Signals and Targets Triggered by Self-Incompatibility in Plants: Recognition of “Self ” Can Be Deadly - Communication in Plants: Neuronal Aspects of Plant Life - page 77

6.1.2
Self-Incompatibility
One aspect of pollen-pistil interactions that has been the focus of much re-
searchisSI.Thisisageneticallycontrolledmechanismwhichallowsplants
to prevent inbreeding. Essentially, SI is a cell-cell recognition system that
allows the discrimination of genetically related pollen (“self” or incompat-
ible pollen) from genetically unrelated pollen (“non-self” or compatible
pollen). For detailed reviews on the different types of SI, the reader is di-
rected to three recent reviews (Franklin-Tong and Franklin 2003; Hiscock
and McInnis 2003; Kao and Tsukamoto 2004).
In Papaver pollen, the cellular and molecular bases of the SI system have
been investigated in detail (Franklin-Tong and Franklin 2003). The pistil
component, the S protein (Foote et al. 1994), is a small (about 15-kDa)
secreted protein which acts as a ligand for the pollen component, which is
thought to be a plasma membrane receptor (Franklin-Tong and Franklin
2003). During an incompatible interaction, several events are triggered in
the pollen. A rapid influx of extracellular Ca 2+ and large increases in [Ca 2+ ] i
precede the dissipation of the tip-focused [Ca 2+ ] i gradient, and comprise
the initial second messenger signals to downstream targets (Franklin-Tong
et al. 1993, 1995, 1997, 2002). These targets include the rapid reorganization
and depolymerization of F-actin (Geitmann et al. 2000; Snowman et al.
2002), which we discuss in more detail later. SI also involves the activation
of several protein kinases leading to the phosphorylation of a number of
proteins. These include p26, a soluble inorganic pyrophosphatase (Rudd et
al. 1996; Rudd and Franklin-Tong 2003). Phosphorylation of p26 and the
inhibition of its activity by increases in [Ca 2+ ] i are believed to interfere
with pollen tube growth. A mitogen-activated protein (MAP) kinase, p56,
is also phosphorylated (Rudd and Franklin-Tong 2003; Rudd et al. 2003).
The timing of p56 activation (Rudd et al. 2003), after arrest of pollen tube
growth, suggests that p56 is not involved in tip-growth inhibition, but
instead may signal to events occurring downstream. SI also triggers PCD
(Jordan et al. 2000; Thomas and Franklin-Tong 2004) and this is discussed
later.