Abstract
Self-incompatibility (SI) in crucifers is controlled by a large number of haplotypes at the S-locus. Each S-haplotype encodes a pollen-borne ligand SP11 and its stigmatic receptor, SRK, and their S-haplotype-specific interaction triggers an SI response in the stigma epidermis. The SI phenotype of pollen of an S-heterozygote is determined by the relationship between the two S-haplotypes it carries, and dominant/recessive relationships are often observed between the two S-haplotypes. These dominance hierarchies are determined at the RNA level: the SP11transcript from a recessive S-haplotype is greatly diminished in the presence of a dominant S-haplotype. In addition, weshow that the 5' promoter sequence of recessive SP11 is specifically methylated in the S-heterozygote. This promoter region is essential for SP11 transcription, and its methylation occurs specifically in the anther immediately prior to the initiation of SP11 transcription. These results suggest that tissue-specific monoallelic de novo DNA methylation is involved in determining the dominance interactions in cruciferous SI. Furthermore, possible mechanisms to explain recessive SP11 allele-specific methylation will be discussed.
