4.5 Article

l-glutamate inhibits blue mould caused by Penicillium expansum in apple fruits by altering the primary nitrogen and carbon metabolisms

Journal

INTERNATIONAL JOURNAL OF FOOD SCIENCE AND TECHNOLOGY
Volume 56, Issue 12, Pages 6591-6600

Publisher

WILEY
DOI: 10.1111/ijfs.15325

Keywords

apples; blue mould; induced resistance; l-glutamate; Penicillium expansum

Funding

  1. Scientific and Technological Innovation Foundation in Shanxi Agricultural University [2017YJ31, 2017YJ32]
  2. Shanxi Provincial Key Research and Development Project [201903D211007-1, 201703D211001-06-03]

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The research showed that glutamate can effectively inhibit blue mould rot on apples by disrupting the balance of primary nitrogen and carbon metabolisms.
Although several studies have shown the ability of l-glutamate (glutamate) to mitigate the stress imposed by pathogens, the underlying mechanism is still in its infancy. To gain further knowledge, this study focussed on the effect of glutamate on primary nitrogen and carbon metabolisms during apple-Penicillium expansum interaction. The obtained result showed that glutamate could effectively restrict blue mould rot development in apples, but had no direct impact on fungal growth in vitro. The application of glutamate increased the level of nitrogen in apples, resulting in a disrupted balance of carbon and nitrogen. Consistently, the key enzymes glutamine synthetase (GS) and glutamate synthase (GOGAT) involved in the GS/GOGAT cycle, and the deaminating activity of glutamate dehydrogenase (GDH), forming 2-oxoglutarate and ammonium from glutamate, were promptly stimulated by glutamate. Interestingly, glutamate led to considerable consumption of the tricarboxylic acid (TCA) cycle intermediates, such as isocitric acid and citric acid, accompanied by the enhancement of malate dehydrogenase and succinate dehydrogenase activities. Collectively, exogenous application of glutamate might confer blue mould resistance in apples, at least in part, by redirecting host's primary nitrogen and carbon metabolisms, such as the activation of the GS/GOGAT cycle, deaminating activity of GDH and the TCA cycle.

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