fz²¹ fz2^C1, fz¹⁵ fz2^C1 and fz²⁵ fz2^C1 double homozygous clones in the wing result in notching of the wing margin and loss of margin bristles in the mutant tissue.

fz¹⁹ fz2^C1 double homozygous clones in the wing result in wing margin defects.

fz²⁰ fz2^C1 double homozygous clones in the wing do not result in loss of wing margin bristles in the mutant tissue.

fz¹⁵ fz2^C1 double mutant clones exhibit cone cell loss 42 hours after pupal formation.

fz¹⁵ fz2^C1 double mutant clones exhibit reduced numbers of cone cells in third instar larval eye discs compared to controls.

The increased bouton number at the neuromuscular junction that is seen in homozygous Vps35^EY14200 larvae is not suppressed by fz2^C1/+.

Cell clones expressing vg^Scer\UAS.cKa under the control of Scer\GAL4^αTub84B.PL that are also mutant for fz¹⁵ and fz2^C1 (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 ; fz2^C1 double mutant clone induced 48-72hrs after egg laying in wild-type and ft⁸ mutant wing imaginal discs do not survive, whereas, there twin cells do. However, when induced during late larval development, these mutant clones display modest survival.

fz¹⁵ ; fz2^C1 mutant clones induced 24 hrs after egg laying in ft⁸ mutant wing imaginal discs survive but appear undergrown by comparison with their wild-type twins.

A W^GMR.PU background generates a severe ventral-to-dorsal misrouting phenotype in fz2^C1 mutant clone retina.

Generation of "iro" mutant clones (ara^DFM3 caup^DFM3 mirr^DFM3 mutants) in the eye results in dorsal axons projecting to the ventral lamina in 32.4% of cases. In "iro" fz2^C1 double mutant clones, 'dorsal-to-ventral' R axon misroutings are observed in 3.5% of the cases. Instead, abnormal bundles of dorsal axons are found.

No axons from fz¹⁵, fz2^C1 dorsal cluster neuron clones reach the medulla, while 37% of all axons from wild-type neurons reach the medulla.

Wnt5⁴⁰⁰/+; fz2^C1/+ brains show a small but significant decrease in the number of dorsal cluster neuron axons that reach the medulla compared to Wnt5⁴⁰⁰/+ brains.

fz²¹ fz2^C1 double homozygous clones in the dorsal air sac primordium grow normally and populate the tip of the air sac primordium to the same degree as wild-type clones.

Germband extension occurs normally in around 80% of fz¹⁵ fz2^C1 homozygous embryos from mothers carrying fz¹⁵ fz2^C1 germ line clones.

The addition of fz¹⁵ and fz2^C1 has no effect on the interneuron phenotype seen in drl^Scer\UAS.cCa, Scer\GAL4^eg-Mz360 animals.

fz2^C1 fz¹⁵ double mutant clones occasionally cause the differentiation of ectopic ommatidia on the dorsal adult head and these clones show overgrowth.

Embryos derived from fz¹⁵ fz2^C1 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).

The viability but not polarity defects of fz2^C1 fz^H5 double mutant clones in the wing are rescued by fz2^{2-2-2.αTub84B}, fz^{1-1-1.αTub84B}, fz::fz2^{1-1-2.αTub84B}, fz::fz2^{1-2-2.αTub84B}, fz::fz2^{1-2-1.αTub84B}, fz::fz2^{2-1-1.αTub84B} or fz::fz2^{2-2-1.αTub84B}.

Embryos derived from fz¹⁵ fz2^C1 female germline clones show defects in tracheal invagination, branch fusion and dorsal trunk formation.

In mutant wing clones in combination with fz¹⁵, 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, fz2^C1 clones resembles that of dsh⁷⁵. Embryos mutant zygotically and maternally for fz¹⁵ and fz2^C1 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 arm^{Δ.Scer\UAS.T:Ivir\HA1}, Scer\GAL4^h-1J3 the naked sections of the embryonic cuticle are partially restored. In combination with wg^{Scer\UAS.T:Ivir\HA1}, Scer\GAL4^h-1J3 the naked sections of the embryonic cuticle are not restored. Embryos doubly mutant for fz¹⁵ and fz2^C1 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.