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General Information
Symbol
Dmel\fz15
Species
D. melanogaster
Name
FlyBase ID
FBal0004931
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
fzH51
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G14367034A

Reported nucleotide change:

T?A

Amino acid change:

W500term | fz-PA; W500term | fz-PC

Reported amino acid change:

W500term

Comment:

TGG to TGA nonsense mutation at amino acid 500.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology

Polytene chromosomes normal.

Nature of the lesion
Statement
Reference

Amino acid replacement: W500term.

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

axon & dorsal cluster neuron

trichome & adult abdomen | somatic clone

trichome & adult abdomen | somatic clone | cell non-autonomous

trichome & pleural membrane, with Scer\GAL4en-e16E, fzUAS.cSa

trichome & pleural membrane | somatic clone

trichome & pleural membrane | somatic clone, with Scer\GAL4Ubx.PdC, fzUAS.cSa

trichome & pleural membrane | somatic clone | cell non-autonomous

trichome & pleural membrane | somatic clone | cell non-autonomous, with Scer\GAL4Ubx.PdC, fzUAS.cSa

Detailed Description
Statement
Reference

Homozygous fz15 mutants are viable but exhibit planar polarity defects.

Mutant adults have an average of 3.9 +/- 0.3 extra tarsal joints in the leg compared to wild type.

fz15/fz30 transheterozygous mutants exhibit 'rough' eyes. A Fourier transform of the mutant eye image reveals a set of concentric circles reflecting a non-ordered arrangement, instead of distinct reflexes up to the fourth order, as in wild-type. More intense regions arranged as apexes of hexagons, reflecting the existence of small regions of the eye surface with dense hexagonal ommatidial packing, can also be seen in the Fourier transform of these mutants. The diffraction pattern from the cornea of these transheterozygotes is noticeably smeared and only reflexes of the first order arranged in the hexagon apexes are observed. This confirms the limited periodicity of ommatidial arrangement and the existence of only small regions with dense hexagonal packing of ommatidia in the mutant flies.

While the borders of the wild-type ommatidia are tightly aligned to each other, irregular infiltrations of the lens material fill the gap between the lenses of fz15/fz30 transheterozygous mutants. These infiltrations indicate that the packing of the mutant lenses is less compact, making them more loosely aligned to each other, explaining the 'rough' appearance and the lack of regularity.

The surface of the ommatidial lens at the nano-scale represents the array of nipples with a cross-section of 250nm and height of 30nm. fz15/fz30 transheterozygous mutant nipples are shorter by 5nm but have the same broadness as those of wild-type flies.

fz23/fz15 mutant clones in the wing non-autonomously disrupt wing membrane ridges.

fz15 mutant border cells are predominantly found at the lagging edge of border cell clusters compared to wild-type cells that show a strong preference to migrate at the leading edge of the cluster.

In border cell clusters where both polar follicle cells are mutant for fz15 there is no preference for non-mutant border cells to take up the leading edge positions in the cluster. In border cell clusters where only one polar follicle cell is mutant for fz15, this mutant cell is observed towards the lagging end of the border cell cluster, whereas the polar cell retaining wild-type function is observed towards the leading edge of the cluster.

Border cell clusters from fz21/fz23 mutants show an average of 38.4 actin protrusions, reduced compared to the average of 94.8 in wild-type clusters.

fz15/fz21 clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes towards the clone.

In fz15/+ adult brains, there is a significant reduction in the number of dorsal cluster neuron axons that cross toward the medulla compared to wild-type brains.

Most larvae from fz15/fz21 mothers crossed with fz15/+ fathers have cuticles with normal morphology; only 2 of 30 exhibit fusions between segments. Another 2 mutants exhibit misplaced actin-based protrusions in denticle row 1.

fz15 somatic clones in the abdominal pleura have strong effects on planar cell polarity: the polarity of hair within the clone is randomised, except for the most anterior row of cells within the clone (normal polarity) and the most posterior row of cells within the clone (reversed polarity - hairs pointing into the clone). This reversal of hairs at the posterior of the clone extends behind the clone for about 2-4 rows of cells. This phenotype occurs wherever the clones are made, dorsally or ventrally, regardless of compartment, or of the presence of compartment boundaries.

fz15/fz21 ovaries show only very minor abnormalities.

The wings of fz15/fz25 animals have a trichome (wing hair) swirling pattern that is distinct from that due to ds33k/dsUAO71. Wing hairs in these wings form away from cell edges.

Only 47.1 +/- 8.9 % of ommatidia in fz37/fz15 flies have the correct chiral shape.

