Table 1 Loss-of-function phenotypes of frizzled genes

Drosophila

fz ^-/-

Disruption of planar cell polarity in sensory bristles, dorsal epidermis, and ommatidia

[1,39]

Drosophila

Dfz2 ^-/-

Viable

[22] (see also [40-42])

Drosophila

Fz^-/-; Dfz2^-/-

Wg signal transduction is abolished in embryos and the wing imaginal disk

[22]

Drosophila

fz^-/-; Dfz2 deficiency

Mimics loss of wg in embryonic epidermal patterning, neuroblast specification, midgut morphogenesis, and heart formation

[40-42]

Drosophila

fz^RNAi; Dfz2^RNAi

Defects in embryonic patterning that mimic wg loss of function

[43]

Drosophila

Dfz3 ^-/-

Suppresses a hypomorphic wg mutation

[44]

C. elegans

mom-5 ^-/-

Embryos lack endoderm and overproduce pharyngeal tissue

[45]

C. elegans

mig-1 ^-/-

Abnormal migration of the Q neuroblast

[46]

C. elegans

Lin-17 ^-/-

Disruption of a variety of asymmetric cell divisions

[47]

Mouse

mfz3 ^-/-

Severe defects in major axon tracts within the forebrain

[48]

Mouse

mfz4 ^-/-

Defects in cell survival in the cerebellum; vascular defects in retina, cochlea, and cerebellum

[26,49]

Mouse

mfz5 ^-/-

Embryonic lethal (at day 10.75) because of defects in yolk-sac angiogenesis

[50]

Human

hFZD4 ^+/-

Familial exudative vitreoretinopathy

[25]

Xenopus

Xfz3 ^MO

Loss of neural crest induction

[51]

Xenopus

Xfz7 ^AS

Depletion of maternal Xfz7 disrupts dorsal anterior development

[52]

Xenopus

Xfz7 ^MO

Severe gastrulation defect arising from inability of involuted anterior mesoderm to separate from the ectoderm

[24]