Insights into the evolution of self‐compatibility in Lycopersicon from a study of stylar factors

Summary To elucidate the molecular basis of loss of self‐incompatibility in Lycopersicon , S‐RNases and HT‐proteins were analysed in seven self‐compatible (SC) and three self‐incompatible (SI) taxa. No or low stylar RNase activity was a common feature in most SC taxa examined, in contrast to the uniformly high levels of activity found in all SI species. The S‐RNase gene is most likely deleted in the four red‐fruited SC taxa ( L. esculentum, L. esculentum var. cerasiforme, L. pimpinellifolium and L. cheesmanii ) because S‐RNase genes could not be amplified from genomic DNA. S‐RNase genes could, however, be amplified from the genomes of the three green‐fruited SC taxa examined. L. chmielewskii and L. hirsutum f . glabratum show a decreased accumulation of transcripts, possibly reflecting changes in the 5′ flanking regions of the S‐RNase genes. The remaining green‐fruited SC species, L. parviflorum , has a functional S‐RNase gene in its genome that is expressed at high levels in the style, suggesting a genetic factor responsible for the low S‐RNase activity. Together these results argue for several independent mutations in the S‐RNase gene over the course of Lycopersicon diversification, and that loss of S‐RNase function is unlikely to the primary cause of the loss of self‐incompatibility. We also examined the HT‐B genes that play a role in self‐incompatibility. HT‐B transcripts were markedly reduced in the styles of all the SC taxa examined. A scenario is described where a mutation causing reduced transcription of HT‐B in an ancestral SI species was central to the loss of self‐incompatibility in Lycopersicon .