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General Information
Symbol
Dmel\ft8
Species
D. melanogaster
Name
FlyBase ID
FBal0004794
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ftfd, fatfd, fat8, ftl(2)fd, l(2)ftfd, l(2)fd
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Reported amino acid change:

S981term

Comment:

Ser981 (AGC) is changed to a stop codon in the ft8 allele.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: S981term.

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 ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

ft8/ftG-rv transheterozygous pharates exhibit severe hair orientation defects in the anterior dorsal abdomen, as compared to controls.

Wing discs of ft8 mutant larvae are overgrown.

Homozygous clones generated using the eyFLP system result in overgrowth of the head capsule and slightly larger eyes than normal.

ft8/ft8 eyes (created by the EGUF method in otherwise heterozygous animals) contain significantly increased number of interomatidial cells (IOC) in the pupal retina compared to wild-type.

ftG-rv/ft8 transheterozygotes rarely survive to third instar larval stage (but never to adulthood) and the survivors display decreased number of photoreceptor cells in the eye disc and overgrown wing discs compared to wild-type.

ftG-rv/ft8; ftT:SV5\V5 wings are normal; ftG-rv/ft8; ftΔD.T:SV5\V5 wings are slightly overgrown, rounder and have decreased spacing between the crossveins compared to controls; ftG-rv/ft8; ftΔF.T:SV5\V5 wings are not enlarged but have greatly reduced spacing between the crossveins.

ft8/ftG-rv and ft8/ft61 imaginal discs are larger and have more folds than controls.

ft8 mutant wing disc clones do not show neoplastic transformation.

Homozygous clones in the eye show progressive retinal degeneration. This phenotype is cell autonomous. Autophagic vesicles with partially degraded content accumulate with age in the mutant photoreceptor cells compared to wild-type cells.

ftG-rv/ft8 mutant larvae show a decrease in the number of glial cells in the eye disc and a lack of glial overgrowth.

ftG-rv/ft8 stage 16 embryos have shorter dorsal trunks than normal, although they are contiguous.

Wing and eye imaginal discs show overgrowth in ft8/ftG-rv pupae. The pupal abdomens are not overgrown, but show planar cell polarity defects.

ft8/ft422 mutant imaginal disc clones are significantly larger than wild-type discs.

Clones of ft8/ft422 mutant tissue generated in imaginal discs via the Flp/FRT technique outgrow their wild-type twinspot clones and exhibit a rounded shape, in contrast to the jagged appearance of wild-type clones.

ft8/ft422 mutant tissue is overrepresented in comparison with wild-type tissue, and eyes containing ft8/ft422 mutant tissue are rough in appearance.

Imaginal discs heterozygous for ft8 are normal in size and shape and give rise to normally sized and patterned adult organs.

Eye and wing imaginal discs mutant for ft8/ft422 exhibit substantial increases in size and display a 'rippled' morphology compared to wild-type discs, which are mostly flat.

When reared at 18oC, ft8/ft422 mutants are lethal at the early pupal stages of development.

ft8 mutant tissue re-enters the cell cycle in an ectopic fashion several ommatidial rows posterior to the morphogenetic furrow, where wild-type counterpart cells are quiescent. An increase in the number of cells in S phase is also found in clones of ft8 mutant tissue in anterior portions of eye imaginal discs, suggesting that cells lacking ft proliferate more quickly than wild-type cells in populations of cells that are proliferating asynchronously.

ft8 tissue exhibits moderate increases in the number of interommatidial cells.

ft8 mutant retinal clones may exhibit a slight increase in apoptosis compared to wild-type.

ft8 clones in the leg induce outgrowths in 12 out of 50 cases and cause the appearance of vesicles in the cuticular tissue of the legs in 40 out of 50 cases.

ft8 clones generated in the wing disc are abnormally large and round.

In ft8/ftG-rv mutants, the polarity of hairs and bristles on the adult cuticle is disturbed, resulting in swirling patterns of hairs and bristles in many tissues.

ft8 mutant clones generated on the abdomen show severely disturbed hair polarity. These clones exhibit some hairs at an angle greater than 90o relative to the normal orientation.

32 out of 33 ft8 clones in the eye include ommatidia rotated more than 90o away from the normal position.

The wing discs of ftG-rv/ft8 larvae show extensive tissue overgrowth during the late third instar.

