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General Information
Symbol
Dmel\dppd6
Species
D. melanogaster
Name
FlyBase ID
FBal0003003
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dppd-6, dpp6
Mutagen
Nature of the Allele
Mutagen
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

Deletion of control elements.

Inversion breakpoint within the regulatory disk region, effectively deleting some of the regulatory sequences that direct expression in imaginal discs.

Breakpoint allele.

Caused by aberration
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

No wing phenotypes are seen in dppd6 heterozygotes.

dppd6/dppd14 flies are viable and have small wings.

dppd6/dppd14 wings are rescued by the expression of dppScer\UAS.cSa.T:Ivir\HA1 under the control of Scer\GAL4dpp.blk1 except for ectopic vein materials around longitudinal vein L3.

The size and morphology of dppd6/dppd14 mutant wings are almost completely rescued by the expression of dppMFSI.Scer\UAS.T:Ivir\HA1 via Scer\GAL4dpp.blk1 except for ectopic vein material around L3.

The size and morphology of dppd6/dppd14 mutant wings are almost completely rescued by the expression of dppMFSI.III.Scer\UAS.T:Ivir\HA1 via Scer\GAL4dpp.blk1 except for ectopic vein material around L3.

dppd6 mutant embryos display an increased number of hematopoietic cells in the lymph gland of embryos compared to wild-type, and the lymph gland is still hypertrophic in third instar larvae and there is an overabundance of plasmatocyte precursors. There is no significant difference in the number of crystal cell precursors in these larvae.

dppd6 mutant larvae fed on S. typhimurium experience a developmental delay of 1 full day from hatching to pupation, and infection results in eventual lethality of these animals. Under normal conditions, dppd6 mutant larvae generate 38% more blood cells per larvae compared to wild-type. There is significantly more (74%) blood cells observed in 3-day fed infected mutant larvae than in non-infected mutant larvae. There is no significant difference in the number of crystal cells between infected mutant and wild-type larvae. In the absence of infection 48% of blood cells in mutant larve are new plasmatocytes, compared to 31% in controls. Within 1 day of infection, the level of new plasmatocytes decreases to 23% and continues to decrease over subsequent days, reduced compared to levels in wild-type infected larvae. Infected dppd6 mutant larvae are significantly impaired in their ability to produce lamellocytes, whereas infected wild-type larvae show >10-fold increase in the percentage of circulating lamellocytes.

Stage 15 dppd6 embryos contain a significantly greater number of zfh1-expressing pericardial cells than normal, but show no change in the number of Mef2 expressing cardiac cells. Hyperplasia of the zfh1-expressing pericardial cells is still seen in stage 17 mutant embryos.

dppd6 embryos show expanded cell proliferation in the dorsal mesoderm during stage 12 compared to wild-type embryos, and cell division in the dorsal mesoderm persists in dppd6 embryos throughout stage 13 (in contrast to wild type, where cell division is absent in the dorsal mesoderm in stage 13).

In the anterior region of the heart (the aorta), mutant first instar larvae show no difference in heart rate or pulse distance compared to controls. However, in the posterior region (the heart proper), the mutant larvae show a considerable reduction in the systolic distance (mutant cells do not approach each other as closely as wild-type cells do) and the diastolic distance (mutant cells do not separate from each other as far as wild-type cells do). The mutant larvae have a 44% reduction in the average pulse distance per beat, an indication that the beat volume is significantly reduced. The heart rate in the posterior region of the heart is comparable to wild type.

Heterozygotes do not have an ectopic wing vein phenotype.

dppd6/dpphr4 wings have only two veins, L3 and L5 and are missing L2 and L4 completely. dppd6/dpphr27 mutants have wings that are significantly reduced in size and that are missing L3 and L5. The wings of dppd5/dppd6 mutants are so small that the identification of patterning defects is obscured.

Wing size is reduced in dpphr4/dppd6 flies.

dppd12/dppd6 flies show a considerable loss of taste bristles but do not show a loss of pseudotrachae or a significant change in gross mediproboscis morphology.

Approximately 50% of eggs laid by heterozygous females have shortened and abnormally shaped respiratory appendages.

dppd6/dpphr27 flies show partial fusions of the L2 and L3 and the L4 and L5 wing veins. The wing is compressed along the A/P axis compared to wild type.

dppd6/dppd12 flies have a reduced number of ommatidia. The adults are weak, short-lived (live for 2-3 days) and have abnormalities in the wing, leg, antenna and external genitalia. The tarsal and meta-tarsal segments of all legs are abnormal in dppd6/dppd12 flies, due to loss of claws and fusion of the tarsal segments. The dorsal parts of the leg are sometimes ventralised. The tibia and femur are progressively less affected, while the trochanter and coxa are almost wild type. The number of sex comb bristles is generally higher than normal. dppd6/dppd12 flies have defects in the distal segments of the antenna. The arista is usually absent and a conical projection is present on the third segment (which presumably represents the fused 4th, 5th and 6th antennal segments). Most dppd6/dppd12 males completely lack external genitalia while some have abnormal external genitalia. There is little effect on the female genitalia. The leg and antennal discs of dppd6/dppd12 larvae are deformed.

