FlyBase Allele Report: Dmel\lab[14]

General Information

Symbol

Dmel\lab¹⁴

Species

D. melanogaster

Name

FlyBase ID

FBal0011527

Feature type

allele

Associated gene

Dmel\lab

Associated Insertion(s)

Carried in Construct

Also Known As

lab^vd1

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

amorphic allele - genetic evidence

Mutagen

X ray

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Popperl et al., 1995, Chouinard and Kaufman, 1991, Merrill et al., 1989)

loss of function allele

Mutagen

X ray

(Merrill et al., 1989)

Progenitor genotype

Cytology

Polytene chromosomes normal.

(Diederich et al., 1989, Merrill et al., 1989)

Description

Less than a 2kb deletion.

(Diederich et al., 1989)

insertion

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

3R:6,675,277..6,677,591 [-]

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.

(Diederich et al., 1989)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

ameliorates Huntington's disease

modeled by Hsap\HTT^{Q138.UAS.mRFP1}

(Weiss et al., 2012)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

lethal | heat sensitive (with lab²)

(Dubreuil et al., 2001)

lethal - all die before end of larval stage | recessive

(Hoppler and Bienz, 1994)

lethal - all die during embryonic stage | recessive

(Lutz et al., 1996)

some die during embryonic stage | recessive

(Lutz et al., 1996)

some die during larval stage | recessive

(Hoppler and Bienz, 1994)

visible (with lab²)

(Dubreuil et al., 2001)

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 31^oC. Viability at 31^oC is only 2-4%. The lab²/lab¹⁴ adults retain a full complement of copper cells at 31^oC 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.

(Dubreuil et al., 2001)

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%.

(Hirth et al., 2001)

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

(Dubreuil et al., 1998)

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

(Hirth et al., 1998)

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).

(Mohler et al., 1995)

Nondefective in gonad assembly.

(Warrior, 1994)

No salivary gland defects.

(Panzer et al., 1992)

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

(Tremml and Bienz, 1992)

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

(Immergluck et al., 1990)

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.

(Merrill et al., 1989)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

lab¹⁴ has lethal phenotype, suppressible by Ggal\Hoxb1^lab

(Lutz et al., 1996)

Suppressor of

Statement

Reference

lab[+]/lab¹⁴ is a suppressor | partially of lethal | pharate adult stage phenotype of Hsap\HTT^{Q138.UAS.mRFP1}, Scer\GAL4^elav-C155

(Weiss et al., 2012)

Phenotype Manifest In

Suppressed by

Statement

Reference

lab¹⁴ has larval tritocerebrum phenotype, suppressible by vvl^UAS.cCa/Scer\GAL4^lab.PH

(Meier et al., 2006)

lab¹⁴ has embryonic tritocerebrum phenotype, suppressible by pb^UAS.A/Scer\GAL4^lab.PH

(Hirth et al., 2001)

lab¹⁴ has embryonic tritocerebrum phenotype, suppressible by Scer\GAL4^lab.PH/Antp^UAS.cMb

(Hirth et al., 2001)

lab¹⁴ has embryonic tritocerebrum phenotype, suppressible by Scer\GAL4^lab.PH/Dfd^UAS.cBa

(Hirth et al., 2001)

lab¹⁴ has embryonic tritocerebrum phenotype, suppressible by Scer\GAL4^lab.PH/Scr^UAS.cMa

(Hirth et al., 2001)

lab¹⁴ has embryonic tritocerebrum phenotype, suppressible by Scer\GAL4^lab.PH/Ubx^UAS.cMa

(Hirth et al., 2001)

lab¹⁴ has embryonic tritocerebrum phenotype, suppressible by abd-A^UAS.cGa/Scer\GAL4^lab.PH

(Hirth et al., 2001)

NOT suppressed by

Statement

Reference

lab¹⁴ has embryonic/larval tritocerebral commissure phenotype, non-suppressible by vvl^UAS.cCa/Scer\GAL4^lab.PH

(Meier et al., 2006)

lab¹⁴ has frontal connective phenotype, non-suppressible by vvl^UAS.cCa/Scer\GAL4^lab.PH

(Meier et al., 2006)

lab¹⁴ has embryonic tritocerebrum phenotype, non-suppressible by Abd-B^UAS.cCa/Scer\GAL4^lab.PH

(Hirth et al., 2001)

Other

Statement

Reference

Ggal\Hoxb1^lab, lab¹⁴ has cephalopharyngeal skeleton phenotype

(Lutz et al., 1996)

Additional Comments

Genetic Interactions

Statement

Reference

vvl^Scer\UAS.cCa; Scer\GAL4^lab.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.

(Meier et al., 2006)

Expression of pb^Scer\UAS.A under the control of Scer\GAL4^lab.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 Dfd^Scer\UAS.cBa under the control of Scer\GAL4^lab.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 Scr^Scer\UAS.cMa under the control of Scer\GAL4^lab.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 Antp^Scer\UAS.cMb under the control of Scer\GAL4^lab.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 Ubx^Scer\UAS.cMa under the control of Scer\GAL4^lab.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-A^Scer\UAS.cGa under the control of Scer\GAL4^lab.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-B^Scer\UAS.cCa under the control of Scer\GAL4^lab.PH does not rescue the tritocerebral defects seen in lab¹⁴ embryonic brains.

(Hirth et al., 2001)

Xenogenetic Interactions

Statement

Reference

One copy of lab¹⁴ significantly rescues the lethality seen when Hsap\HTT^{Q138.Scer\UAS.T:Disc\RFP-mRFP} is expressed under the control of Scer\GAL4^elav-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.

(Weiss et al., 2012)

Ggal\Hoxb1^lab 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.

(Lutz et al., 1996)

Complementation and Rescue Data

Rescued by

lab¹⁴ is rescued by Scer\GAL4^lab.PH/lab^UAS.cMa

(Hirth et al., 2001)

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

2092