Kapuganti J. Gupta,1
Luis A. J. Mur,2 and
1Department of Plant Sciences, University of Oxford, South Parks Road, Oxford OX1 3RB, U.K.; 2Aberystwyth University, Institute of Biological, Environmental and Rural Science, Edward Llwyd Building, Aberystwyth, SY23 3DA U.K.; 3Max-Planck-Institute of Molecular Plant Physiology, Am Mühlenberg 1, D-14476 Golm-Potsdam, Germany
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Accepted 16 November 2013.
Inoculations with saprophytic fungus Trichoderma spp. are now extensively used both to promote plant growth and to suppress disease development. The underlying mechanisms for both roles have yet to be fully described so that the use of Trichoderma spp. could be optimized. Here, we show that Trichoderma asperelloides effects include the manipulation of host nitric oxide (NO) production. NO was rapidly formed in Arabidopsis roots in response to the soil-borne necrotrophic pathogen Fusarium oxysporum and persisted for about 1 h but is only transiently produced (approximately 10 min) when roots interact with T. asperelloides (T203). However, inoculation of F. oxysporum–infected roots with T. asperelloides suppressed F. oxysporum–initiated NO production. A transcriptional study of 78 NO-modulated genes indicated most genes were suppressed by single and combinational challenge with F. oxysporum or T. asperelloides. Only two F. oxysporum–induced genes were suppressed by T. asperelloides inoculation undertaken either 10 min prior to or after pathogen infection: a concanavlin A-like lectin protein kinase (At4g28350) and the receptor-like protein RLP30. Thus, T. asperelloides can actively suppress NO production elicited by F. oxysporum and impacts on the expression of some genes reported to be NO-responsive. Of particular interest was the reduced expression of receptor-like genes that may be required for F. oxysporum–dependent necrotrophic disease development.
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