The external genitalia of dppd6/dppd12 males are reduced to a small ring like structure. dppd6/dppd12 females show duplication of the thorn bristles accompanied by an absence of long bristles.

Small, rough eyes.

Heterozygotes are phenotypically wild-type. Wings derived from dppd6/dpps4 animals lack only the anterior crossvein.

dppd6/dppd8 transheterozygotes have defects in both wing and leg development. Mutants can produce ventral wing hinge structures in transdetermined legs.

70 to 100% of homozygous males show loss of tarsi and claws and have small wings and eyes. 35 to 70% of homozygous males show duplication of leg structures, and 10 to 35% of homozygous males have duplicated antennal structures.

dpphr4/dppd6 transheterozygotes exhibit reduced wings to approximately half wild type size and no defects in eyes or legs.

Homozygotes exhibit greatly reduced wings and eyes and loss of tarsal claws at the tips of the legs. Transheterozygotes with dpphr4 have wings approximately half size and normal legs and eyes. When in combination with Df(2L)C28/Mad+ the transheterozygotes exhibit more severe phenotype, further reduction in wing blade, slight reduction in the eye and loss of tarsal claws. Trisomy for Mad (Dp(2;3)JS20) partially ameliorates transheterozygote phenotype, wings are of normal size and show residual vein fusions.

dppd6/dpphr4 individuals have a nearly full size wing, except for the absence of the anterior crossvein, a reduction in the distance between L4 and L5 and a small amount of ectopic vein between L2 and L3.

The medulla neuropil is reduced to a size similar to that produced by inactivating wg prior to 44hr AEL. The number of ommatidia is correspondingly reduced. The number of outer proliferative center cells incorporating BrdU is markedly decreased in the Fas2 expressing domain of wg and dpp early third instar brains.

dppd6/dppd14 clones are associated with defects in the wing, but not the notum. dppd6/dppd14 clones in the posterior compartment are associated with normal venation.

Adults lack distal portion of appendages.

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

dppd6/dppd12 has visible phenotype, enhanceable by B1

dppd6 has visible | recessive phenotype, enhanceable by mxcG43

NOT Enhancer of
Statement
Reference

dppd6/dppd6 is a non-enhancer of visible | recessive phenotype of mxcG43

Suppressor of
Statement
Reference

dppd6/dpp[+] is a suppressor of neuroanatomy defective phenotype of spin10403

dppd6/dpp[+] is a suppressor | partially of visible phenotype of Scer\GAL4[-], SnooGS-C517T

dppd6/dpp[+] is a suppressor | partially of visible phenotype of Scer\GAL4Tub.PU, SnooGS-C517T

dppd6/dpp[+] is a suppressor of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

dppd6 is a suppressor of visible phenotype of upd1GMR.PB

NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

dppd6/dppd12 has tarsal segment phenotype, enhanceable by B1

dppd6/dppd12 has tibia phenotype, enhanceable by B1

dppd6/dppd12 has antenna phenotype, enhanceable by B1

dppd6/dppd12 has arista phenotype, enhanceable by B1

dppd6/dppd12 has femur phenotype, enhanceable by B1

dppd6/dppd12 has leg phenotype, enhanceable by B1

dppd6/dppd12 has male genitalia phenotype, enhanceable by B1

dppd6/dppd12 has ommatidium phenotype, enhanceable by B1

dppd6 has tarsal segment phenotype, enhanceable by mxcG43

dppd6 has leg | ectopic phenotype, enhanceable by mxcG43

dppd6 has wing phenotype, enhanceable by mxcG43

dppd6 has eye phenotype, enhanceable by mxcG43

dppd6 has antenna | ectopic phenotype, enhanceable by mxcG43

dpphr4/dppd6 has wing phenotype, enhanceable by vri[+]/vri1

dpphr4/dppd6 has wing phenotype, enhanceable by vri2/vri[+]

Suppressed by
Statement
Reference

dpps4/dppd6 has anterior crossvein phenotype, suppressible by gbb1

NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

dppd6/dpp[+] is a suppressor of eye disc phenotype of spin10403

dppd6/dpp[+] is a suppressor of glial cell phenotype of spin10403

dppd6/dpp[+] is a suppressor | partially of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, SnooGS-C517T

dppd6/dpp[+] is a suppressor | partially of wing vein | ectopic phenotype of Scer\GAL4[-], SnooGS-C517T

dppd6/dpp[+] is a suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

dppd6 is a suppressor of eye phenotype of upd1GMR.PB

NOT Suppressor of
Statement
Reference

dppd6 is a non-suppressor of hemocyte | embryonic stage phenotype of zfh12

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

A high frequency of tumour growth occurs below the anal plates of the terminalia in chromosomally female flies homozygous for ix1 and dppd6, or homozygous for ix1 and trans-heterozygous for dppd5/dppd6 or dppd6/dppd-ho.

