Agriculture Reference
In-Depth Information
be involved early in the primary pathway of the signalling cascade, which leads to
SI (Rudd & Franklin-Tong, 2003). This significantly bolsters the argument that the
DNA fragmentation observed in SI is a result of PCD and not necrosis. Further,
this result suggests that the initial reversible cessation of tube growth is not only
reversible, but also temporary. This raises the interesting question as to whether
the signalling events involved in the initial reversible inhibition of tube growth are
truly functionally involved in the operation of this SI system or are an indirect effect
that results from elevation of [Ca
2
+
]
i
within the pollen tube. Ca
2
+
is a promiscuous
secondary messenger and while its elevation appears to be required for the activation
of PCD, other [Ca
2
+
]
i
regulated pathways will also be affected, some of which are
very likely to be involved in tip growth. The answer to this question lies in the timing
of the various processes
in vivo
. Can activation of PCD alone at the stigma surface
terminate the growth of all pollen tubes before they reach the ovules? PCD is not a
particularly rapid process; in the hypersensitive response in tomato leaves, necrotic
lesions appear after
16 h (Hoeberichts
et al.
, 2003). Although it is unclear how
long a pollen tube would continue to grow after the induction of PCD, it is entirely
possible that some pollen tubes would have sufficient time to effect fertilisation. The
function of the rapid reversible inhibition of pollen tube growth is, thus, likely to
be to stop the pollen tubes while PCD comes into effect, and in so doing strengthen
the SI response.
∼
10.3.7 Model for the mechanism of self-incompatibility in P. rhoeas
The data described above suggest that SI in
P. rhoeas
is mediated by a number of sig-
nal transduction cascades that are activated within incompatible pollen grains/tubes.
The stigmatic S-proteins are well established as encoding female
S
-specificity, and
function to communicate the S-genotype of the stigma to incoming pollen grains.
The pollen
S
-specificity component has not been conclusively identified, but is
thought to be an S-protein receptor located at the surface of pollen tubes. SBP both
binds S-proteins and is located in the plasma membrane, but S-protein binding ap-
pears to be irrespective of
S
-genotype, suggesting that this protein functions as an
accessory receptor (Hearn
et al.
, 1996). It remains possible, however, that binding
of S-protein to the pollen receptor occurs in both cross- and self-interactions but
that the result differs, as is proposed in Solanaceous SI.
Figure 10.3 illustrates a working model for the mechanism of SI in
P. rhoeas
.
Binding between an S-protein and its cognate pollen
S
-receptor is envisaged to trig-
ger intracellular signalling cascade(s) involving Ca
2
+
acting as a secondary messen-
ger (Franklin-Tong
et al.
, 1993). Within approximately 1 min of the initial signal,
there is an influx of extracellular Ca
2
+
, which, together with release of Ca
2
+
from
internal stores, leads to an increase in cytosolic [Ca
2
+
]
i
in the tube shank (Franklin-
Tong
et al.
, 2002). Elevation of cytosolic [Ca
2
+
]
i
, has multiple rapid effects. The
initial series of events are fully capable of stopping pollen tube growth, but are re-
versible. First is the loss of the apical [Ca
2
+
]
i
gradient, which may well be responsible
for the initial arrest of pollen tube growth. Second is the rapid phosphorylation of
