Biomedical Engineering Reference
In-Depth Information
2002
); the
approximated
palmitoyltransferase (
Matakatsu & Blair, 2008
); and
small GTPases such as
Rho1
(
Strutt et al., 1997; Yan et al., 2009
) and Go
(
Purvanov et al., 2010
). An interesting and unexpected group of genes
that are required for normal PCP function in ion transport including the
Na
þ
/H
þ
exchanger
Nhe2
(
Simons et al., 2009
), a component of the
vesicle ATPase (
Buechling et al., 2010; Hermle, Saltukoglu, Grunewald,
Walz, & Simons, 2010
), and an organic anion transporter,
oat30B
(
Mummery-Widmer et al., 2009
). The effect of Nhe2 was suggested to
be mediated through an effect on the interaction of Dsh and plasma
membrane lipids. Many of the genes noted above produce mutant
phenotypes that suggest they could function in concert with or affect the
function of either the
fz/stan
or the
ds/ft
pathways. For example, the
PCP phenotype that results from a loss of
grh
function in wing cells was
shown to be associated with a loss of
stan
expression in the mutant cells
(
Lee & Adler, 2004
). A notable and interesting exception was the
identification of
chascon
and
jitterbug
, which affect notum PCP by
impacting the tendons that attach the indirect flight muscles to the notum
(
Olguin, Glavic, & Mlodzik, 2011
). In this case, a loss of the ability of
the tissue to respond to the mechanical tension produced by the IFMs
appears to be the mechanism responsible for the PCP mutant phenotype.
3.5. Genome-wide screen for PCP genes
A genome-wide screen based on transgene-mediated RNAi that was
designed to identify genes that played a role in Notch signaling also identi-
fied many genes required for PCP (
Mummery-Widmer et al., 2009
). In this
screen,
pannier-Gal4
was used to drive transgene expression.
pannier
is
expressed in the central region of the notum; hence, it is an ideal driver
to use to look for effects on bristle sense organ determination and differen-
tiation. Effects on PCP in this screen were manifested by the misalignment
of notum bristles. Satisfyingly, this screen identified in order of the strength
of phenotype
fz
,
Vang
,
frtz
,
pk
,
stan
,
fy
,
in
,
ft
, and
ds
. Thus, most of the
fz/stan
and
ds/ft
pathway genes were identified confirming that the screen was very
effective. The screen failed to identify
dgo
,
fj
, and
mwh
. The failure to identify
dgo
and
mwh
is not surprising as null alleles of
dgo
and
mwh
do not show a bristle
polarity phenotype (
Feiguin et al., 2001; Strutt &Warrington, 2008; Yan et al.,
2008
).This is not thecase for
fj
and the failure to identify
fj
may simply reflect the
transgene not knocking down the expression enough to produce a mutant
phenotype. It is unlikely that this screen identified all of the genes that play a
role in PCP. Some genes would likely be missed due to the knockdown not
