W320term | fz2-PA; W320term | fz2-PB; W320term | fz2-PC; W320term | fz2-PD; W320term | fz2-PE; W320term | fz2-PF; W320term | fz2-PG
TGG to TAG mutation in codon W320
In the in the wild type, the W320 residue is at the junction between the coding sequence of the amino-terminal extracellular domain (which contains the CRD) and the remainder of the protein, which includes all seven transmembrane domains.
Nucleotide substitution: G?A.
Amino acid replacement: W320term.
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 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.
Generation of "iro" mutant clones (araDFM3 caupDFM3 mirrDFM3 mutants) in the eye results in dorsal axons projecting to the ventral lamina in 32.4% of cases. In "iro" fz2C1 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.
The viability but not polarity defects of fz2C1 fzH5 double mutant clones in the wing are rescued by fz22-2-2.αTub84B, fz1-1-1.αTub84B, fz::fz21-1-2.αTub84B, fz::fz21-2-2.αTub84B, fz::fz21-2-1.αTub84B, fz::fz22-1-1.αTub84B or fz::fz22-2-1.αTub84B.
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, 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.
fz2Scer\UAS.6x.T:Hsap\MYC; Scer\GAL4BG487 completely rescues the reduction in bouton number at neuromuscular junctions seen in fz2C1/Df(3L)ED4782 larvae. This reduction in bouton number is not rescued by fz2ΔSGKTLESW.Scer\UAS.T:Hsap\MYC; Scer\GAL4BG487 or fz2C.Scer\UAS.NLS.T:Hsap\MYC; Scer\GAL4BG487.
fz2Scer\UAS.6x.T:Hsap\MYC; Scer\GAL4BG487 completely rescues the reduction in bouton number at neuromuscular junctions seen in fz2C1/Df(3L)ED4782 larvae, and partially rescues bouton morphology defects in these animals. This reduction in bouton number is not rescued by fz2ΔSGKTLESW.Scer\UAS.T:Hsap\MYC; Scer\GAL4BG487 or fz2C.Scer\UAS.NLS.T:Hsap\MYC; Scer\GAL4BG487.