Expression of ftΔICD.Scer\UAS.T:Ivir\HA1, under the control of either Scer\GAL4Act5C.PI or Scer\GAL4da.G32, enhances the wing disc tissue overgrowth phenotype of ftG-rv/ft8 mutants.

Mutant ft8 clones, generated through FLP-induced recombination are significantly larger than their wild-type twin-spots (by approximately 1.92 times). There are also small, but reproducible increases in BrdU labeling in ft8 mutant cells ahead of the morphogenetic furrow, indicating an increase in cell division. There is also a marked delay in the onset of the second mitotic wave.

ft8 mutant clones in pupal retinas exhibit a significant increase in the number of secondary cells per ommatidium (wild-type 6, ft8 9).

Induction of ft8 mutant clones in the eye results in heads that are much larger than those of wild-type siblings, with a dramatic overgrowth of the head capsule.

Ommatidia are more widely-spaced in ft8 mutant clones, indicating an excess of interommatidial cells in the larval eye disc.

In contrast to wild-type cells, ft8 mutant eye cell clones fail to arrest the cell cycle after the second mitotic wave and continue to proliferate. This ectopic proliferation occurs only in developmentally uncommitted cells, but not in differentiating photoreceptor cells.

ft8/ftG-rv mutant animals die during the early stages of pupal development and show severely overgrown imaginal disc derivatives.

Late third instar ft8/ftG-rv wing discs exhibit disproportionate overgrowth of the proximal wing pouch compared to other parts of the wing disc.

Planar polarity is disrupted in ft8/ftchance eyes; dorsal and ventral ommatidia are intermixed and no obvious equatorial line can be drawn.

Wild-type ommatidia on the polar side of homozygous clones in the eye frequently show planar polarity inversions.

Very large ft8 somatic clones in the wing often show marked swirls. These swirls show no reproducible pattern in a given region from one wing to another. In these large clones the cell-cell alignment shows continuity within and across clone boundaries. In contrast, in very small clones in the wing the orientation of pre-hairs is always normal.

About 40% of ommatidia within somatic clones in the adult eye frequently have reversed dorsal ventral polarity. Occasional reversals of polarity are also seen in wild-type ommatidia bordering the polar side of the mutant tissue. When homozygous mutant clones are made specifically in the equatorial R3/R4 precursor, almost all (91%) of the consequent ommatidia are in the reverse polarity. When clones are made specifically in the polar R3/R4 precursor, all of the consequent ommatidia are in the wild-type polarity. The mutant photoreceptor precursor eventually becomes an R4 photoreceptor 95% of the time (50% in wild-type).

Mutant imaginal discs do not show an obvious duplication of structures, but overgrow in multiple directions. Mutant clones make outgrowths which are not deficient in bristles, having more than wild type tissue. Some form vesicles with internally facing bristles.

Cell death is abundant in homozygous wing imaginal discs.

Hyperplastic imaginal disc overgrowth, affecting all discs. Discs implanted into wild type hosts for metamorphosis overgrow and form normal imaginal structures. ft8/ft4 mutant larvae do not grow beyond the maximum size seen for wild type larvae.

Cause a hyperplastic tumour-like overgrowth of the imaginal discs resulting in large discs that contain many convoluted and abnormal folds of epithelial cells. During metamorphosis mutant discs differentiate into defective adult structures. Homozygotes die during the pupal stage.

Eggs derived from homozygous germ-line clones are apparently normal, but the resulting embryos do not develop to the stage of cuticle formation. Females that contain homozygous germ-line clones deposit all their eggs during the first four days of adulthood.

Homozygous 10 day-old larvae have smaller salivary glands than wild-type. Few of the larvae form prepupae.

Hyperplastic growth. Imaginal discs show normal gap-junctional communication.

Imaginal discs overgrow in homozygous larvae. The wing discs have an abnormal folding pattern. Outgrowth occurs from the proximal folds region. Pupariation is delayed by about 3.2 days at 25oC. Homozygous ft8 wing discs transplanted into wild-type adult hosts continue to overgrow, suggesting that the wing disc overgrowth caused by ft8 is disc-autonomous. A few homozygotes die as pharate adults, with abnormal legs, eyes, antennae and wings, the legs being most severely affected. Transheterozygous combinations of ft8 with other ft alleles generally produce the same phenotype as in homozygous ft8 animals, although ft8 in combination with ft1, ft2 or ft3 produces viable, "fat" flies.

