FlyBase Allele Report: Dmel\fu[1]

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.

(Narbonne-Reveau et al., 2006)

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.

(Besse et al., 2002)

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.

(Glise et al., 2002)

Hemizygous mutants raised at 18^oC 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.

(Inaki et al., 2002)

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.

(Aza-Blanc et al., 2000)

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

(Delattre et al., 1999)

The wings of hemizygotes show a distal and proximal fusion of wing veins L3 and L4. In fu¹ and kn^col-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.

(Vervoort et al., 1999)

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.

(Alves et al., 1998)

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

(Biehs et al., 1998)

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.

(Epps et al., 1997)

Medial head structures are absent and replaced by frons material.

(Royet and Finkelstein, 1996)

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

(Therond et al., 1996)

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.

(Pham et al., 1995)

fu¹/fu^v22 females are viable and have non-tumorous ovaries.

(Forbes et al., 1993)

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.

(Held, 1993)

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

(Diaz-Benjumea and Garcia-Bellido, 1990)

Anomalies of adult cuticular structures and tumorous ovaries.

(Preat et al., 1990)

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.

(Busson et al., 1988)

Embryos derived from fu¹/fu^10C 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/fu^10C 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/fu^1A4 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.

(Martinez Arias, 1985)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

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

(Delattre et al., 1999)

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

(Delattre et al., 1999)

Suppressed by

Statement

Reference

fu¹ has visible phenotype, suppressible by Scer\GAL4^en-e16E/Xlae\Gli1^UAS.Tag:MYC

(Aza-Blanc et al., 2000)

fu¹ has visible | recessive phenotype, suppressible by Su(fu)^LP

(Delattre et al., 1999)

fu¹ has visible | recessive phenotype, suppressible by Scer\GAL4^ptc-559.1/ci^UAS.Tag:HA

(Alves et al., 1998)

Enhancer of

Statement

Reference

fu¹ is an enhancer of lethal | pupal stage phenotype of Scer\GAL4^da.G32, Su(fu)^UAS.cDa

(Dussillol-Godar et al., 2006)

Suppressor of

Statement

Reference

fu¹ is a suppressor of increased cell death phenotype of bi^omb-1, puc^E69

(Adachi-Yamada and O'Connor, 2002)

fu¹ is a suppressor | partially of visible phenotype of Scer\GAL4^en-e16E, Xlae\Gli1^UAS.Tag:MYC

(Aza-Blanc et al., 2000)

fu¹ is a suppressor of visible | dominant phenotype of hh^Mrt

(Alves et al., 1998)

fu¹ is a suppressor of visible phenotype of Scer\GAL4^en-e16E, hh^UAS.cIa

(Alves et al., 1998)

Other

Statement

Reference

ci^Ce-4, fu¹ has visible | recessive phenotype

(Alves et al., 1998)

ci^Ce-4, fu¹ has visible | dominant phenotype

(Alves et al., 1998)

Phenotype Manifest In

Enhanced by

Statement

Reference

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

(Delattre et al., 1999)

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

(Delattre et al., 1999)

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

(Delattre et al., 1999)

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

(Delattre et al., 1999)

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

(Vervoort et al., 1999)

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

(Vervoort et al., 1999)

fu¹ has wing vein L3 phenotype, enhanceable by oro¹

(Epps et al., 1997)

fu¹ has wing vein L4 phenotype, enhanceable by oro¹

(Epps et al., 1997)

fu¹ has lateral ocellus phenotype, enhanceable by oro¹

(Epps et al., 1997)

fu¹ has wing vein L3 phenotype, enhanceable by oro²

(Epps et al., 1997)

fu¹ has wing vein L4 phenotype, enhanceable by oro²

(Epps et al., 1997)

fu¹ has lateral ocellus phenotype, enhanceable by oro²

(Epps et al., 1997)

Suppressed by

Statement

Reference

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

(Besse et al., 2002)

