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General Information
Symbol
Dmel\fu1
Species
D. melanogaster
Name
FlyBase ID
FBal0004834
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
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

Point mutation within the kinase domain.

Class I fu allele, affects the catalytic domain but does not change the open reading frame.

Carried on 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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

macrochaeta & tarsal segment 5 | distal

microchaeta & tarsal segment 1

microchaeta & tarsal segment 2

microchaeta & tarsal segment 3

microchaeta & tarsal segment 4

microchaeta & tarsal segment 5

Detailed Description
Statement
Reference

70% of ovarioles in 4 day old fu1 homozygous females are tumorous. Tumorous follicles in these ovarioles consist of tens to hundreds of germ-line cells with small, non-polyploid nuclei enveloped by a regular follicular epithelium. No increase in the rate of cell division of germline stem cells in the stem cell niche of the germarium is seen in these animals.

Mutant ovaries contain some egg chambers with more than the normal number of 16 germline cells. Egg chambers that contain more than 16 germline cells show nurse cells with varying degrees of polyploidy within a given chamber, suggesting that cysts of different ages are developing together.

Mutants show fusion of wing veins L3 and L4 both proximally and distally, with intervein tissue remaining between the two veins in the medial part of the wing.

Hemizygous mutants raised at 18oC exhibit cuticle defects in the medial region of all three leg types. The region of tarsal segment 5 flanked by longitudinal bristle rows 1 and 8 show an almost complete loss of microchaetae. The distal-most sensory bristle is lost in 16% of legs. Mutant flies possess a normal pair of tarsal claws, and no appreciable difference is seen in claw-to-claw distance.

Growth in the region between wing veins 3 and 4 is inadequate in mutant flies, as can be seen by proximal fusion of veins 3 and 4.

The phenotype of fu1 in a wild-type background is a proximal and distal fusion of wing veins L3 and L4.

The wings of hemizygotes show a distal and proximal fusion of wing veins L3 and L4. In fu1 and kncol-1 double heterozygotes, wing veins L3 and L4 are fused for most of their lengths. This is an enhancement of the phenotype of either mutation alone.

Wings of homozygous flies show thickening of vein 3 and lack vein 4 proximally. At the wing margin, the anterior double row bristles extend up to the fourth vein. Homozygous clones in the wing only generate a mutant phenotype if they are located in the region extending between veins 3 and 4; clones anterior to vein 3 or in the posterior compartment are wild-type. Clones that have a mutant phenotype have extra veins which often have campaniform sensillae characteristic of vein 3. These clones also have supernumerary sensillae and show a reduction of the anterior crossvein. Vein 4 is not affected. The clones do not cross the anterior/posterior compartment boundary.

Wing veins L3 and L4 are shifted closer together than normal in fu1 flies.

Wing vein L4 fails to form and vein L3 is thickened from the proximal base to midway between the anterior and posterior crossveins in the wings of hemizygous males. L3 curves towards the posterior compartment and makes contact with L4 at the wing margin. Hemizygous males also lack the anterior ocellus and bristles surrounding the ocelli.

Medial head structures are absent and replaced by frons material.

When in combination with decreasing doses of Su(fu)+ the fu wing phenotype is suppressed. Increasing doses of Su(fu)+ enhances the wing phenotype.

Heterozygotes carrying one copy of Su(fu)+ display a partially suppressed wing phenotype. The presence of P{SUFU100} or P{SUFU200} in these individuals produces viable males with a fu1 wing phenotype, the transposons fully compensate the decreased amount of Su(fu)+ product. With P{SUFU000} males are recovered with partially rescued fu wing phenotype, consistent with lack of Su(fu)+ function. Heterozygotes carrying two copies of Su(fu)+ display a fu wing phenotype. When the number of Su(fu)+ doses (via P{SUFU100}) in males is greater than two viability decreases, the decrease in viability is correlated with an enhancement of the fu wing phenotype. Decrease in viability is more pronounced when the transgene is provided by the mother. Viability of males is not affected by a decrease in Su(fu)+ activity.

fu1/fuv22 females are viable and have non-tumorous ovaries.

Second leg bristles missing from tarsal row 4, 1 and interrow 3.5 and additional bristles in row 5 and 8 and interrow 2.5.

Narrow wings with short connecting extra veins between LIII and LIV.

Anomalies of adult cuticular structures and tumorous ovaries.

weak wing phenotype - veins L3 and L4 fused only proximally; intermediate viability phenotype - ratio of the number of fused flies to wild type in fu/+ X fu/Y is 0.5-0.75; weak fecundity phenotype - ratio of eggs laid by fu/fu versus fu/+ sisters is 0.5-1.0; intermediate maternal effect on segmentation.

Embryos derived from fu1/fu10C mothers have a weak phenotype. Additional rows of denticles with reversed polarity are seen behind the wild-type denticle belts. At least one third of homozygous fu1 embryos derived from fu1/fu10C mothers do not develop; some are not fertilised and some stop cleavage after a few cell divisions. The remainder form a normal cellular blastoderm which may be reduced in size and contain very little yolk compared to wild-type. These embryos generally gastrulate normally. At approximately 5.5 hours of development, cells along the germ band appear loose and dead cells can be seen first in the cephalic mesoderm and then in the posterior mesodermal regions. Extensive cell death is seen in the mesoderm and ectoderm of 7-8 hour embryos, but not in the endodermal derivatives, which develop normally during this period. During germ band shortening, occasional pairwise fusion of segments can be seen, especially in the more posterior segments, and the ventral cord is often discontinuous. Development of the embryo from 9.5-20 hours is relatively normal. All segments of embryos derived from fu1/fu1A4 mothers are smaller than wild-type. Denticles are present over the entire ventral surface. The anterior rows of denticles are very distorted and the posterior compartments of the segments are virtually non-existent.

