Polytene chromosomes normal.
axon & dorsal cluster neuron
trichome & adult abdomen | somatic clone
trichome & adult abdomen | somatic clone | cell non-autonomous
trichome & pleural membrane | somatic clone
trichome & pleural membrane | somatic clone | cell non-autonomous
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.
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.
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.
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).
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.
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.