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	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]

*MO, morpholino oligos; AS, antisense oligos; RNAi, RNA interference. See also [6].
Huang and Klein Genome Biology 2004 5:234 doi:10.1186/gb-2004-5-7-234