pupal lethal

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

ft8 has lethal phenotype, suppressible | partially by Dlish04/Dlish04

ft8 has increased cell number | somatic clone | larval stage phenotype, suppressible by yki[+]/ykiB5

ft8/ftG-rv has hyperplasia phenotype, suppressible | partially by wgspd-fg

NOT suppressed by
Enhancer of
Statement
Reference

ft8 is an enhancer of visible | recessive phenotype of l(2)gd11

Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference

ft8/ftG-rv has eye disc | pupal stage phenotype, suppressible by appe6

ft8 has wing disc | somatic clone phenotype, suppressible by d1

ft8 has leg | somatic clone phenotype, suppressible by dGC13

ft8 has microchaeta | somatic clone phenotype, suppressible | partially by dGC13

ft8 has eye disc | somatic clone | larval stage phenotype, suppressible by yki[+]/ykiB5

ft8/ftG-rv has wing disc phenotype, suppressible | partially by wgspd-fg

ft8 has wing | pharate adult stage phenotype, suppressible | partially by vg1

NOT suppressed by
Enhancer of
Statement
Reference

ft8 is an enhancer of imaginal disc phenotype of l(2)gd11

ft8 is an enhancer of wing disc phenotype of l(2)gd11

ft8 is an enhancer of haltere disc phenotype of l(2)gd11

ft8 is an enhancer of genital disc phenotype of l(2)gd11

ft8 is an enhancer of macrochaeta phenotype of l(2)gd11

ft8 is an enhancer of wing vein phenotype of l(2)gd11

Suppressor of
Statement
Reference

ft8 is a suppressor of arista | supernumerary phenotype of obk1

Other
Additional Comments
Genetic Interactions
Statement
Reference

Expression of DlishGD7133 RNAi under the control of Scer\GAL4hh.PU suppresses (in the posterior) the wing disc overgrowth characteristic for ft8 mutant larvae.

The complete lethality of ft8 homozygotes is partially suppressed by combination with Dlish04 in homozygous state and the wings of the double mutant adults are mispatterned but of nearly normal size (while ft8 mutant larval wing discs are strongly overgrown).

Double homozygous ft8, RtGEFp1036 clones generated using the eyFLP system result in substantial overgrowth of the head, particularly in the ptilinum.

Double homozygous ft8, exe1 clones generated using the eyFLP system result in substantial overgrowth of the head, particularly in the ptilinum.

Gitex21C mutants carrying ft8 clones generated using the eyFLP system show substantial overgrowth of the head, particularly in the ptilinum.

The supernumerary inter-ommatidial cells in the pupal retina phenotype characteristic for ft8/ft8 eyes (created by the EGUF method in otherwise heterozygous animals) cannot be restored by combination with ZyxΔ41/ZyxΔ41.

The low rate of survival of ftG-rv/ft8 transheterozygotes to third instar larval stage (and never to adulthood), the loss of photoreceptor cells in the eye discs or the overgrowth of the wing disc cannot be suppressed by combination with ZyxΔ41/ZyxΔ41.

Scer\GAL4αTub84B.PL-mediated expression of Fbxl7Scer\UAS.T:Zzzz\FLAG suppresses ft8/ft61, but not ft8/ftG-rv, phenotypes, resulting in viable flies.

ft8 l(2)gl4 double mutant clones in the proximal domain of the wing disc exhibit overproliferation and neoplastic transformation. Clones in the distal domain are eliminated.

Flies expressing wtsScer\UAS.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL rescue the lethality and third instar larval wing disc overgrowth phenotypes seen in ft8/ftG-rv mutants, but the wing hair phenotypes are still present. Rather than pointing distally as in wild type, the wing hairs in these flies are misoriented and swirling patterns can be observed. A strong planar cell polarity defect is also seen in the abdominal hairs and the wing anterior-posterior crossvein distance is reduced.

Expression of ftT:SV5\V5 fully rescues the planar cell polarity defects seen in ft8/ftG-rv mutant wings and abdomens expressing wtsScer\UAS.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL. The reduced anterior-posterior crossvein distance phenotype is also suppressed.

Flies expressing ftΔEGF.T:SV5\V5 (co-expressed with wtsScer\UAS.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL) in a ft8/ftG-rv mutant background do not exhibit any wing phenotypes compared to flies expressing wtsScer\UAS.T:Hsap\MYC alone.

