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A comparative transcriptomic and proteomic analysis of hexaploid wheat’s responses to colonization by Bacillus velezensis and Gaeumannomyces graminis both separately and combined

2019-08-06

Abstract:

Tritrophic interactions involving a biocontrol agent, a pathogen and a plant have been analyzed predominantly from the perspective of the biocontrol agent. To explore the adaptive strategies of wheat in response to beneficial, pathogenic and combined microorganisms, we performed the first comprehensive transcriptomic, proteomic and biochemical analysis in wheat roots after exposure to Bacillus velezensis CC09 (Bv), Gaeumannomyces graminis var. tritici (Ggt) and their combined colonization, respectively. The transcriptional/translational programming of wheat roots inoculated with beneficial Bv showed mild alterations compared to that of pathogenic Ggt. However, the combination of Bv and Ggt activated a larger transcriptional/translational program than for each single microorganism, but the gene expression pattern was similar to that of individual infection by Ggt, suggesting a prioritization of defense against Ggt infection. Surprisingly, pathogen-associated molecular pattern-triggered immunity and effector-triggered immunity made wheat pre-treated with Bv more sensitive to subsequent Ggt infection. Additionally, Bv triggered a salicylic acid (SA)-dependent mode of induced systemic resistance that resembles pathogen-induced systemic acquired resistance (SAR). Wheat plants mainly depend on SA-mediated resistance, and not that mediated by jasmonic acid (JA), against the necrotrophic pathogen Ggt. Moreover, SA-JA interactions resulted in antagonistic effects regardless of the type of microorganisms in wheat. Further enhancement of SA-dependent defense responses such as lignification to the combined infection was shown to reduce the level of induced JA-dependent defense against subsequent infection with Ggt. Altogether, our results demonstrate how the hexaploid monocot wheat responds to beneficial/pathogenic microorganisms and prolongs the onset of ‘take-all’ disease through modulation of cell reprogramming and signaling events.


Text link :

 https://apsjournals.apsnet.org/doi/abs/10.1094/MPMI-03-19-0066-R 

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