FB2024_03 , released June 25, 2024
Allele: Dmel\dlp1
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General Information
Symbol
Dmel\dlp1
Species
D. melanogaster
Name
FlyBase ID
FBal0190800
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

Imprecise excision of the P{PZ}Q5 element, resulting in a 504bp deletion that begins at the insertion site and extends 2bp beyond the putative ATG for the dlp open reading frame. 8bp of the P{PZ} element inverted repeat sequence remain.

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

dlp1/dlp2 larvae have a normal number of boutons at the neuromuscular junction. Mean active zone area is significantly decreased and the number of active zones per bouton is significantly increased compared to wild type.

The amplitude of the evoked excitatory junctional potential (EJP) is increased compared to wild type at the neuromuscular junction of dlp1/dlp2 larvae. The amplitude and frequency of miniature EJPs is normal. Quantal content is increased.

dlp1/Df(3L)fz-D21 mutants show axon guidance defects. At the third instar larval stage, half of mutants show thickening of the lamina plexus, and 80% show crossovers between ommatidial axon bundles and abnormal photoreceptor process expansion outside the lamina plexus. Mosaic studies show that dlp1 homozygous photoreceptors misguide axons to the lamina plexus, but do not affect axon guidance to the medulla. At the pupal level, 80% of dlp1/Df(3L)fz-D21 mutants have brains with irregularities in the R7 and R8 medulla termini, ~50% show medulla cartridge crossover and ~20% show misrouting of R7/R8 axons. Electrophysiological analysis shows that dlp1/Df(3L)fz-D21 flies have grossly abnormal ERGs, with defective photoreceptor polarization and complete absence of on- and off-transients. Mosaic flies with dlp1 mutant photoreceptors and wild-type brains have normal ERGs, suggesting that the ERG defect is due to the presence of mutation in the optic lobe, not the eye.

dlp1/dlp2 mutants show axon guidance defects. At the third instar larval stage, ~30% of mutants show thickening of the lamina plexus, and >60% show crossovers between ommatidial axon bundles and abnormal photoreceptor process expansion outside the lamina plexus. At the pupal level, 80% of dlp1/dlp2 mutants have brains with irregularities in the R7 and R8 medulla termini and over 20% show medulla cartridge crossover. The eyes of dlp1/Df(3L)fz-D21 adults show a rough eye phenotype with eyes that are reduced in size. However, the mutant eyes contain all photoreceptors and ommatidial polarity is normal. Differentiation of dlp1/dlp2 photoreceptors is not defective.

Less than 5% of dlp1 mutants survive to adulthood. dlp1/dlp2 embryos from dlp1 germline clone females and dlp2 males show a severe segment polarity defect with denticles covering the ventral surface. Rare dlp1/Df(3L)fz-D21 escapers show a ~50% reduction in ommatidia and disordered ommatidial structure compared to wild type. Both dlp1/dlp2 and dlp1/Df(3L)fz-D21 escapers show patterning defects at the anterior margin, with ectopic mechanosensory bristles on both dorsal and ventral surfaces, that are positioned further from the wing margin than bristles in wild type. This phenotype is fully penetrant for both mutants, but the number of ectopic bristles varies. Expression of dlpScer\UAS.cBa, under the control of Scer\GAL4ap-md544, in a dlp1/+ background leads to bristle loss at the anterior wing margin. BrdU incorporation shows that the zone of nonproliferating cells along the DV boundary of the third instar wing disc in dlp1/Df(3L)fz-D21 larvae is expanded compared to dlp1/+ controls. The average width of the wing pouch is reduced in these mutants.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

dlp1/dlp[+] is a suppressor of increased cell number | female | adult stage | heat sensitive phenotype of Mmp2Y53N/Mmp2W307stop

dlp1/dlp[+] is a suppressor of increased cell number | female | adult stage | heat sensitive phenotype of Df(2R)BSC132/Mmp2Y53N

NOT Suppressor of
Statement
Reference
Phenotype Manifest In
NOT suppressed by
Statement
Reference

dlp1/dlp2 has eye photoreceptor cell & axon phenotype, non-suppressible by SdcUAS.cSa/Scer\GAL4da.G32

NOT Enhancer of
Statement
Reference

dlp1 is a non-enhancer of anterior fascicle & axon | ectopic phenotype of Larbypass

Suppressor of
Statement
Reference

dlp1/dlp[+] is a suppressor of stalk follicle cell | increased number | heat sensitive phenotype of Df(2R)BSC132/Mmp2Y53N

dlp1/dlp[+] is a suppressor of stalk follicle cell | increased number | heat sensitive phenotype of Mmp2Y53N/Mmp2W307stop

dlp1/dlp[+] is a suppressor of wing sensillum phenotype of Hsepid12

dlp1/dlp[+] is a suppressor | partially of wing phenotype of NotumUAS.cGa, Scer\GAL4ap-md544

NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The increase in average cell number in the stalks between egg chambers which is seen in Mmp2Y53N/Df(2R)BSC132 and Mmp2Y53N/Mmp2W307stop females after being shifted to the restrictive temperature is dominantly suppressed if the females also carry a single copy of dlp1.

A heterozygous dlp1

background does not result in a decreased number of chemosensory bristles in a Hsepid12 homozygous mutants.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is not affected if the embryos are also heterozygous for dlp1.

The dlp1 mutation does not increase the frequency of the Larbypass ISNb bypass phenotype.

Expression of SdcScer\UAS.cSa, under the control of Scer\GAL4da.G32, fails to rescue the axon guidance defects of dlp1/dlp2 mutants.

Heterozygosity for dlp1 partially suppresses the wingless phenotype seen when NotumScer\UAS.cGa is expressed under the control of Scer\GAL4ap-md544. Approximately 40% of such flies display a winglet on one side of the body, but are usually wingless on the other side. These winglets often display substantially normal wing patterning, although this phenotype is variable.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments

Expression of dlpScer\UAS.cBa without a driver is sufficient to rescue the eye phenotype, but not the wing phenotype of dlp1/Df(3L)fz-D21 mutants.

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Mutant
Wild-type
Stocks (0)
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (11)