Lessons from the root apex - Intercellular Communication in Plants - page 211

(Benkova et al. , 2003). On the basis of this study, Benkova et al. (2003) suggested a
model of primordium development in which the pericycle cells at the site of future
initiation start accumulating auxin, possibly due to PIN-dependent auxin transport.
In the context of establishment of the vascular network, Sachs (1988, 1991)
proposed a model in which vascular tissue is established through a positive feedback
loop where auxin is a limiting factor that induces auxin transport capability and
polarity. On the basis of the studies with various gnom alleles, Geldner et al. (2004)
proposed a model in which a similar mechanism results in the establishment of
the embryonic axis and the initiation of lateral roots. In embryos corresponding to
strong gnom alleles, as a result of grossly misaligned auxin transporters the basal part
of the embryo lacks sufficient auxin to be able to initiate a primary root meristem.
Instead, auxin accumulates in the apical domain at the presumptive site of synthesis,
leading to cotyledon fusion (Fig. 8.4A). The absence of auxin transport also results
in a randomization of cell division and expansion, which increases axis diameter.
During lateral root development some pericycle cells start to accumulate auxin and
divide and they thus deplete auxin from the surrounding cells, which in turn inhibits
their proliferation. The observed simultaneous peak of auxin within the primordium
and the auxin-mediated lateral inhibition may be explained by the assumption that in
a stage I primordium PIN1 is localized in a bipolar manner (in both apical and basal
sides of the cell). When PIN1 fails to take on the bipolar localization, auxin peaks
would lead to homogeneous proliferation of the pericycle, as in gnom R5 (Geldner
et al. , 2004). Since PIN1 localizes to the newly formed cell plates after a division
(Geldner et al. , 2001), in gnom R5 mutants this would lead to daughter cells having
opposing PIN1 polarities (Fig. 8.4B). Geldner et al. (2004) propose that after a
division a weak bias in the auxin signal results in one of the cells changing polarity,
and that GNOM is essential at this step. Subsequent cell divisions would be polarized
in the direction set by the first two cells, leading to the 90˚ degree shift in polarity
from the primary root axis (Fig. 8.4C). The retargeting of PIN proteins would cause
the auxin flow to be redirected and allow auxin from the primary root vasculature
to flow through the centre of the new lateral root primordium. At the tip of the new
lateral root the flow is directed away from the meristem through the lateral rootcap,
creating a 'fountain' model of auxin flow (Benkova et al. , 2003).

8.4.3 Molecular genetics of epidermal patterning

The epidermis, the outermost layer of cells in the mature root, is composed of alter-
nating files of trichoplasts, which give rise to hair cells (H cells), and atrichoplasts,
which give rise to non-hair cells (N cells) (Dolan et al. , 1994; Galway et al. , 1994). In
Arabidopsis ,several mutants impaired in epidermal cell pattering have been iden-
tified. Three of these mutants, werewolf (wer ), transparent testa glabra ( ttg ) and
glabra2 ( gl2 ), show a hairy root phenotype due to ectopic root hair cell production.
This implies that the normal role of the WER, TTG and GL2 is either to promote
N cell differentiation or to repress root hair cell differentiation (DiCristina et al. ,
1996; Galway et al. , 1994; Masucci et al. , 1996; Lee & Schiefelbein, 1999). A fourth