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

fu1 has visible | recessive phenotype, enhanceable by Dvir\Su(fu)cDa

Suppressed by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

fu1 is a suppressor of visible | dominant phenotype of hhMrt

fu1 is a suppressor of visible phenotype of Scer\GAL4en-e16E, hhUAS.cIa

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference

fu1 has wing vein L3 phenotype, enhanceable by Dvir\Su(fu)cDa

fu1 has wing vein L4 phenotype, enhanceable by Dvir\Su(fu)cDa

fu1 has wing vein L3 phenotype, enhanceable by kn[+]/kncol-1

fu1 has wing vein L4 phenotype, enhanceable by kn[+]/kncol-1

fu1 has wing vein L3 phenotype, enhanceable by oro1

fu1 has wing vein L4 phenotype, enhanceable by oro1

fu1 has lateral ocellus phenotype, enhanceable by oro1

fu1 has wing vein L3 phenotype, enhanceable by oro2

fu1 has wing vein L4 phenotype, enhanceable by oro2

fu1 has lateral ocellus phenotype, enhanceable by oro2

Suppressed by
Statement
Reference

fu1 has ovariole phenotype, suppressible | partially by Su(fu)LP/Su(fu)LP

fu1 has ovariole phenotype, suppressible | partially by cos[+]/cos1

fu1 has wing vein L3 phenotype, suppressible by Su(fu)LP

fu1 has wing vein L4 phenotype, suppressible by Su(fu)LP

fu1 has phenotype, suppressible | partially by Su(fu)LP

fu1 has phenotype, suppressible by Su(fu)12d

fu1 has phenotype, suppressible by Su(fu)LP

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

fu1 is a suppressor of wing cell phenotype of Scer\GAL471B, smoΔFU.UAS

fu1 is a suppressor of wing phenotype of biomb-1, pucE69

fu1 is a suppressor of wing vein L2 phenotype of hhMrt

fu1 is a suppressor of wing | anterior | distal phenotype of hhMrt

Other
Additional Comments
Genetic Interactions
Statement
Reference

In escaper flies that express Su(fu)Scer\UAS.cDa, under the control of Scer\GAL4da.G32, in a fu1 background, the wing phenotype is enhanced compared to flies expressing the transgene in a wild-type background. fu1, Su(fu)Scer\UAS.cDa, Scer\GAL4da.G32 wings show anterior duplications but also have a truncated vein 2, an enlargement of the domain between vein 2 and the margin, and veins 3 and 4 are completely fused with a large delta at the margin. These flies also show an enhancement of the leg phenotype seen in Su(fu)Scer\UAS.cDa, Scer\GAL4da.G32 flies.

biomb-1, pucE69 double heterozygotes exhibit a strong wing notch and cell death increase phenotype. These phenotypes are suppressed by the addition of fu1.

The phenotype of fu1 in a Su(fu)LP/Su(fu)LP background is wild type. The phenotype of fu1 in a Su(fu)LP/+ background is characterised by an absence of the crossvein between wing veins L3 and L4.

The fu1 wing phenotype cannot be rescued by Scer\GAL4 driven expression of knScer\UAS.cVa.

fu1; ciCe-4/+ flies generally die as pupae, although some adults eclose. The latter have small wings, a reduced thorax and lack the scutellum. Expression of ciScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ptc-559.1 partially rescues the fu1 wing phenotype; the interval between veins 3 and 4 is restored, but the double row bristles still reach the fourth vein at the margin. fu1 completely suppresses the wing phenotype caused by hhScer\UAS.cIa expressed under the control of Scer\GAL4en-e16E. Suppresses the wing phenotype of hhMrt heterozygotes.

The fu1 wing and ocellus phenotypes are dominantly enhanced by oro1 and oro2, with the addition of one copy of oro1 or oro2 increasing the deformity of the wings and reducing the size of the posterior ocelli.

When in combination with Su(fu)LP, Su(fu)12d, Df(3R)kar3Q or Df(3R)kar-Sz11 heterozygotes individuals display a partially suppressed fu phenotype. When in combination with cos3 individuals display no cos phenotype. ptc mutations do not suppress the fu phenotype, fu1; ptc9/ptc9 embryos show no naked cuticle.

Xenogenetic Interactions
Statement
Reference

The wing overgrowth phenotype caused by expression Xlae\Gli1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4en-e16E is partially suppressed by fu1, while the defect seen in the intervein region between veins 3 and 4 in fu1 flies is partially rescued by the expression Xlae\Gli1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4en-e16E.

The addition of Dvir\Su(fu)cDa to fu1 flies that are either heterozygous for Su(fu)LP or are Su(fu)+ results in an increase in fusions of wing veins L3 and L4.

Complementation and Rescue Data
Rescued by
Partially rescued by
Comments

Wing and embryonic phenotypes rescued by fu+t5.1.

Mutant phenotype has been rescued by the introduction of the wild type fu gene by P element mediated transformation.

Images (1)
Stocks (4)
Notes on Origin
Discoverer

Bridges, 4th Nov. 1912.

Comments
Comments

Not rescued by: knScer\UAS.cVa { Scer\GAL4unspecified }

Maternal germline clonal analysis demonstrates a maternal effect, defects in segment polarity, that is rescuable by introduction of the wild-type copy of the gene from the father.

Class I fu allele.

Class I mutation based on interaction with Su(fu)LP, suppression of embryonic and adult phenotype.

Class I allele.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (53)