Lessons from the vegetative shoot apex - Intercellular Communication in Plants - page 156

is predicted to increase the number of stem cells and the size of the central zone (see
below). Although CLV3 is likely to be a ligand, there is currently no biochemical
evidence to support a physical interaction between CLV3 and CLV1.
6.4.3 The wuschel mutant
The function of the CLV pathway in limiting the number of stem cells in the cen-
tral zone is balanced by the cell-proliferating activity of WUSCHEL ( WUS ). wus
mutants have meristems that terminate after the emergence of the first few leaves.
However, adventitious meristems subsequently form and produce a few more leaves
before terminating. Repeated rounds of initiation and termination cause wus plants
to appear bushy or tousled ( wuschel is German for 'tousled hair'; Laux et al. , 1996).
WUS encodes a putative homeobox transcription factor that is expressed in a few
cells of the L3 layer directly beneath the stem cells (Mayer et al. , 1998). It has
been proposed that WUS -expressing cells define a region of the meristem called
the organising centre, which promotes stem cell identity on overlying cell lay-
ers non-cell autonomously (Mayer et al. , 1998). Recent work supports this view,
as induced WUS expression in patches of cells within the meristem causes stem
cell identity and proliferation in adjacent non- WUS -expressing cells (Gallois et al. ,
2002).
6.4.4 The CLAVATA-WUSCHEL regulatory loop
Genetic studies place WUS downstream of the CLV pathway and therefore a likely
target of CLV regulation (Laux et al. , 1996; Schoof et al. , 2000). In the absence
of CLV activity, the domain of WUS expands, suggesting that the larger meristem
size of clv mutants might be caused by an increase of WUS activity (Brand et al. ,
2000; Schoof et al. , 2000). This was tested directly by enlarging the domain of WUS
expression using the CLV1 promoter. Transgenic plants expressing this construct
had a clv -like phenotype (Schoof et al. , 2000). Conversely, when the domain of
CLV3 expression was increased, the resulting wus -like phenotype correlated with a
reduction of WUS expression (Brand et al. , 2000). This phenotype was dependent
on CLV1 activity, suggesting that the function of the CLV signalling pathway is to
restrict WUS expression and in doing so antagonise stem cell accumulation.
But what promotes CLV expression? Several lines of evidence point to a WUS -
regulated signal promoting CLV3 expression. Firstly, stem cell formation and CLV3
expression can be induced ectopically when WUS is expressed in lateral organs
(Schoof et al. , 2000; Brand et al. , 2002; Lenhard et al. , 2002). And secondly, when
CLV3 is ectopically expressed in the L3 region of the meristem, both WUS and
endogenous CLV3 expression (in L1 and L2 layers) is reduced or lost completely
(Brand et al. , 2000). Thus, WUS acts non-cell autonomously to promote CLV3
expression in the overlying cells of the central zone. However, the dependence of
CLV3 expression on WUS activity is not absolute, as CLV3 is still expressed in the
adventitious and axillary meristems of wus mutants (Brand et al. , 2002). Expression