4.7 Article

Metabolic response induced by parasitic plant-fungus interactions hinder amino sugar and nucleotide sugar metabolism in the host

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SCIENTIFIC REPORTS
卷 6, 期 -, 页码 -

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NATURE PUBLISHING GROUP
DOI: 10.1038/srep37434

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资金

  1. Rural Development Administration of Korea [PJ011646]
  2. Bio-Synergy Research Project of the Ministry of Science, ICT and Future Planning through the National Research Foundation [NRF-2012M3A9C4048796]
  3. National Research Foundation of Korea grant - Korean government (MSIP) [2009-0083533]
  4. Basic Science Research Program through the National Research Foundation of Korea [NRF-2016R1E1A2020743]
  5. National Research Foundation of Korea [2016R1E1A2020743, 2012M3A9C4048796, 2009-0083533] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Infestation by the biotrophic pathogen Gymnosporangium asiaticum can be devastating for plant of the family Rosaceae. However, the phytopathology of this process has not been thoroughly elucidated. Using a metabolomics approach, we discovered the intrinsic activities that induce disease symptoms after fungal invasion in terms of microbe-induced metabolic responses. Through metabolic pathway enrichment and mapping, we found that the host altered its metabolite levels, resulting in accumulation of tetrose and pentose sugar alcohols, in response to this fungus. We then used a multiple linear regression model to evaluate the effect of the interaction between this abnormal accumulation of sugar alcohol and the group variable (control/parasitism). The results revealed that this accumulation resulted in deficiency in the supply of specific sugars, which led to a lack of amino sugar and nucleotide sugar metabolism. Halting this metabolism could hamper pivotal functions in the plant host, including cell wall synthesis and lesion repair. In conclusion, our findings indicate that altered metabolic responses that occur during fungal parasitism can cause deficiency in substrates in pivotal pathways and thereby trigger pathological symptoms.

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