Mosaic ommatidia at the boundaries of homozygous clones can show incorrect chirality. In incorrect chiral ommatidia where the mosaic boundary separates the R3/R4 pair, the R4 cell is invariably mutant and the R3 cell is wild type. In these cases the presumptive R3 cell has developed as an R4 cell. The R3/R4 pair can also either both be mutant or both be wild-type in mosaic ommatidia with incorrect chirality. Chirally incorrect ommatidia that have wild-type R3 and R4 cells can occur at any position along the border of the clone, but are predominantly found at the polar side of the clone. Mosaic ommatidia at the boundaries of homozygous clones can show correct chirality. In those ommatidia with mosaicism between R3/R4, the R3 cell is almost always wild type and the R4 cell is almost always mutant. Mosaic ommatidia at the boundaries of homozygous clones are occasionally symmetrical, and in these cases both members of the R3/R4 pair are generally mutant. Expression of fzhs.sev in a fz15 background in either the presumptive R3 or R4 cell in mosaic ommatidia causes the cell expressing fzhs.sev to become an R3 cell and the other to become an R4 cell.

Ommatidial orientations are disturbed, chiral shape is choosen randomly.

Non-autonomous phenotype in wing clones.

strong thoracic bristle phenotype strong wing-hair disorientation

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

fz15 has neuroanatomy defective phenotype, enhanceable by Wnt5400/Wnt5[+]

Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

fz15 is a non-enhancer of visible phenotype of upd1GMR.PB

NOT Suppressor of
Statement
Reference

fz15 is a non-suppressor of visible phenotype of upd1GMR.PB

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

fz15 has axon & dorsal cluster neuron phenotype, enhanceable by Wnt5400/Wnt5[+]

Suppressed by
Statement
Reference

fz15 has trichome & abdomen | cell non-autonomous | somatic clone phenotype, suppressible by Vangstbm-6/Vangstbm-6

fz15 has trichome & abdomen | cell non-autonomous | somatic clone phenotype, suppressible by stan3/stan3

fz15 has trichome & abdomen | somatic clone phenotype, suppressible by stan3/stan3

NOT suppressed by
Statement
Reference

fz15 has trichome & abdomen | cell non-autonomous | somatic clone phenotype, non-suppressible by pkpk-sple-13/pkpk-sple-13

fz2C1, fz15 has phenotype, non-suppressible by wgUAS.Tag:HA/Scer\GAL4h-1J3

Enhancer of
Statement
Reference

fz[+]/fz15 is an enhancer of axon & dorsal cluster neuron phenotype of Wnt5400

fz15 is an enhancer of cardioblast phenotype of fz2C1

fz15 is an enhancer of wing disc phenotype of fz2C1

fz15 is an enhancer of scutum phenotype of fz2C1

fz15 is an enhancer of macrochaeta phenotype of fz2C1

fz15 is an enhancer of wing margin bristle | ectopic phenotype of fz2C1

fz15 is an enhancer of embryo phenotype of fz2C1

fz15 is an enhancer of embryonic epidermis phenotype of fz2C1

fz15 is an enhancer of denticle belt phenotype of fz2C1

fz15 is an enhancer of neuroblast NB4-2 phenotype of fz2C1

NOT Enhancer of
Statement
Reference

fz15 is a non-enhancer of eye phenotype of upd1GMR.PB

NOT Suppressor of
Statement
Reference

fz15 is a non-suppressor of eye phenotype of upd1GMR.PB

Other
Additional Comments
Genetic Interactions
Statement
Reference

fz15/fz21 enhances the wing defects caused by expressing kermitScer\UAS.cLa under the control of Scer\GAL4Bx-MS1096, with a significant increase in the number of wing cells with multiple hairs.

fz15 fz2C1 double homozygous clones in the wing result in notching of the wing margin and loss of margin bristles in the mutant tissue.

fz15 fz2C1 double mutant clones exhibit cone cell loss 42 hours after pupal formation.

fz15 fz2C1 double mutant clones exhibit reduced numbers of cone cells in third instar larval eye discs compared to controls.

Vangstbm-6/Vangstbm-6 fz15/fz21 clones in the pupal wing (32 hours after puparium formation) have negligible effects on the polarity of trichomes in neighbouring cells. Trichome polarity is also relatively unperturbed within the double mutant clones.

Clones expressing VangScer\UAS.cBa under the control of Scer\GAL4Act5C.PI in a fz15/Df(3L)fz-D21 background do not affect the polarity of trichomes in the surrounding non-clonal tissue.

