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General Information
Symbol
Dmel\dve01738
Species
D. melanogaster
Name
FlyBase ID
FBal0060453
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dve1, dve-lacZ, dveP1738, dve1-lacZ
Key Links
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 in intron 1.

P{PZ} insertion in the second intron.

Insertion of a P{PZ} element in the second intron.

Insertion components
P{PZ}dve01738
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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

The ratio of the cross-section areas of the accessory gland/ejaculatory bulb is significantly reduced compared to wild type in males expressing dveKK115422 under the control of Scer\GAL4dve.13 in a dve01738/+ background. Binucleation of main type cells is relatively normal in the mutant accessory glands.

The number of eggs laid per day by females mated to males expressing dveKK115422 under the control of Scer\GAL4dve.13 in a dve01738/+ background is reduced and these females show high re-mating activity (comparable to those of virgin female controls) at 48 hours after the first mating.

Homozygous clones in the male accessory gland do not contain cells with secondary morphology.

dve01738/dveNP3060 trans-heterozygotes show normal morphology and function.

dve01738/dveE181 and dve01738/Df(2R)01D01W-L186 trans-heterozygotes exhibit substantially impaired proventriculus function.

dve01738 homozygotes exhibit a reduction in copper absorption and acid secretion in the midgut. dve01738/dveE181 trans-heterozygotes exhibit a milder phenotype, with dve01738/dveNP3060 trans-heterozygotes milder still, while dve01738 heterozygotes exhibit a mild reduction in copper absorption and acid secretion compared to wild-type.

dve01738 clones in the leg are frequently associated with ectopic joint structures in the tarsal segments, whereas clones in the femur or tibia are not associated with ectopic joints. Clones encompassing multiple tarsal segments induce extra joints in each segment, though clones spanning the joint have no effect on endogenous joint morphology. Clones spanning several joints induce only one ectopic partial joint per segment, which tends to appear in the middle of the segment. The curvature of the ectopic joints is reversed relative to the endogenous joints. No obvious effects on bristle polarity are observed.

Wings of mutant flies are smaller and shorter than normal. The wings lack a region that encompasses most of the distal costa and a small part of the adjacent wing blade. The mutant wings are also reduced in size along the anterior-posterior axis. Wing vein 2 is interrupted in the proximal part and the distal part of wing vein 5 is missing. The size of the area of the wing outlined by wing veins 3 and 4, and the anterior crossvein and wing margin is similar in size in mutant and wild-type animals. The cell density in the area of the wing outlined by wing veins 3 and 4 is very similar in mutant and wild-type animals. The distance between wing vein 3 and 4, measured by the numbers of cells between them, is the same in mutant and wild-type animals. The cell density in the region anterior to wing vein 3 is similar in mutant and wild-type animals, but the distance between wing vein 3 and the anterior margin is reduced in mutant animals, indicating that this area consists of fewer cells in the mutant. The distance from vein 4 to the posterior wing margin is reduced in mutant animals compared to wild type, and cell density in this region is also lower than wild-type in the mutant animals, indicating that this region consists of fewer, larger cells in mutant animals compared to wild type. Mutant third larval instar wing discs are abnormal; the anlage of the dorsal part of the wing pouch is shorter than normal. In early pupae, the wing pouch is smaller than normal and has a small indentation at the anterior wing margin. The fold adjacent to the wing blade appears to be reduced in mutant wing discs. Homozygous clones induced in the wing disc are smaller than their wild-type twin clones. Clones in the regions of the disc extending from the anterior wing margin to vein 3 and from vein 4 to the posterior margin are about half the size of their wild-type counterparts. In addition, nearly half the wild-type clones in these regions do not have a mutant counterpart (suggesting that the mutant cells have died). Clones in the region from wing vein 3 to 4 are about two-thirds the size of their wild-type counterparts.

Homozygous clones in the wing result in ectopic margin bristles (which can be derived from mutant or wild-type tissue) and wing margin notches.

Homozygotes die as first instar larvae. Passage of food is blocked at the proventriculus in these larvae. The specification of the proventriculus primordium occurs normally in homozygous embryos. At stage 17, the endoderm outer wall structure of the proventriculus shows a collapsed phenotype and the ingrowth of the ectodermal valve cells into the endoderm fails. The number of outer wall cells is wild-type and no cell death occurs in the defective outer wall.

Homozygous larvae show normal locomotion behaviour immediately after hatching, however they develop into small larvae and die within a day of hatching. Food accumulates in the proventriculus, in contrast to control larvae where it is present throughout the length of the gut. The proventriculus is not correctly formed; cell migration of the foregut epithelium into the anteriormost midgut is greatly delayed and the internalisation is only temporary. Constriction of the midgut normally occurs in the midgut of homozygous embryos and the arrangement of the stage 17 midgut appears normal. The arrangement of copper cells appears disorganised in hemizygous larvae.

Larvae have a nonfunctional proventriculus, leading to lethality at the first instar stage.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference

dve01738/dve[+] is a suppressor of visible | heat sensitive phenotype of peb1

Phenotype Manifest In
Suppressor of
Statement
Reference

dve01738/dve[+] is a suppressor of eye | heat sensitive phenotype of peb1

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

A. Spradling.

Comments
Comments

Excision of the P{PZ} element reverts the lethal phenotype.

Excision of the P{PZ} element results in viable, fertile flies indicating that the phenotype is caused by the P{PZ} insertion.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (19)