The S locus receptor kinase and the S locus glycoproteins are encoded by genes located at the S locus, which controls the self-incompatibility response in Brassica. In class II self-incompatibility haplotypes, S locus glycoproteins can be encoded by two different genes, SLGA and SLGB. In this study, we analyzed the sequences of these genes in several independently isolated plants, all of which carry the same S haplotype (S2). Two groups of S2 haplotypes could be distinguished depending on whether SRK was associated with SLGA or SLGB. Surprisingly, SRK alleles from the two groups could be distinguished at the sequence level, suggesting that recombination rarely occurs between haplotypes of the two groups. An analysis of the distribution of polymorphisms along the S domain of SRK showed that hypervariable domains I and II tend to be conserved within haplotypes but to be highly variable between haplotypes. This is consistent with these domains playing a role in the determination of haplotype specificity.

During the course of evolution, recognition mechanisms that prevent self-fertilization. in flowering plants have been selected. These mechanisms, named self-incompatibility, allow self-pollen rejection by the pistil. In most cases, the self-incompatibility response is under die genetic control of a single multiallelic locus, the S (Self-incompatibility) locus. Depending on the genetic control of the self-pollen rejection, two major classes of self-incompatibility systems have been described. The most common systems correspond to the gametophytic self-incompatibility, which has been well characterized in the Solanacene and in the Papaveraceae. The second type of self-incompatibility systems corresponds to the sporophytic self-incompatibility, particularly well studied in the Brassicaceae. In the review article, we present recent advances in understanding the molecular events that lead to pollen recognition and rejection in both systems. Interestingly, different molecules and signaling pathways of a have been recruited during evolution of flowering plants to answer the same biological question: how to discriminate male partners and to efficiently prevent self-fertilization by the pistil of hermaphroditic flowers ? The origin and molecular evolution of these multiallelic systems is discussed.

Self-incompatibility (SI) is a widespread mechanism in flowering plants that prevents self-fertilization. Self-pollen recognition relies on the products of genes located at the S (self-incompatibility) locus. Significant progress towards understanding molecular interactions allowing stigmatic cells to recognize and reject self-pollen in Brassica has been made during the past two years. Thus, the male and female determinants responsible of the self-incompatibility (SI) response have been identified. The structural features of these molecules strongly suggest that SI response is triggered by a ligand-receptor interaction.

During the course of evolution, recognition mechanisms that prevent self-fertilization in flowering plants have been selected. These mechanisms, named self-incompatibility, allow self-pollen rejection by the pistil. In most cases, the self-incompatibility response is under the genetic control of a single multiallelic locus, the S (Self-incompatibility) locus. Depending on the genetic control of the self-pollen rejection, two major classes of self-incompatibility systems have been described. The most common systems correspond to the gametophytic self-incompatibility, which has been well characterized in the Solanaceae and in the Papaveraceae. The second type of self-incompatibility systems corresponds to the sporophytic self-incompatibility, particularly well studied in the Brassicaceae. In the review article, we present recent advances in understanding the molecular events that lead to pollen recognition and rejection in both systems. Interestingly, different molecules and signalling pathways have been recruited during evolution of flowering plants to answer the same biological question: how to discriminate male partners and to efficiently prevent self-fertilization by the pistil of hermaphroditic flowers? The origin and molecular evolution of these multiallelic systems is discussed.

The self-incompatibility response has been defined as the inability of a fertile hermaphrodite seed-plant to produce zygotes after self-pollination. Many members of the genus Brassica exhibit sporophytic self-incompatibility, rejection of self-pollen occurring on the stigma surface. Over the last 15 years a number of genes have been implicated in the self-incompatibility response in Brassica. These include both genes at the S locus, which are potentially involved in the recognition of self-pollen, and genes at unlinked loci, which are though to be involved in processes downstream of the recognition event such as signal transduction and self-pollen rejection. Here we review data from recent studies that have focused on determining the function of these genes, and their respective gene products, in the self-incompatibility response.

Self-incompatibility in Brassica is controlled by a single, highly polymorphic locus that extends over several hundred kilobases and includes several expressed genes. Two stigma proteins, the S locus receptor kinase (SRK) and the S locus glycoprotein (SLG), are encoded by genes located at the S locus and are thought to be involved in the recognition of self-pollen by the stigma. We report here that two different SLG genes, SLGA and SLGB, are located at the S locus in the class II, pollen-recessive S15 haplotype. Both genes are interrupted by a single intron; however, SLGA encodes both soluble and membrane-anchored forms of SLG, whereas SLGB encodes only soluble SLG proteins. Thus, including SRK, the S locus in the S15 haplotype contains at least three members of the S gene family. The protein products of these three genes have been characterized, and each SLG glycoform was assigned to an SLG gene. Evidence is presented that the S2 and S5 haplotypes carry only one or the other of the SLG genes, indicating either that they are redundant or that they are not required for the self-incompatibility response.