
Reference

One copy of lab14 significantly rescues the lethality seen when Hsap\HTTQ138.Scer\UAS.T:Disc\RFP-mRFP is expressed under the control of Scer\GAL4elav-C155 using the P{UAS-HTT.Q138.mRFP}A insertion line. The number of axonal aggregates seen in the peripheral nerves of third instar larvae is not reduced.

Ggal\Hoxb1lab rescues the embryonic lethality of lab14 mutants. The head skeleton of rescued larvae resembles the wild type, though there is a slight abnormality in the mouthparts.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Diederich.

R. Diederich.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (36)