Lessons from the vegetative shoot apex - Intercellular Communication in Plants - page 151

6.4 Signalling involved in meristem maintenance

The shoot apical meristem of most plants remains relatively constant in size unless
responding to a changing environment or developmental signals. The stability of
size reflects a balance between cell proliferation in the central and peripheral zones
and the recruitment of cells into organ formation in the peripheral and rib zones.
Meristems that have lost this balance occur naturally and are distinguished by gen-
erating broad flat stems and/or flowers that have many more organs than normal.
The shoot apical meristem of these plants often grows as a band or ring rather than
as a point, a property termed fasciation .
The genetic basis of meristem maintenance has been extensively studied in Ara-
bidopsis , where mutant screens have identified plants with abnormal meristems.
One class of mutant has meristems that get progressively larger as the plant grows,
whereas the other class fails to form and/or maintain the shoot apical meristem.
Much progress has been made in characterising these mutants and identifying genes
involved in meristem function. In many instances these genes encode proteins that
are involved in cell signalling, some of which are examined in detail in the following
sections. Other genes whose protein products are either not known to be involved
in signalling or have yet to be identified are listed in Table 6.1.

6.4.1 The CLAVATA mutants
Mutations in the three Arabidopsis CLAVATA loci cause a progressive enlargement of
the shoot apical meristem during the growth of the plant. clv mutants also have more
leaves and flowers than do wild-type plants and produce flowers with an increased
number of organs (Leyser & Furner, 1992; Clark et al. , 1993, 1995; Kayes & Clark,
1998). The presence of additional carpels in the clv gynoecium gives it a club-
shaped appearance, which led to these mutants being named ' clavatus ' from the
Latin meaning club-like. The dramatic increase in the size of clv meristems results
from an accumulation of cells within the central zone, a defect that may arise in
several ways. One possibility is that the CLV pathway might regulate the rate of cell
divisions within the central zone. The loss of CLV activity would therefore lead to an
increase in the rate of cell proliferation within the central zone and an accumulation
of cells. Alternatively, the CLV pathway might promote the transition of cells from
the central zone into the peripheral zone. In this scenario, the increased accumulation
of cells in the central zone of clv mutants is not associated with a change in the rate
of cell division. Careful observations of both cell size and frequency of divisions in
clv meristems have shown that there is a slight decrease in cell division rates within
the central zone, supporting the second scenario (Laufs et al. , 1998b).
Genetic interactions between all three clv loci show that they function in the same
genetic pathway. However, unlike the other clv mutants, clv2 displays additional
organ defects implying that its function is not limited to meristem maintenance
(Kayes & Clark, 1998). In addition, genetic studies show that the activity of CLV1