Table 1.

Loss-of-function phenotypes of frizzled genes

Species	Genotypes*	Phenotypes	References
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	fzRNAi; Dfz2RNAi	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]

*MO, morpholino oligos; AS, antisense oligos; RNAi, RNA interference. See also [6].