Loss of the anterior crossvein is seen in 74% of dppd6 Df(2R)en-SFX31 double heterozygous flies.

Loss of the anterior crossvein is seen in dppd6 en54 double heterozygous flies.

The glial overmigration phenotype seen in spin10403 eye discs is significantly suppressed if the animals are also heterozygous for dppd6.

There are no hematopoietic cells in the lymph gland of dppd6, zfh12 double mutant embryos.

The frequency of the SnooGS-C517T/SnooGS-C517T ectopic wing vein phenotype is significantly suppressed if the flies are also carrying one copy of dppd6.

The frequency of the ectopic wing vein phenotype caused by expression of SnooGS-C517T under the control of Scer\GAL4tub is significantly suppressed if the flies are also carrying one copy of dppd6.

Flies that express tkvScer\UAS.cNa, under the control of Scer\GAL4tub, in a dpphr4/dppd6 background, have smaller wings than flies expressing the transgene in a wild-type background and than dpphr4/dppd6 flies that do not express tkvScer\UAS.cNa.

The severity of the leg defects seen in dppd6/dppd16 flies is enhanced by B1. There is an overall shortening in length along the proximal-distal axis of the leg and complete or partial fusion or even total loss of tarsal segments. The tibia and femur are deformed, showing shortening, bulging and disorganised bristle patterns. The coxa and trochanter are not so strongly affected. The sex comb of the prothoracic leg, when present, is always duplicated in these flies. The antenna phenotype of dppd6/dppd16 flies is enhanced by B1; the arista, 4th and 5th segments are completely absent and the 2nd and 3rd segments are widened and deformed and have defects in the bristle pattern. B1 ; dppd6/dppd16 flies completely lack ommatidia. All B1 ; dppd6/dppd16 males completely lack external genitalia.

The anterior crossvein is restored in dppd6/dpps4 flies carrying one copy of gbb1. The wing is reduced in size in these animals and viability is significantly reduced.

Very few wgAct5C.PS; dppd6/dppd8 flies exhibit wg-induced transdetermination, legs with wing tissue.

Does not enhance the phenotype of mxcG43 hemizygotes. The dppd6 phenotypes are enhanced if the flies are also hemizygous for mxcG43.

vri1/+ or vri2/+ causes a further reduction in wing size and wing veins of dpphr4/dppd6 transheterozygotes. Eyes are smaller and rough and legs are truncated.

If dppd6/dpphr4 flies are also heterozygous for (paternally contributed) sax1 or sax2, L2 is lost and L4 and L5 fused. Whereas dppd5/dppd6 legs are normal, if the flies are also heterozygous for sax1 or sax2 then legs tend to lack tarsal claws.

Scer\GAL4dpp.blk1 driven expression of gbbScer\UAS.cSa or gbbScer\UAS.cSb is unable to rescue the mutant phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Not rescued by
Comments

dppd6/dppd14 wings are rescued by the expression of dppScer\UAS.cSa.T:Ivir\HA1 under the control of Scer\GAL4dpp.blk1 except for ectopic vein materials around longitudinal vein L3.

The size and morphology of dppd6/dppd14 mutant wings are almost completely rescued by the expression of dppMFSI.Scer\UAS.T:Ivir\HA1 via Scer\GAL4dpp.blk1 except for ectopic vein material around L3.

The size and morphology of dppd6/dppd14 mutant wings are almost completely rescued by the expression of dppMFSI.III.Scer\UAS.T:Ivir\HA1 via Scer\GAL4dpp.blk1 except for ectopic vein material around L3.

The expression of dppMFSII.Scer\UAS.T:Ivir\HA1 via Scer\GAL4dpp.blk1 fails to rescue the wing phenotype of dppd6/dppd14 mutants.

Eye and wing phenotypes can be rescued by Scer\GAL4dpp.blk1 driving the expression of dppScer\UAS.cSa.

Belongs to the disk-III class of alleles.

Allele class: d-III

Images (0)
Mutant
Wild-type
Stocks (3)
Notes on Origin
Discoverer
Comments
Comments

dpp class III allele.

Clonal analysis shows a requirement for dpp+ function in cells adjacent to the anterior-posterior compartment boundary of the wing primordium.

Intermediate disk dpp allele.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (45)