TY - JOUR
T1 - The apical determinants aPKC and dPatj regulate frizzled-dependent planar cell polarity in the Drosophila eye
AU - Djiane, Alexandre
AU - Yogev, Shaul
AU - Mlodzik, Marek
N1 - Funding Information:
We are grateful to M. Bhat, Z. Chen, C. Klambt, J. Knoblich, D. St. Johnston, D. Strutt, the Bloomington Drosophila Stock Center, and the DSHB for flies and antibodies. We thank J. Delaney, A. Jenny, T. Klein, and I.L. Torres for critical reading. A.D. thanks I.L. Torres for support and the many improvements to this manuscript. A.D. was supported by postdoctoral fellowships from the Assoc. pour le Recherche sur le Cancer (ARC) and EMBO. This work was supported by a NIH grant to M.M.
PY - 2005/5/20
Y1 - 2005/5/20
N2 - Planar cell polarity (PCP) is a common feature of many vertebrate and invertebrate epithelia and is perpendicular to their apical/basal (A/B) polarity axis. While apical localization of PCP determinants such as Frizzled (Fz1) is critical for their function, the link between A/B polarity and PCP is poorly understood. Here, we describe a direct molecular link between A/B determinants and Fz1-mediated PCP establishment in the Drosophila eye. We demonstrate that dPatj binds the cytoplasmic tail of Fz1 and propose that it recruits aPKC, which in turn phosphorylates and inhibits Fz1. Accordingly, components of the aPKC complex and dPatj produce PCP defects in the eye. We also show that during PCP signaling, aPKC and dPatj are downregulated, while Bazooka is upregulated, suggesting an antagonistic effect of Bazooka on dPatj/aPKC. We propose a model whereby the dPatj/aPKC complex regulates PCP by inhibiting Fz1 in cells where it should not be active.
AB - Planar cell polarity (PCP) is a common feature of many vertebrate and invertebrate epithelia and is perpendicular to their apical/basal (A/B) polarity axis. While apical localization of PCP determinants such as Frizzled (Fz1) is critical for their function, the link between A/B polarity and PCP is poorly understood. Here, we describe a direct molecular link between A/B determinants and Fz1-mediated PCP establishment in the Drosophila eye. We demonstrate that dPatj binds the cytoplasmic tail of Fz1 and propose that it recruits aPKC, which in turn phosphorylates and inhibits Fz1. Accordingly, components of the aPKC complex and dPatj produce PCP defects in the eye. We also show that during PCP signaling, aPKC and dPatj are downregulated, while Bazooka is upregulated, suggesting an antagonistic effect of Bazooka on dPatj/aPKC. We propose a model whereby the dPatj/aPKC complex regulates PCP by inhibiting Fz1 in cells where it should not be active.
UR - https://www.scopus.com/pages/publications/19344363080
U2 - 10.1016/j.cell.2005.03.014
DO - 10.1016/j.cell.2005.03.014
M3 - Article
C2 - 15907474
AN - SCOPUS:19344363080
SN - 0092-8674
VL - 121
SP - 621
EP - 631
JO - Cell
JF - Cell
IS - 4
ER -