The dual effects of methyl salicylate on ripening and expression of ethylene biosynthetic genes in tomato fruit
Chang-Kui Ding and Chien Yi Wang
Plant Science Volume 164, Issue 4 , April 2003, Pages 589-596
2003
บทคัดย่อ
Tomatofruit(Lycopersicon esculentum Mill. cv. Sun Bright) at three ripening stages (mature green, breaker and turning) were treated with three different concentrations of methyl salicylate (MeSA) vapor to investigate the impact on ripening and ethylene production. The tomato ripening process, including the development of red color, ethylene production andrespirationrate, was enhanced by 0.1 mM of MeSA during the mature green stage and 0.01 mM of MeSA during the breaker stage. But infruitat the turning stage, even a low concentration of MeSA (0.01 mM) retarded the ripening process. High concentration (0.5 mM) of MeSA prevented red color development, ethylene production andrespirationin all maturity stages. Northern hybridization experiments on mature greenfruit,involving four cDNAs encoding ACC synthase and ACC oxidase, showed that the abundance of LE-ACS2 and LE-ACS4 mRNAs increased during storage concomitant with a burst in ethylene production. These increases in mRNAs of LE-ACS2 and LE-ACS4 with ripening were suppressed by treatment with 0.5 mM of MeSA. But in 0.1 mM MeSA treatedfruit,the transcript of LE-ACS2 had a large increase at day 1 and day 3 compared with untreatedfruit.The abundance of LE-ACS4 was undetectable in untreatedfruitat day 0, but accumulated with 0.1 mM MeSA treatedfruit.Transcripts for the LE-ACS6 gene were undetectable after day 1 in the mature green stage. The transcripts for the LE-ACO1 gene, which were present at harvest in mature greenfruit,increased greatly during ripening in storage. These increases in LE-ACO1 mRNA with ripening were delayed by treatment with both 0.1 and 0.5 mM MeSA. The results suggest that increased ethylene production by 0.1 mM MeSA in tomatofruitis possibly mediated by depressing the negative feedback regulation of the LE-ACS6 genes and increasing the expression of LE-ACS2 and LE-ACS4 through positive feedback regulation.