The tomato long shelf-life fruit phenotype: Knowledge, uncertainties and prospects

The long shelf-life (LSL) phenotype is characteristic of diverse Mediterranean tomato landraces and is defined by the outstanding durability of the fruit, showing no symptoms of deterioration for up to ten months after harvest. The genetic basis behind this abnormal phenotype is yet to be fully characterized, though many ripening-related mutants have been identified and studied during the past decades. New technologies have allowed for a deeper understanding of the genetic background of this trait and have revealed that the LSL phenotype is dependent on more traits beyond the ethylene synthesis and response pathways. Nevertheless, full determination of ethylene synthesis levels in mutants of commercial interest, such as rin, nor and alc, warrants some further research as to describe to what extent these mutations affect ethylene response. Available data suggests that singular mutations are not enough to lead to the LSL phenotype. Particularly, the role of the alc allele is not entirely clear, as newer studies suggest this mutation alone is not responsible for this phenotype in landraces that naturally present it, summed to the fact that Italian LSL landraces do not harbor this particular allele. The molecular traits underlying the LSL phenotype have been increasingly studied for the past decades and it becomes clear that it is far more complex than originally believed, and that traits other than the alc mutation must be involved in this phenotype. This review aims to recapitulate the research performed in this area and highlight the questions that are still to be answered to fully explain the basis of this outstanding fruit phenotype.

Automated summary

The long shelf-life (LSL) phenotype is characteristic of Mediterranean tomato landraces, yet the genetic basis behind it is still not completely defined. New technologies have revealed that the LSL phenotype is dependent on traits beyond ethylene synthesis and response pathways. Current research indicates that singular mutations may not be enough to lead to the LSL phenotype.