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

(Besse et al., 2002)

fu¹ has wing phenotype, suppressible by Scer\GAL4^en-e16E/Xlae\Gli1^UAS.Tag:MYC

(Aza-Blanc et al., 2000)

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

(Delattre et al., 1999)

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

(Delattre et al., 1999)

fu¹ has wing phenotype, suppressible by Scer\GAL4^ptc-559.1/ci^UAS.Tag:HA

(Alves et al., 1998)

fu¹ has phenotype, suppressible by Su(fu)^LP

(Preat et al., 1993, Preat, 1992)

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

(Preat, 1992)

NOT suppressed by

Statement

Reference

fu¹ has wing vein L3 phenotype, non-suppressible by kn^UAS.cVa/Scer\GAL4^unspecified

(Vervoort et al., 1999)

fu¹ has wing vein L4 phenotype, non-suppressible by kn^UAS.cVa/Scer\GAL4^unspecified

(Vervoort et al., 1999)

Enhancer of

Statement

Reference

fu¹ is an enhancer of wing phenotype of Scer\GAL4^da.G32, Su(fu)^UAS.cDa

(Dussillol-Godar et al., 2006)

fu¹ is an enhancer of prothoracic leg phenotype of Scer\GAL4^da.G32, Su(fu)^UAS.cDa

(Dussillol-Godar et al., 2006)

fu¹ is an enhancer of sex comb | increased number phenotype of Scer\GAL4^da.G32, Su(fu)^UAS.cDa

(Dussillol-Godar et al., 2006)

fu¹ is an enhancer of metathoracic leg phenotype of Scer\GAL4^da.G32, Su(fu)^UAS.cDa

(Dussillol-Godar et al., 2006)

fu¹ is an enhancer of wing | anterior phenotype of Scer\GAL4^71B, ptc^D584N.UAS

(Johnson et al., 2002)

fu[+]/fu¹ is an enhancer of wing vein L4 phenotype of kn^col-1

(Vervoort et al., 1999)

fu[+]/fu¹ is an enhancer of wing vein L3 phenotype of kn^col-1

(Vervoort et al., 1999)

Suppressor of

Statement

Reference

fu¹ is a suppressor of wing cell phenotype of Scer\GAL4^71B, smo^ΔFU.UAS

(Malpel et al., 2007)

fu¹ is a suppressor of wing phenotype of bi^omb-1, puc^E69

(Adachi-Yamada and O'Connor, 2002)

fu¹ is a suppressor of wing vein | ectopic phenotype of Scer\GAL4^71B, ptc^D584N.UAS

(Johnson et al., 2002)

fu¹ is a suppressor | partially of wing phenotype of Scer\GAL4^en-e16E, Xlae\Gli1^UAS.Tag:MYC

(Aza-Blanc et al., 2000)

fu¹ is a suppressor of wing vein L2 phenotype of hh^Mrt

(Alves et al., 1998)

fu¹ is a suppressor of wing | anterior | distal phenotype of hh^Mrt

(Alves et al., 1998)

fu¹ is a suppressor of first posterior wing cell phenotype of Scer\GAL4^en-e16E, hh^UAS.cIa

(Alves et al., 1998)

fu¹ is a suppressor of wing vein L3 phenotype of Scer\GAL4^en-e16E, hh^UAS.cIa

(Alves et al., 1998)

fu¹ is a suppressor of dorsal row of double row of wing sensilla phenotype of Scer\GAL4^en-e16E, hh^UAS.cIa

(Alves et al., 1998)

fu¹ is a suppressor of ventral row of double row of wing sensilla phenotype of Scer\GAL4^en-e16E, hh^UAS.cIa

(Alves et al., 1998)

Other

Statement

Reference

Scer\GAL4^da.G32, Su(fu)^UAS.cDa, fu¹ has wing vein L2 phenotype

(Dussillol-Godar et al., 2006)

Scer\GAL4^da.G32, Su(fu)^UAS.cDa, fu¹ has wing vein L3 phenotype

(Dussillol-Godar et al., 2006)

