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General Information
Symbol
Dmel\Dll17
Species
D. melanogaster
Name
FlyBase ID
FBal0001014
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
DllSA1
Key Links
Mutagen
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

5.5kb deletion removing the exon encoding the amino terminal two thirds of the homeodomain.

about 6 kb deletion around about 120 kb; removes middle exon; Coordinates estimated from Cohen, Broenner, Kuettner, Jurgens and Jaeckle (1989); origin undefined; positive values extend to left.

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

macrochaeta & leg | somatic clone

wing & macrochaeta | somatic clone

Detailed Description
Statement
Reference

Dll17/Dll3 mutant larvae show a significantly impaired behavioural response to an attractive odorant (EtOAc). Some larvae show dorsal organ malformations but there appears to be no correlation between the larvae with cuticular defects and those with olfactory impairment. Motor activity appears normal, and allowing more time for the larva to respond (10 minutes rather than 5 minutes) does not change the response indices.

Heterozygous Dll17 mutant larvae show a significantly impaired response to an attractive odorant (EtOAc). No malformations are seen in in the cuticular components of the dorsal organ.

Heterozygous Dll17 mutant embryos have fewer neurons and fewer support cells in the dorsal organ (DO) and terminal organ than wild type animals. No cell death is seen (TUNEL staining) and the remaining neurons exhibit aberrant morphologies. The DO dendrites are loosely associated rather than tightly bundled.

Large minute clones of Dll17 result in almost all portions of distiproboscis being eliminated. The mediproboscis is not eliminated by these clones.

The basal capsule of the arista is almost normal in heterozygous flies.

Dll3/Dll17 animals die as pharate adults. They show truncations of the antenna, such as deletion of antennal segment 3 and the arista. A complete loss of the tarsal segments and shortening of both the femur and tibia is seen in the legs.

Dll17 somatic clones do not develop anal plates in males, or dorsal anal plates in females. Clones do not show any detectable alterations in the male external genitalia. Clones do not affect the development of the female ventral anal plates.

Dll17 somatic clones produce areas of defective cuticle and are unable to form anal plates.

The distribution of homozygous clones along the proximodistal axis of the leg differs from the distribution of control clones; the ratio of distal-to-proximal clones is 2:1 for control clones and 1:4 for homozygous Dll17 clones, suggesting that homozygous Dll17 clones are lost distally. Homozygous clones in the tarsal segments segregate out of the surrounding wild-type imaginal disc epithelium. Vesicles of homozygous Dll17 tissue are sometimes seen inside the tarsal segments of the legs of adult flies.

Homozygous clones can be recovered in the dorsal femur when they are generated at any stage in development (from embryo to mid-third instar larva), although early in development their frequency is reduced compared to wild-type clones. When the leg is composed almost entirely of Dll17 tissue then the region more distal to the coxa is represented by only a small stump of tissue. The characteristic hairs and bristles found at the wing margin are deleted in homozygous clones at the margin. The effect of these clones is autonomous.

Homozygous clones induced in the leg discs do not proliferate. Homozygous clones induced in the leg during the first and second larval instar stages are only found in the pleural and coxa regions and produce no morphological abnormalities. Homozygous clones induced in the leg during the third larval instar stage are frequently seen in the distal regions of the leg. The majority of clones in the trochanter and tibia-tarsus region form vesicles that invaginate inside the appendage. These clones often contain bristles and trichomes that do not resemble those in the vicinity of the clone. Clones in the femur and proximal tibia contain bristles without bracts. Homozygous clones induced in the antenna during the first larval instar stage are able to differentiate the aI antennal segment and a small part of the aII antennal segment, but are unable to form the rest of the aII segment, segment aIII or the arista. Homozygous clones induced in the antenna during the third larval instar stage tend to form vesicles that are separated from the surrounding tissue in segments aII and aIII. Clones in the arista often differentiate bracted bristles, suggesting an antennal to leg transformation. Homozygous clones induced in the wing during the larval stage affect the wing margin; the triple row of bristles in the anterior compartment and the double row of long hairs in the posterior compartment are eliminated. Clones away from the margin often affect vein differentiation in the vicinity of the margin. This affect can be nonautonomous as wild-type cells in the vicinity of the clone are often affected. The clones develop socketed bristles in the posterior compartment and also develop a halo of pigment.

Dll null mutant embryos produced both leg and imaginal discs following in vivo culture.

Embryos have normal mouth hooks and ventral organs, but missing an average of 5 cirri from the anterior row and 7 cirri from the posterior row. Also the ventral organ often includes extra papillae of unknown origin.

Wnt5 expression in head and thoracic segments is absent in embryos presumed to be homozygous for this allele.

Greatly reduced femur and tibia, associated with normal trochanter and coxa.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

A Dll17 mutant background partially suppresses the ectopic leg tissue phenotype seen when btdScer\UAS.cSa clones are generated under the control of Scer\GAL4tub.PU using the MARCM system. These clones cannot generate distal leg fates, but are able to produce what appears to be proximal leg tissue.

Dll17 danrex35 or Dll17 Df(3R)ex56 double heterozygotes show ectopic tarsal bristles in the basal capsule of the arista.

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

Some Dll17/Df(2R)ED4065 animals carrying Dll+m312 survive until the pharate adult stage. These animals show severe truncation and malformation of the medial and distal leg segments. The distal tibia and tarsal regions are absent, the femur is shortened and the trochanter is deformed. The bristles on the femur lack bracts, in contrast to wild type. Mechanosensory bristles of the wing margin are missing.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Clonal analysis indicates that the requirement for Dll in the femur and most of the tibia is lost by about the early third larval instar stage.

Strong Dll allele.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
References (43)