Epigenetic mechanisms for breakdown of self-incompatibility in interspecific hybrids

As a major agent of rapid speciation, interspecific hybridization has played an important role in plant evolution. When hybridization involves species that exhibit self-incompatibility (Sl), this prezygotic barrier to self-fertilization must be overcome or lost to allow selling. How SI, a normally dominant trait, is lost in nascent hybrids is not known, however. Here we demonstrate that hybrid self-fertility can result from epigenetic changes in expression of the S-locus genes that determine specificity in the SI response. We analyzed loss of Sl in synthetic hybrids produced by crossing self-fertile and self-incompatible species in each of two crucifer genera. We show that SI is lost in the stigmas of A. thaliana-lyrata hybrids and their neo-allotetraploid derivatives and in the pollen of C. rubella-grandiflora hybrids and their homoploid progenies. Aberrant processing of S-locus receptor kinase gene transcripts as detected in Arabidopsis hybrids and suppression of the S-locus cysteine-rich protein gene as observed in Capsella hybrids are two reversible mechanisms by which Sl might break down upon interspecific hybridization to generate self-fertile hybrids in nature.