Scer\GAL4^da.G32, Su(fu)^UAS.cDa, fu¹ has wing margin phenotype

(Dussillol-Godar et al., 2006)

Scer\GAL4^da.G32, Su(fu)^UAS.cDa, fu¹ has wing vein L4 phenotype

(Dussillol-Godar et al., 2006)

Scer\GAL4^71B, fu¹, ptc^D584N.UAS has first posterior wing cell phenotype

(Johnson et al., 2002)

Scer\GAL4^71B, fu¹, ptc^D584N.UAS has first basal wing cell phenotype

(Johnson et al., 2002)

Su(fu)^LP, fu¹ has anterior crossvein phenotype

(Delattre et al., 1999)

ci^Ce-4, fu¹ has scutellum phenotype

(Alves et al., 1998)

ci^Ce-4, fu¹ has wing phenotype

(Alves et al., 1998)

ci^Ce-4, fu¹ has adult thorax phenotype

(Alves et al., 1998)

Additional Comments

Genetic Interactions

Statement

Reference

In escaper flies that express Su(fu)^Scer\UAS.cDa, under the control of Scer\GAL4^da.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\GAL4^da.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\GAL4^da.G32 flies.

(Dussillol-Godar et al., 2006)

bi^omb-1, puc^E69 double heterozygotes exhibit a strong wing notch and cell death increase phenotype. These phenotypes are suppressed by the addition of fu¹.

(Adachi-Yamada and O'Connor, 2002)

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.

(Delattre et al., 1999)

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

(Vervoort et al., 1999)

fu¹; ci^Ce-4/+ flies generally die as pupae, although some adults eclose. The latter have small wings, a reduced thorax and lack the scutellum. Expression of ci^{Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^ptc-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 hh^Scer\UAS.cIa expressed under the control of Scer\GAL4^en-e16E. Suppresses the wing phenotype of hh^Mrt heterozygotes.

(Alves et al., 1998)

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.

(Epps et al., 1997)

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.

(Preat et al., 1993)

Xenogenetic Interactions

Statement

Reference

The wing overgrowth phenotype caused by expression Xlae\Gli1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^en-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\Gli1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^en-e16E.

(Aza-Blanc et al., 2000)

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.

(Delattre et al., 1999)

Complementation and Rescue Data

Rescued by

fu¹ is rescued by fu^hs.PT

(Therond et al., 1999)

fu¹ is rescued by fu^+t5.1

(Therond et al., 1993)

fu¹ is rescued by fu^+t5.1

(Preat et al., 1990)

Partially rescued by

fu¹ is partially rescued by fu^UAS.cAa/Scer\GAL4^dpp.blk1

(Alves et al., 1998)

Comments

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

(Therond et al., 1993)

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

(Preat et al., 1990)

Images (1)

Holtzman, S. and Kaufman, T. (2013)

Mutant

Wild-type

Stocks (4)

1533

106372

105695

107535

In(1)Bar^M1, y² oc¹ ptg¹ Bar^M1/Insc, fu¹/R(YL)/C(1;YS)1, y² oc¹ ptg¹ fu¹

Notes on Origin

Discoverer

Bridges, 4th Nov. 1912.

Comments

Not rescued by: kn^Scer\UAS.cVa { Scer\GAL4^unspecified }

(Vervoort et al., 1999)

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.

(Perrimon et al., 1989)

Class I fu allele.

(Pham et al., 1995)

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

(Therond et al., 1996)

Class I allele.

(Robbins et al., 1997)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

fu¹

(Ranieri et al., 2014, Cheng et al., 2012, Casso et al., 2011, Ayers et al., 2009, Christensen et al., 2009.2.28, Cook et al., 2008.9.3, Malpel et al., 2007, Dussillol-Godar et al., 2006, Narbonne-Reveau et al., 2006)

Name Synonyms

Secondary FlyBase IDs

References (53)

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