The pathogenic fungus Colletotrichum musae infects developing green bananas (Musa spp. AAA group), but remains latent until the fruit ripens. The aim of this research was to determine whether the appearance of disease symptoms is regulated by chitinase gene expression following treatment of fruit with benzothiadiazole (BTH) and methyl jasmonate (MeJA), and with physical (heat) and chemical (H2O2 and Ca2+-related) treatments. In bananas inoculated with C. musae, BTH and MeJA lowered disease severity and stimulated higher gene expression compared with the untreated controls during ripening. However, in naturally infected bananas, BTH and MeJA treatments slightly reduced transcription of the chitinase gene in green bananas, but they prolonged gene expression in ripe bananas and significantly reduced disease severity. The combination of H2O2 and the NADPH oxidase inhibitor, diphenylene iodonium, down-regulated chitinase gene expression and compromised disease resistance compared with H2O2 alone. Heat treatment (HT) or the combination of HT followed by CaCl2 reduced disease, but only the latter significantly upregulated chitinase gene expression. The combination of HT and a calcium ionophore (A23187) resulted in different disease indicies and different levels of gene expression depending upon the order of application: HT followed by A23187 induced higher gene expression and lower disease. The results suggest that disease resistance of green bananas could be related to high and prolonged levels of chitinase gene expression, and chitinase could be involved in harvested banana's anthracnose resistance activated by different defense pathway signals, such as BTH, MeJA, H2O2, and Ca2+.
Nitrogen regulates chitinase gene expression in a marine bacterium