Self‐incompatibility (SI) is a genetically controlled cell–cell recognition system that acts as a barrier to self pollination in a wide range of flowering plant species. Several different SI mechanisms have been identified.

Keywords: S‐receptor kinase (SRK); S‐RNAase; F‐box; actin depolymerization; calcium signalling; programmed cell death (PCD)

Figure 1.

Proposed mechanisms for the self‐incompatibility reaction in the S‐RNAase system. The products of the female S gene, the S‐RNAases, are secreted into the transmitting tissue of the style. Pollen growing through the style encounters the S‐RNAases. If the pollen carries an S haplotype corresponding to either of the haplotypes present in the style, then inhibition occurs. Two models have been proposed for the inhibition mechanism. Compatible (Sx‐, left) and incompatible (Sa‐, right) pollinations are shown on an SaSb pistil. Symbols for pistil factors (S‐RNAase, HT‐B and 120 K) and pollen factor (SLF) are shown below: (a) S‐RNAase degradation model. S‐RNAase enters the pollen tube cytoplasm from the ECM (arrows). A compatible nonself‐S‐RNAase/SLF interaction (left) results in ubiquitylation and degradation of S‐RNAases by the 26S proteasome, so there is no cytotoxic action and pollen tube growth continues. An incompatible self‐S‐RNAase/SLF interaction (right) does not result in S‐RNAase degradation; cytotoxicity results in RNA degradation and so incompatible pollen tube growth is inhibited. (b) S‐RNAase compartmentalization model. S‐RNAase, 120 K and HT‐B are taken up by endocytosis and sorted to a vacuole. In a compatible interaction (left), S‐RNAase remains compartmentalized, so although S‐RNAase is present it is not cytotoxic because it is sequestered. Degradation of HT‐B in compatible pollen tubes is mediated by a hypothetical pollen protein (PP). How S‐RNAase gains access to SLF (arrow, question mark) is not known. In an incompatible interaction (right), HT‐B is not degraded and the vacuolar compartment containing S‐RNAases degrades. S‐RNAase is released into the cytoplasm and RNA is degraded by its cytotoxic action, and pollen tube growth is inhibited. Adapted from McClure and Franklin‐Tong . With kind permission of Springer Science and Business Media.

Figure 2.

A proposed model for the self‐incompatibility mechanism in Papaver rhoeas. Incompatible pollen undergoes an S haplotype‐specific interaction. Secreted stigmatic S‐proteins interact with the pollen S receptor. An haplotype‐specific interaction such as binding S1 protein to S1 pollen results in triggering an intracellular Ca2+ signalling cascade(s), involving large‐scale Ca2+ influx and increases in [Ca2+]i. A series of events then occur in the incompatible pollen. Within 1 min there is a dissipation of the tip‐focused calcium gradient that is required for continued pollen growth and the activation of calcium‐dependent protein kinase (CDPK). The CDPK phosphorylates Pr‐p26.1, a soluble inorganic pyrophosphatase (sPPase). Both calcium and phosphorylation inhibit sPPase activity, resulting in a reduction in the biosynthetic capability of the pollen, thereby inhibiting growth. Dramatic changes to pollen cytoskeleton organization are apparent within 1 min, with extensive depolymerization of the F‐actin accompanying this, also predicted to cause rapid arrest of tip growth. p56‐MAPK is activated and may signal to PCD. PCD is triggered, involving key features of PCD including caspase‐like activity, cytochrome c leakage and DNA fragmentation. This ensures that incompatible pollen does not start to grow again. Adapted from McClure and Franklin‐Tong . With kind permission of Springer Science and Business Media.

Figure 3.

A proposed model for the Brassica self‐incompatibility reaction. In Brassica the SI response occurs within the stigma. When a pollen grain alights on the papilla surface the pollen coat flows to form an adhesive ‘foot’, thus making a connection with the surface of the stigmatic papilla. The pollen S locus cysteine‐rich (SCR/SP11) protein is carried within this coating and when this is allelic with the recipient stigma, an incompatible reaction is induced. SCR binds to the extracellular domain of the S receptor kinase (SRK), which results in the activation of the kinase. The role of the S locus glycoprotein (SLG) in this recognition event is unclear, as evidence suggests it is not essential for the SI reaction. However in some S haplotypes it does appear to enhance the SI response. MLPK (M locus protein kinase) a membrane localized protein is a positive effector of SI and may form a complex with SRK. Following activation SRK interacts with ARC1 in a phosphorylation‐dependent manner. This ultimately leads to pollen rejection by some, as yet, unknown mechanism.



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Further Reading

Anderson MA, Cornish EC, Mau S‐L et al. (1986) Cloning of cDNA for a stylar glycoprotein associated with expression of self‐incompatibility in Nicotiana alata. Nature 321: 38–44.

Foote HCC, Ride JP, Franklin‐Tong VE et al. (1994) Cloning and expression of a distinctive class of self‐incompatibility (S) gene from Papaver rhoeas L. Proceedings of the National Academy of Sciences of the USA 91: 2265–2269.

Nasrallah JBK, Kao T‐H, Goldberg ML and Nasrallah ME (1985) A cDNA clone encoding an S‐locus‐specific glycoprotein from Brassica oleracea. Nature 318: 263–267.

Takayama S and Isogai A (2005) Self‐incompatibility in plants. Annual Reviews of Plant Biology 56: 467–489.

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How to Cite close
Franklin‐Tong, Veronica, and Franklin, Christopher(Apr 2007) Self‐incompatibility. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0002041.pub2]