Introduction of SLG (S locus glycoprotein) alters the phenotype of endogenous S haplotype, but confers no new S haplotype specificity in Brassica rapa L.

Self-incompatibility (SI) in Brassicaceae is genetically controlled by the S locus complex in which S locus glycoprotein (SLG) and S receptor kinase (SRK) genes have been identified, and these two genes encoding stigma proteins are believed to play important roles in SI recognition reaction. Here we introduced the SLG(43) gene of Brassica rapa into a self-incompatible cultivar, Osome, of B. rapa, and examined the effect of this transgene on the SI behavior of the transgenic plants. Preliminary pollination experiments demonstrated that Osome carried S-52 and S-60, and both were codominant in stigma, but S-52 was dominant to S-60 in pollen. S-43 was found to be recessive to S-52 and codominant with S-60 in stigma. The nucleotide sequence of SLG(43) was more similar to that of SLG(52) (87.8% identity) than to that of SLG(60) (74.8% identity). Three of the ten primary transformants (designated No. 1 to No. 10) were either completely (No. 9) or partially (No. 6 and No. 7) self-compatible; the SI phenotype of the stigma was changed from (SS60)-S-52 to S-60, but the SI phenotype of the pollen was not altered. In these three plants, the mRNA and protein levels of both SLG(43) and SLG(52) were reduced, whereas those of SLG(60) were not. All the plants in the selfed progeny of No. 9 and No. 6 regained SI and they produced a normal level of SLG(52). These results suggest that the alteration of the SI phenotype of the stigma in the transformants Nos. 6, 7, and 9 was the result of specific co-suppression between the SLG(43) transgene and the endogenous SLG(52) gene. Three of the transformants (Nos. 5, 8 and 10) produced SLG(43) protein, but their SI phenotype was not altered. The S-60 homozygotes in the selfed progeny of No. 10 which produced the highest level of SLG(43) were studied because S-43 was codominant with S-60 in the stigma. They produced SLG(4)3 at approximately the same level as did (SS60)-S-43 heterozygotes, but did not show S-43 haplotype specificity at the stigma side. We conclude that SLG is necessary for the expression of the S haplotype specificity in the stigma but the introduction of SLG alone is not sufficient for conferring a novel S haplotype specificity to the stigma.