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First published online January 16, 2004
doi: 10.1242/10.1242/jcs.00973

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Planar polarity from flies to vertebrates

Manolis Fanto^* and Helen McNeill

Cancer Research UK, 44 Lincoln's Inn Fields, London, WC2A 3PX, UK

View larger version (26K): [in a new window]   Fig. 1. PCP is evident in the coordinate organization of wing hairs and eye ommatidial clusters in the fly. Mutations in PCP genes cause cells to lose their planar organization, yet maintaining their individual cell polarity. Loss of PCP genes in the wing can cause misorientation of hairs, or multiple hairs to form in a single cell. Loss of PCP genes in the eye can cause alterations in degree of rotation, dorsal-ventral inversions, and loss of the chiral, asymmetric organization of the ommatidia. Cells appear to have lost their `compass' yet maintain their identity.

View larger version (51K): [in a new window]   Fig. 2. Development of PCP in the wing and eye. (A) Wing cells display only apical-basal polarity until the pupal stage. Planar polarity is first evident by the production of a single, actin-rich structure at the distal edge of a cell. This develops into a hair. (B) Ommatidial preclusters emerge from a moving wave of differentiation, marked by an indentation called the morphogenetic furrow. As ommatidial preclusters begin to differentiate, they begin to rotate. Ommatidia in one half of the eye will rotate clockwise, and the ventral ommatidia will rotate counterclockwise. This rotation occurs in two steps of 45°, and results in dorsal ommatidia having opposite orientations from ventral ommatidia. A symmetry-breaking step occurs after rotation, resulting in ommatidia with different chiralities in the dorsal and ventral fields.

View larger version (22K): [in a new window]   Fig. 3. Polarized subcellular distribution of PCP genes in wing and eye cells. (A) Pupal wing cells show a transient accumulation of PCP proteins on either the proximal or distal cell membranes. Fz and Dsh accumulate on the distal membranes, Stbm and Pk accumulate on proximal membranes, and Fmi and Diego appear to be enriched on both proximal and distal membranes. All are depleted from anterior and posterior membranes. (B) PCP proteins accumulate specifically on subsets of ommatidial precursor cells, most importantly at the R3/R4 interface, shown here. Fz and Dsh accumulate on the R3 cell at the R3/R4 interface, whereas Stbm is enriched in the R4 cell at the R3/R4 interface. Other photoreceptor cells (not shown) show polarized distributions of some components, but importantly cell in-between ommatidial clusters show no polarized accumulation of PCP proteins.

View larger version (44K): [in a new window]   Fig. 4. Fj and Ds impart positional information in the eye and wing. Fj and Ds are transmembrane proteins that are expressed in opposing gradients in the eye (A) and the wing (B). The distribution of these proteins defines the equatorial-polar axis in the eye, and the distalproximal axis in the wing. Disrupting the polarized distribution of Fj and Ds perturbs planar polarity in both the eye and wing.

View larger version (86K): [in a new window]   Fig. 5. Mutations in vertebrate PCP genes lead to a PCP defect in the inner ear. Scanning electron micrographs of the inner ear from wild-type mice (A and B) and mice homozygous for mutations in a vertebrate homologue of flamingo (C), called crash (Crsh/Crsh). At (A) 3-5 months, wild-type stereocilia form regularly organized arrays, with the apex of the stereocilia pointing in one direction. This organization is evident in wild-type at E18.5 (B). In Crsh homozygotes at E18.5, the outer hair cells (OHCs) are extensively misrotated, showing a clear defect in PCP. Arrows show new axis of polarity. [Figure reproduced, with permission, from Curtin et al. (Curtin et al., 2003)].