Expression of ftΔICD.T:SV5\V5 partially rescues the planar cell polarity defects seen in ft8/ftG-rv mutant wings and abdomens expressing wtsScer\UAS.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL. The reduction in anterior-posterior crossvein distance appears to be partially rescued, although crossveins are often incomplete, making it difficult to calculate. The abdominal and wing hair polarity defects are also partially suppressed.

Expression of btl::ftftICD.T:Ivir\HA1,T:λ\cI-DD under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals rescues disc overgrowth, allows eclosion and improves hair planar cell polarity defects in the wing and abdomen.

Expression of dsScer\UAS.cTa under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals does not detectably improve hair planar cell polarity defects in the abdomen.

dGC13 suppresses the retinal neurodegeneration seen in ft8 clones.

ykiB5/+ partially suppresses the retinal neurodegeneration seen in ft8 clones.

Expression of ykiScer\UAS.cHa under the control of Scer\GAL4tub.PU within ft8 clones suppresses the retinal degeneration normally seen in them.

The lethality and overgrowth phenotypes of ftG-rv/ft8 animals are rescued by Scer\GAL4tub.PU-mediated overexpression of wtsScer\UAS.T:Hsap\MYC. However, these animals still show obvious planar cell polarity phenotypes in multiple tissues.

The disc overgrowth phenotypes of ft8/ftG-rv pupae are suppressed by appe6 and the abdominal planar cell polarity (PCP) and lethality phenotypes are reduced in the double mutants compared to the ft8/ftG-rv single mutant. The double mutant adults have PCP defects in proximal portions of the wing, but not in the distal wing.

ft8/ft422 mutants, heterozygous for wtsx1 exhibit a significant increase in size, both from wild-type and the ft8/ft422 double mutant, and display an even more 'rippled' morphology.

ft8/ft422 mutants, heterozygous for ykiB5 exhibit a size and morphology similar to those of wild-type discs, indicating suppression of the ft8/ft422 phenotype through ykiB5.

ft8/ft422 mutants, heterozygous for ykiB5 progress to the late pupal stage of development, with some surviving to adulthood. ft8 ykiB5/ft422 flies display defects in the size and morphology of eyes, wings, and some bristles.

ft8/exe1 double mutants display only a subtle increase in interommatidial cell number, as in ft8 or exe1 single mutants implying that both ft and ex are dispensible for the majority of pupal retinal apoptosis. Significant apoptosis is observed in both exe1 and ft8/exe1 mutant tissue, 28 hours after pupal formation.

In eye-discs mosaic for ft8, the expression hpoScer\UAS.cUa under the control of Scer\GAL4GMR.PF induces apoptosis as in wild-type tissue.

In eye-discs mosaic for ft8, the expression exScer\UAS.cBa under the control of Scer\GAL4GMR.PF induces apoptosis as in wild-type tissue.

Nl1N-ts1;ft8/ft422 double mutant larvae grown at restrictive temperature show distal wing growth.

ft8, dGC13 double mutant clones in the leg do not induce outgrowths or the appearance of vesicles in the cuticular tissue, a phenotype seen when ft8 single mutant clones are generated in the leg.

ft8, d1 double mutant clones generated in the wing are normal in size and shape like d1 single clones, while ft8 single mutant clones are abnormally large and round.

dGC13 partially suppresses the polarity phenotype of ft8. This is evidenced by comparison of ft8 and dGC13 single mutant clones with ft8, dGC13 double mutant clones in the abdomen. While all (39/39) ft8 clones have a polarity phenotype, only 54% of ft8, dGC13 clones show this phenotype (vs 3% of dGC13 clones). The ft8 single mutant clones exhibit some hairs at an angle greater than 90o relative to the normal orientation, while only 26% of ft8, dGC13 clones had hairs of this angle.

The polarity phenotype of ft8, dGC13 double mutant clones in the eye is similar to that of ft8 single mutant clones (28 vs 32 out of 33 clones including ommatidia rotated more than 90o away from the normal position, respectively.

dsUAO71, ftG-rv/ft8 double mutant larvae show an enhancement of the wing disc overgrowth phenotype of ftG-rv/ft8 single mutants.

Overexpression of hpoScer\UAS.cPa in the developing eye, under the control of Scer\GAL4GMR.PF induces cell death in ft8 mutant cells.