Cell clones expressing vgScer\UAS.cKa under the control of Scer\GAL4αTub84B.PL that are also mutant for fz15 and fz2C1 (generated using the MARCM technique) are present in the wing disc 48 hours after heat-shock, with increased clone size further away from the dorsal-ventral boundary. However, at 72 hours after heat shock these mutant clones disappear as a result of cell death. Nonautonomous effects on growth and patterning are also seen in these mutant wing discs.

fz15, fz2C1 double mutant clones in the wing pouch fail to grow and survive. However, when induced late during larval development, these mutant clones display modest survival. fz15, fz2C1 double mutant clones induced 24 hours before dissection survive but appear undergrown compared to their wild-type twins.

fz15, fz2C1 double mutant clones induced in ft8 mutant discs during early larval stages fail to survive.

No axons from fz15, fz2C1 dorsal cluster neuron clones reach the medulla, while 37% of all axons from wild-type neurons reach the medulla.

Wnt5400/+; fz15/+ brains show a synergistic reduction in the number of dorsal cluster neuron axons that reach the medulla.

Hairs around fz15 somatic clones in the abdomens of pkpk-sple-13 homozygous flies point inwards, towards the clones, irrespective of whether they are anterior or posterior to the clone or located in regions of normal or reversed polarity.

The non-autonomous effect of fz15 somatic clones on planar polarity in the abdomen is suppressed by Vangstbm-6/Vangstbm-6.

A stan3/stan3 background blocks planar repolarisation both inside and outside fz15 homozygous clones in the adult abdomen.

Germband extension occurs normally in around 80% of fz15 fz2C1 homozygous embryos from mothers carrying fz15 fz2C1 germ line clones.

fz15 fz2C1/fz15 fz2C1 embryos produce cuticles with a lawn of denticles. Naked cuticle is restored in these embryos, by expression of arr::fz2arr.intra.Scer\UAS.T:Hsap\MYC with Scer\GAL4en-e16E.

The addition of fz15 and fz2C1 has no effect on the interneuron phenotype seen in drlScer\UAS.cCa, Scer\GAL4eg-Mz360 animals.

fz2C1 fz15 double mutant clones occasionally cause the differentiation of ectopic ommatidia on the dorsal adult head and these clones show overgrowth.

When ft8 homozygous mutant clones are made in the R3/R4 precursors of fz37/fz15 mutant flies, The mutant photoreceptor precursor eventually becomes an R3 photoreceptor 61% of the time (50% in wild-type).

Embryos derived from fz15 fz2C1 double mutant female germline clones lack all the dorsal trunk of the tracheal system (apart from minute vestiges of material found in the posterior part).

fz22-2-2.hs.2sev does not rescue the tissue polarity defect seen in fz37/fz15 eyes. fz::fz22-2-1.hs.2sev does not rescue the tissue polarity defect seen in fz37/fz15 eyes. fz::fz22-1-1.hs.2sev does not rescue the tissue polarity defect seen in fz37/fz15 eyes. fz::fz21-2-2.hs.2sev does not rescue the tissue polarity defect seen in fz37/fz15 eyes. fz::fz21-1-2.hs.2sev significantly rescues the tissue polarity defect seen in fz37/fz15 eyes, such that 93.3 +/- 5.0 % of ommatidia have the correct chiral shape. fz::fz21-2-1.hs.2sev significantly rescues the tissue polarity defect seen in fz37/fz15 eyes, such that 76.5 +/- 6.4 % of ommatidia have the correct chiral shape.

Embryos derived from fz15 fz2C1 female germline clones show defects in tracheal invagination, branch fusion and dorsal trunk formation.

In mutant wing clones in combination with fz2C1, the wing margin is defective. Neighboring wild type cells show ectopic wing margin bristles. wg signal transduction is lost: the mutant phenotype of the fz15, fz2C1 clones resembles that of dsh75. Embryos mutant zygotically and maternally for fz15 and fz2C1 cannot transduce wg signalling. They show the wg shortened embryo/"lawn of denticles" phenotype, en expression is lost, midgut constructions fail to form, lab is not-up-regulated, the neuroblasts that generate the RP2 neurons are absent, wg-dependent eve-expressing cardiac myoblasts are lost. In combination with armΔ.Scer\UAS.T:Ivir\HA1, Scer\GAL4h-1J3 the naked sections of the embryonic cuticle are partially restored. In combination with wgScer\UAS.T:Ivir\HA1, Scer\GAL4h-1J3 the naked sections of the embryonic cuticle are not restored. Embryos doubly mutant for fz15 and fz2C1 from heterozygous parents die at the embryo/larval boundary. Double mutant clones in the wing disc are at a growth disadvantage and do not survive in the wing pouch region. Double mutant clones in the mesonotum can fill the entire mesonotum with the bristles showing a frizzled polarity phenotype. Clones of wg- cells that fill the notum have a different phenotype in that fewer dorsocentral bristles form. Embryos and larvae lacking maternal fz and fz2 but having had fz or fz2 provided paternally are apparently normal.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

Adler.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (42)