Biomedical Engineering Reference
In-Depth Information
Abstract
Drosophila has been the key model system for studies on planar cell polarity (PCP). The
rich morphology of the insect exoskeleton contains many structures that display PCP.
Among these are the trichomes (cuticular hairs) that cover much of the exoskeleton, sen-
sory bristles, and ommatidia. Many genes have been identified that must function for the
development of normal PCP. Among these are the genes that comprise the frizzled/starry
night (fz/stan) and dachsous/fat pathways. The mechanisms that underlie the function of
the fz/stan pathway are best understood. All of the protein products of these genes ac-
cumulate asymmetrically in wing cells and there is good evidence that this involves local
intercellular signaling between protein complexes on the distal edge of one cell and the
juxtaposed proximal edge of its neighbor. It is thought that a feedback system, directed
transport, and stabilizing protein
-
protein interactions mediate the formation of distal
and proximal protein complexes. These complexes appear to recruit downstream
proteins that function to spatially restrict the activation of the cytoskeleton in wing cells.
This leads to the formation of the array of distally pointing hairs found on wings.
1. INTRODUCTION TO DROSOPHILA PLANAR CELL
POLARITY
The cuticular surface of insects has a rich morphology that led them to
be the first systems where the development of planar cell polarity (PCP) was
studied in depth (see, e.g.,
Lawrence, 1966
). For the past 30 years, genetic
studies using Drosophila have provided many of the most important insights
that resulted in the blossoming of the field (
Gubb & Garcia-Bellido, 1982;
Held, Duarte, & Derakhshanian, 1986; Wong & Adler, 1993
). These
included the identification of many of the genes that play key roles in
PCP (
Adler, Charlton, & Liu, 1998; Chae et al., 1999; Collier & Gubb,
1997; Collier, Lee, Burgess, & Adler, 2005; Feiguin, Hannus, Mlodzik,
& Eaton, 2001; Gubb & Garcia-Bellido, 1982; Klingensmith, Nusse, &
Perrimon, 1994; Strutt & Warrington, 2008; Taylor, Abramova,
Charlton, & Adler, 1998; Theisen et al., 1994; Usui et al., 1999; Vinson,
Conover, & Adler, 1989; Wolff & Rubin, 1998; Yan et al., 2008; Yang,
Axelrod, & Simon, 2002; Zeidler, Perrimon, & Strutt, 1999
), that the
protein products of these genes accumulate asymmetrically in cells (
Adler,
Zhu, & Stone, 2004; Axelrod, 2001; Bastock, Strutt, & Strutt, 2003;
Feiguin et al., 2001; Shimada, Usui, Yanagawa, Takeichi, & Uemura,
2001; Strutt, 2001; Strutt & Warrington, 2008; Tree et al., 2002; Usui
et al., 1999; Yan et al., 2008
), that many of the proteins interact physically
(
Bastock et al., 2003; Das, Jenny, Klein, Eaton, & Mlodzik, 2004; Jenny,
Darken, Wilson, & Mlodzik, 2003; Jenny, Reynolds-Kenneally, Das,