The growth-promoting effects of ft8 clones induced in the eye is strongly suppressed by one copy of ykiB5.

ft8 clones in a ykiB5/+ mutant background show a reduced growth advantage over their sister twin spots. This reduction of growth advantage is statistically highly significant and is consistent with a placement of yki downstream of ft in proliferation control.

Clones of cells in the eye, doubly-mutant for ft8 and Mer4 exhibit a dramatic increase in the number of interommatidial cells compared to the more moderate increases seen in single mutants.

One copy of exe1 enhances the lethality of ft8/ftG-rv animals. Those that are wild-type for exe1 but mutant for ft8/ftG-rv emerge as 0.32% of the progeny, whereas those that are also mutant for exe1 emerge as 0.269% of the progeny, a small, but statistically significant difference.

Overexpression of hpoScer\UAS.cPa in the developing eye, under the control of Scer\GAL4GMR.PF induces cell death in ft8 mutant cells.

Nearly all ft8 ykiB5/ftG-rv mutant animals develop into adults, although they do not hatch from the pupal case as they have some leg defects and head overgrowths. In contrast, all ft8/ftG-rv mutant animals die during the early stages of pupal development and show severely overgrown imaginal disc derivatives. This indicates that ykiB5 suppresses the overgrowth phenotypes of ft8/ftG-rv mutant imaginal discs.

Overgrowth of the proximal wing disc in ft8/ftG-rv animals is suppressed by wgspd-fg/wgspd-fg.

bonsaik08322 ft8 double mutant animals first exhibit the extreme growth delay seen in bonsaik08322 single mutants, reaching the L3 stage after 6 days instead of the normal 2 days when raised at 25oC. However, in mid-L3, double mutants discs start to grow and quickly show hyperplasia, as is seen in ft8 single mutants.

Clones double mutant for l(2)gd11 and ft8 show extensive overgrowth. Wing discs bend at the hinge region and show many extra folds that probably result from excess proliferation. Discs are initially smaller than wild type or either single mutant but eventually outgrow them. Leg discs are greatly overgrown, approximating the size of a wild type wing disc, and show no sign of duplications, except for the first leg disc. Haltere disc is also overgrown with an occasional duplication of the capitellum pouch. The eye-antennal disc is massively overgrown and becomes the largest disc, with duplications and triplications of the antenna knob and the retinal field. Genital discs duplicate and show many extra folds. Double mutants do not survive to pharate adults. Animals mutant for l(2)gd11 and heterozygous for ft8 die before the pharate adult stage. dppd5 suppresses the duplicative ability of second leg discs in ft8 l(2)gd11/l(2)gd11 mutants. Imaginal discs from ds38k l(2)gd11/l(2)gd11 larvae resemble those of ft8 l(2)gd11/l(2)gd11 rather than l(2)gd11/l(2)gd11 in that wing, haltere, second and third leg discs are duplicated.

Pharate adult wings of ft8 vg1 double mutants are partially restored compared to the single homozygotes. Clones in a vg1 homozygous background frequently show necrotic masses.

Xenogenetic Interactions
Statement
Reference

Expression of ft::Hsap\FAT4T:SV5\V5 partially rescues the planar cell polarity defects seen in ft8/ftG-rv mutant wings expressing wtsScer\UAS.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL. The abdominal hair defects are completely rescued and the reduction in anterior-posterior crossvein distance is partially suppressed.

Expression of one copy of ft::Hsap\FAT4T:SV5\V5 fails to suppress the wing overgrowth phenotypes seen in ft8/ftG-rv mutant flies expressing one copy of ftΔD.T:SV5\V5.

Expression of one copy of ft::Hsap\FAT4T:SV5\V5 partially suppresses the wing crossvein spacing and hair polarity phenotypes seen in ft8/ftG-rv mutant flies expressing one copy of ftΔF.T:SV5\V5.

Complementation and Rescue Data
Fails to complement
Partially rescued by

ft8/ftG-rv is partially rescued by ftΔD.Tag:V5

ft8/ftG-rv is partially rescued by ftΔF.Tag:V5

ft8/ftG-rv is partially rescued by ftΔD.Tag:V5

ft8/ftG-rv is partially rescued by ftΔE.Tag:V5

ft8/ftG-rv is partially rescued by ftΔF.Tag:V5

ft8/ftG-rv is partially rescued by ftmV.Tag:V5

Comments

Expression of either ftΔECD-PH+Hippo.Scer\UAS.T:Ivir\HA1 or ftΔECD-Hippo.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hh.PU suppresses (in the posterior) the wing disc overgrowth characteristic for ft8 mutant larvae.

