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Table 1 Loss-of-function phenotypes of frizzled genes

From: The Frizzled family: receptors for multiple signal transduction pathways

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