Genes involved in the control of ethylene biosynthesis during climacteric of Prunus persica fruit

Peach (Prunus persica) produces climacteric fruit whose ripening is largely dependent on the effects of the gaseous hormone ethylene. Physiological ethylene production is not limited to the ripening stage, but it is present also in stage 1 (S1), when fruit growth is sustained mainly by cell division. The transcriptional regulation of the genes coding for ethylene biosynthetic enzymes showed that at the onset of fruit ripening PpACS1 (1-aminocyclopropane-1-carboxylate synthase) and PpACO1 (1-aminocyclopropane-1-carboxylate oxidase) are the main players. But not much is known on the genes coding for biosynthetic enzymes in non-ripening fruit and on their transcriptional regulation during transition from System-1 to System-2 ethylene production. By means of microarray experiments (4800 probes) and EST database searches followed by qRT-PCR experiments, it has been possible to detect the expression of five ACS and two ACO genes. Of the five ACS and two ACO genes identified, only ACS1, ACS4 and both ACO genes have significant expression in fruit, with ACS1 and ACO1 involved in climacteric production, while ACS4 and ACO2 seem important in basal (System-1) ethylene synthesis. Microarray experiments have highlighted the auxin effect on ripening, disclosing a cross-talk with ethylene, besides the actions carried out autonomously by each of them. The application of the ethylene inhibitor 1-MCP (1-methylcyclopropene), besides being effective in inverting the expression of ethylene-regulated genes, is able to induce auxin-responsive genes, such as GH3, whose expression is widely used as a marker for free IAA. Also ACS1 and ACO2 are induced by 1-MCP, while ACS4, whose basal transcription seem to guarantee System-1 ethylene production, is negatively regulated by the chemical, as ACO1 does. Thus, blocking ethylene perception with 1-MCP seems to trigger the release of free IAA, which stimulates ethylene biosynthesis through the induction of ACS1 transcription.