Biomedical Engineering Reference
In-Depth Information
mom-1
/Porcupine that is required for secretion of Wnts (
Siegfried et al.,
2004; Yamamoto et al., 2011
). Instead, it was suggested that the polarity
is regulated, at least partly, by signals from the germ cells (Z2 and Z3)
that position between Z1 and Z4, as germ cell-less mutants show
abnormal polarity of Z1 and Z4 (
Yamamoto et al., 2011
). Although this
germ cell signal has not been identified, it was reported recently that
mRNA of
mom-2
/Wnt is present specifically in the germ cells of L1
larvae (
Harterink et al., 2011
). Considering that a hypomorphic
mom-2
mutation was used in quintuple Wnt mutants which have normal polarity
of Z1 and Z4, it may still be possible that
mom-2
in the germ cells causes
polarity reversal of Z1 as it does so in P7.p in the vulva. However, in this
case,
mom-2
from germ cells should induce opposite polarity (POP-1 is
higher in the daughter proximal to the
mom-2-
expressing germ cells)
compared to that induced by
mom-2
in EMS or P7.p (POP-1 is higher in
the daughter distal to the
mom-2-
expressing cells). Therefore, it is more
plausible to imagine that non-Wnt signals from the germ cells orient
polarity of Z1 and Z4.
10. FUNCTIONS OF PCP COMPONENTS IN C. ELEGANS
Although the coordination of spindle orientation and polarity in
C. elegans
is conceptually similar to the PCP regulation in
Drosophila
and ver-
tebrates, knowledge about functions of PCP-specific components, such as
Van Gogh and Prickle, in the processes described above has been limited
so far. RNAi of
prkl-1
/Prickle weakly affects polarity of male B cell division
that also involves POP-1 asymmetry (
Wu & Herman, 2006
). A
vang-1
/Van
Gogh mutation can suppress abnormal polarity of P7.p caused by
lin-17
/Fzd
mutations, although the
vang-1
/Van Gogh mutation by itself does not affect
P5.p or P7.p polarity (
Green et al., 2008
). As deletion mutants of
vang-1
,
prkl-1
, and
fmi-1
/Flamingo are viable, it is unlikely that these genes are glob-
ally required for polarity regulation.
vang-1
is also involved in morphogenesis of intestine (
Hoffmann,
Segbert, Helbig, & Bossinger, 2010
). In
vang-1
mutants, some parts of the
intestinal lumen, which is normally surrounded by two cells, are instead sur-
rounded by three cells (
Fig. 3.7
A). As intestine morphogenesis involves cell
intercalation, it was suggested that
vang-1
might regulate cell intercalation
as the case for its vertebrate homologues. VANG-1 is recruited to the apical
surface of intestinal cells by direct interaction with junctional protein
DLG-1/Discs large. The VANG-1 localization also requires DSH-2/
