Natural and Ethephon-Stimulated Ripening of F1 Hybrids of the Ripening Inhibitor (rin) and Non-Ripening (nor) Mutants of Tomato (Lycopersicon esculentum Mill.)

The ripening inhibitor (rin) and non-ripening (nor) mutants each contribute additively as heterozygotes to delay ripening as measured by time from anthesis to the respiratory peak. The rin mutant as a heterozygote has no effect on the magnitude of the respiratory rise, whereas nor reduces the respiratory peak to about 50% of normal. The respiratory rise is further reduced to about 25% of normal in the double mutant hybrid (+ rin, + nor). Peak ethylene and fruit carotene production is reduced about 50% in single mutant hybrids and to 25% of normal in the double mutant hybrid. Polygalacturonase activity 5 days after the respiratory peak in heterozygotes of rin and nor and the double mutant hybrid was 35, 25 and 10% of normal, respectively. Ethephon treatment hastened ripening in all genotypes, but the magnitude of specific ripening events was determined by genotype. The mode of action of these mutants is not directly through endogenous ethylene but probably via a slow change which precedes the ethylene rise and other concomitant ripening changes. It is proposed that polygalacturonase synthesis or activation may represent the primary genetic event which is inhibited in the mutants and attenuated in mutant hybrids.