Expression of ftΔA.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. The rescued animals appear morphologically normal and only a negligible wing hair planar cell polarity phenotype is seen. The abdominal hair polarity phenotype is fully rescued. The intercellular ridges that run from anterior to posterior in the ft8/ftG-rv mutant posterior wings run proximally to distal in rescue animals, as is seen in wild type.

Expression of ftΔB.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. The rescued animals appear morphologically normal and only a negligible wing hair planar cell polarity phenotype is seen. The abdominal hair polarity phenotype is fully rescued. The intercellular ridges that run from anterior to posterior in the ft8/ftG-rv mutant posterior wings run proximally to distal in rescue animals, as is seen in wild type.

Expression of ftΔC.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. The rescued animals appear morphologically normal and only a negligible wing hair planar cell polarity phenotype is seen. The abdominal hair polarity phenotype is fully rescued. The intercellular ridges that run from anterior to posterior in the ft8/ftG-rv mutant posterior wings run proximally to distal in rescue animals, as is seen in wild type.

Expression of ftΔD.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. However the wings of the rescued flies are 29% larger than normal and the distance between the anterior and posterior crossveins in 73% of wild type. Only a negligible wing hair planar cell polarity phenotype is seen. The abdominal hair polarity phenotype is fully rescued. The intercellular ridges continue to run from anterior to posterior as in the ft8/ftG-rv mutant posterior wings, rather than proximally to distal, as is seen in wild type.

Expression of ftΔE.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. However the wings of the rescued flies are 8% larger than normal and the distance between the anterior and posterior crossveins in 87% of wild type. Only a negligible wing hair planar cell polarity phenotype is seen. The abdominal hair polarity phenotype is fully rescued. The intercellular ridges that run from anterior to posterior in the ft8/ftG-rv mutant posterior wings run proximally to distal in rescue animals, as is seen in wild type.

Expression of ftΔF.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. However the wings of the rescued flies are 4% larger than normal and shorter and wider than normal wings. The distance between the anterior and posterior crossveins is also reduced. Wing hair planar cell polarity phenotypes are still present, with the most proximal part of the wing, the costa, the most severely affected. A subtle phenotype is observed in the abdomen. The intercellular ridges continue to run from anterior to posterior as in the ft8/ftG-rv mutant posterior wings, rather than proximally to distal, as is seen in wild type.

Expression of ftΔEGF.T:SV5\V5 fails to rescue the lethality associated with ft8/ftG-rv.

Expression of one copy of ftΔF.T:SV5\V5 partially suppresses the wing overgrowth phenotype seen in ft8/ftG-rv mutant flies expressing one copy of ftΔD.T:SV5\V5.

Expression of one copy of ftΔD.T:SV5\V5 partially suppresses the wing crossvein spacing and hair polarity phenotypes seen in ft8/ftG-rv mutant flies expressing one copy of ftΔF.T:SV5\V5.

Expression of ftΔICD.T:SV5\V5 fails to rescue the lethality associated with ft8/ftG-rv and the wing discs these flies are overgrown compared to controls.

Expression of ftP32.T:SV5\V5 rescues the lethality and wing overgrowth phenotype associated with ft8/ftG-rv.

Expression of ftmI.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. However the wings of the rescued flies are 18% larger than normal. Wing hair polarity defects are partially rescued and the abdominal hair defects are fully rescued.

Expression of ftmV.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. However the wings of the rescued flies are larger than normal.

Expression of ftmIV.T:SV5\V5 rescues the lethality associated with ft8/ftG-rv. The abdominal and wing hair polarity phenotypes are fully rescued.

for both ft alleles in GA22:

Expression of ftScer\UAS.cMa under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals substantially improves hair planar cell polarity defects in the abdomen.

Expression of ftΔECD.Scer\UAS.T:Ivir\HA1 or ftΔECD2.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals rescues disc overgrowth, allows eclosion and substantially improves hair planar cell polarity defects in the wing and abdomen.

Expression of ftICD.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals does not rescue disc overgrowth or eclosion and does not detectably improve hair planar cell polarity defects in the abdomen.

