Profiling changes in primary metabolites and antioxidants during apple fruit decay caused by Penicillium crustosum

Abstract

Penicillium crustosum is one of the causal agents of apple fruit blue mold decay. It produces mycotoxins and it is widely distributed, although a less aggressive pathogen than P. expansum. Changes in sugars (sucrose, glucose, and fructose), organic acids (malic and shikimic), and antioxidants (total glutathione, ascorbate, and phenolics) were monitored in P. crustosum infected apples at 6 and 24 hpi, 3, 5, 7, and 11 dpi. The initial stage of infection (6 hpi) was characterized by a decline in fructose, malic acid, and total phenolic contents, whereas the total glutathione considerably increased. Twenty-four hpi and 3 dpi the strong activation of ascorbate-glutathione cycle correlated significantly with total phenolics and organic acid enhancement at the expense of sugars. At 5 dpi the progress of visible symptoms caused a temporary breakdown of apple defense, leading to degradation of total phenolics, glutathione, and glucose, whereas the fructose as a crucial signal molecule increased significantly. An acclimation of the defense system was achieved at 7 dpi by accumulating fructose, sucrose and antioxidants that further resulted in stable ratio of most of the investigated metabolites at 11 dpi. LDA analysis enabled us to define the fructose, glucose, malic acid and ascorbate-glutathione cycle as crucial temporary marker with balanced cross-induction playing a complex role in apple defense against P. crustosum. In summary, apple fruit reacted on P. crustosum by activating defense mechanisms quickly after inoculation (6 hpi), and stayed at the higher level until 5 dpi when temporary breakdown occurred. Apple fruit managed to recover as metabolites were fairly in balance after 11 dpi. Phenolics were viewed as a wheel of the apple fruit defense mechanism, driven by the ascorbate–glutathione system, while glutathione and fructose are believed to have had a crutial role in signaling.