SummaryTo elucidate the molecular basis of loss of self-incompatibility in Lycopersicon, S-RNases and HTproteins 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 ampli®ed from genomic DNA. S-RNase genes could, however, be ampli®ed 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 re¯ecting changes in the 5¢¯anking regions of the S-RNase genes. The remaining green-fruited SC species, L. parvi¯orum, 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 diversi®cation, 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.
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