Expression of ftΔECDΔN-1.Scer\UAS.T:Ivir\HA1 or ftΔECDΔN-2.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals rescues eclosion and very weakly improves hair planar cell polarity defects in the abdomen.

Expression of ftΔECDΔN-4.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals rescues eclosion but does not detectably improve hair planar cell polarity defects in the abdomen.

Expression of ftΔECDΔN-5.Scer\UAS.T:Ivir\HA1, ftΔECDΔN-6.Scer\UAS.T:Ivir\HA1 or ftΔECDΔICD.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals does not rescue eclosion and does not detectably improve hair planar cell polarity defects in the abdomen.

Expression of ftΔECDΔ9-C.Scer\UAS.T:Ivir\HA1, ftΔECDΔ8-C.Scer\UAS.T:Ivir\HA1, ftΔECDΔ7-C.Scer\UAS.T:Ivir\HA1, ftΔECDΔ6-C.Scer\UAS.T:Ivir\HA1, ftΔECDΔ1-3.Scer\UAS.T:Ivir\HA1, ftΔECDΔ3-4.Scer\UAS.T:Ivir\HA1, ftΔ9-C.Scer\UAS.T:Ivir\HA1 or ftΔ7-C.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals rescues eclosion and strongly improves hair planar cell polarity defects in the abdomen.

Expression of ftΔECDΔ5-C.Scer\UAS, ftΔECDΔ4-C.Scer\UAS.T:Ivir\HA1, ftΔECDΔ2-C.Scer\UAS.T:Ivir\HA1, ftΔECDΔ1-C.Scer\UAS.T:Ivir\HA1, ftΔECDΔ5-6.Scer\UAS.T:Ivir\HA1, ftΔECDΔ3-5.Scer\UAS.T:Ivir\HA1, ftΔECDΔ1-5.Scer\UAS.T:Ivir\HA1, ftΔ6-C.Scer\UAS.T:Ivir\HA1 or ftΔ5-C.Scer\UAS under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals does not rescue eclosion but strongly improves hair planar cell polarity defects in the abdomen of pharate adults.

Expression of ftΔECDΔN-1.Scer\UAS.T:Ivir\HA1 or ftΔECDΔN-2.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals does not rescue hair planar cell polarity defects in the wing.

Expression of ftΔN-1.Scer\UAS.T:Ivir\HA1 or ftΔN-2.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals rescues eclosion and weakly improves hair planar cell polarity defects in the abdomen.

Expression of ftΔN-4.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals weakly rescues eclosion and very weakly improves hair planar cell polarity defects in the abdomen.

Expression of ftΔN-5.Scer\UAS.T:Ivir\HA1, ftΔN-6.Scer\UAS.T:Ivir\HA1 or ftΔICD.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals does not rescue eclosion but very weakly improves hair planar cell polarity defects in the abdomen of pharate adults.

Expression of ftΔ8-C.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act.PU in ftG-rv/ft8 animals weakly rescues eclosion and strongly improves hair planar cell polarity defects in the abdomen.

Expression of ftScer\UAS.cMa or ftΔECD.Scer\UAS in the posterior wing pouch, driven by Scer\GAL4en-e16E, rescues the overgrowth phenotype of ftG-rv/ft8 mutants in this region, but does not rescue overgrowth in the anterior.

Expression of ftΔECD.Scer\UAS, under the control of either Scer\GAL4Act5C.PI or Scer\GAL4da.G32, rescues the lethality of ftG-rv/ft8 mutants and is effective in rescuing the wing disc overgrowth phenotype.

Expression of ftΔECD.Scer\UAS under the control of Scer\GAL4Act5C.PI in ftG-rv/ft8 mutants partially rescues the abdominal planar cell polarity defect.

Expression of ftScer\UAS.cMa under the control of Scer\GAL4Act5C.PI rescues the lethality and wing disc overgrowth phenotype of ftG-rv/ft8 mutants and partially rescues the abdominal planar cell polarity defect.

ftScer\UAS.cMa; Scer\GAL4da.G32 rescues the pupal lethality of ftG-rv/ft8 and substantially rescues planar cell polarity and tarsal segment defects in these animals.

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Homozygous salivary glands can respond to added ecdysterone when incubated in vitro.

Pole cell transplantation and germ-line clonal analysis indicates that the ft product is required in the germ-line for normal egg development and/or subsequent embryogenesis. Analysis of follicle cell mosaics indicates that ft is not required for follicle cell functions.

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