Agriculture Reference
In-Depth Information
of the activator have reached a sufficient level, at a point farthest from the existing
organs (reviewed in Lyndon, 1998).
Changing the size of the meristem without altering the strength of the signal is
expected to alter phyllotaxis, as the region experiencing least inhibition or greatest
activation will be greatly expanded. Several
Arabidopsis
mutants display such alter-
ations including the
clv
and
fasciata
mutants (Leyser & Furner, 1992; Clark
et al.
,
1993) as well as the maize
abphyl1
(
abph1
) mutant (Greyson
et al.
, 1978; Jackson &
Hake, 1999). Similarly, reducing the size of organ primordia allows more organs to
form from a meristem, as seen in the whorled arrangement of the smaller needle-like
organs of the
Antirrhinum phantastica
(
phan
) mutants (Waites & Hudson, 1995).
An alternative, but not necessarily exclusive, mechanism for phyllotaxis is based
on physical forces (Green, 1996). According to this model, tensile and compressive
forces within the meristem determine the site of organ formation. Computer mod-
elling has shown that such a process is capable of accounting for many aspects of
phyllotaxis, including the regular pattern of organ formation and changes in phyl-
lotaxis that arise following disruptions in organ formation (Green, 1992, 1996). As
this mechanism is unlikely to require the action of specific genes, it is hard to test
genetically. However, experiments that alter the physical forces acting within the
meristem have provided some supporting evidence for this model. The sunflower
inflorescence (capitulum) is a large flat meristem that initiates primordia in multiple
spirals. Each primordium develops into a flower and subtending bract. Hernandez
and Green (1993) showed that lateral compression of a developing capitulum led to
the formation of ridges that run parallel to the applied pressure. These ridges fail
to separate into primordia, developing instead as extended (united) bracts that lack
flowers. Thus, applied physical forces can change phyllotaxis in predictable ways
as well as cause changes to primordia development.
6.7.2 The role of auxin in phyllotaxis
Much attention has recently been focused on auxin as a key regulator of phyllotaxis.
It is synthesised in the developing tissue of the shoot, particularly young leaves
(Davies, 1995), and actively moved throughout the plant by a polar transport sys-
tem. When polar auxin transport is inhibited chemically, phyllotaxis is significantly
altered and in many cases organs fail to form, leaving a naked pin-like stem (Okada
et al.
, 1991; Reinhardt
et al.
, 2000). A number of
Arabidopsis
mutants mimic these
effects, including
pin-formed1
(
pin1
; Okada
et al.
, 1999),
pinoid
(
pid
; Bennett
et al.
,
1995) and
monopterous
(
mp
; Berleth & Jurgens, 1993; Przemeck
et al.
, 1996), which
are all implicated in either auxin transport or signalling.
PIN1
encodes an auxin efflux carrier that is expressed in the meristem, developing
primordia and vascular tissue (Galweiler
et al.
, 1998; Vernoux
et al.
, 2000; see also
Chapter 2). The lack of organs on
pin1
stems may reflect the need either to remove
auxin from lateral organ initials or to accumulate auxin, depending on whether auxin
inhibits or promotes primordium formation. Several lines of evidence point to auxin
as a lateral organ promoter. The
pin1
mutant phenotype can be rescued by exogenous
