Abstract
Fusarium oxysporum (Fo) is best known as a host‐specific vascular pathogen causing major crop losses. Most Fo strains, however, are root endophytes potentially conferring endophyte‐mediated resistance (EMR). EMR is a mechanistically poorly understood root‐specific induced resistance response induced by endophytic or nonhost pathogenic Fo strains. Like other types of induced immunity, such as systemic acquired resistance or induced systemic resistance, EMR has been proposed to rely on the activation of the pattern‐triggered immunity (PTI) system of the plant. PTI is activated upon recognition of conserved microbe‐associated molecular patterns (MAMPs) of invading microbes. Here, we investigated the role of PTI in controlling host colonization by Fo endophytes and their ability to induce EMR to the tomato pathogen Fo f. sp. lycopersici (Fol). Transgenic tomato and Arabidopsis plants expressing the Fo effector gene Avr2 are hypersusceptible to bacterial and fungal infection. Here we show that these plants are PTI‐compromised and are nonresponsive to bacterial‐ (flg22) and fungal‐ (chitosan) MAMPs. We challenged the PTI‐compromised tomato mutants with the EMR‐conferring Fo endophyte Fo47, the nonhost pathogen Fom (a melon pathogen), and with Fol. Compared to wild‐type plants, Avr2‐tomato plants became hypercolonized by Fo47 and Fom. Surprisingly, however, EMR towards Fol, induced by either Fo47 or Fom, was unaffected in these plants. These data show that EMR‐based disease resistance is independent from the conventional defence pathways triggered by PTI, but that PTI is involved in restricting host colonization by nonpathogenic Fo isolates.
Highlights
Vascular wilt pathogens cause large losses in important agronomical crops (Michielse & Rep, 2009; Yadeta & Thomma, 2013)
Using the same procedure Fom001 was found to confer endophyte-mediated resistance (EMR) to Fol4287 to an extent similar to Fo47 (Figure 1d) as fresh weight (FW) and disease index (DI) were affected to a comparable extent in this tripartite interaction (Figure 1e,f). These findings show that the nonhost pathogen Fom001 is an endophyte of tomato and confers EMR, reducing disease symptoms caused by a tomato pathogenic Fusarium oxysporum (Fo) strain
We report that the endophyte Fo47 and the melon pathogen Fom001 become hypercolonizers of pattern-triggered immunity (PTI)-compromised tomato plants
Summary
Vascular wilt pathogens cause large losses in important agronomical crops (Michielse & Rep, 2009; Yadeta & Thomma, 2013). The observations that flg22- and chitosan-induced PTI responses are compromised in both MM-∆spAvr tomato and in ∆spAvr Arabidopsis indicate that the Avr effector targets a conserved—and shared—signalling component downstream of the respective PRR receptors, making ∆spAvr transgenic lines a good proxy for a PTI mutant. An effective PTI response to Fo47 appears to be instrumental in controlling the extent of host colonization by a Fo endophyte as MM-∆spAvr plants are hypercolonized, as compared to wild-type and MM-Avr plants. Fo47-inoculated MM wild-type and MM-Avr plants consistently showed the least colonization, while MM-∆spAvr showed a significantly higher amount of fungal biomass in the three tomato lines analysed These data show that a compromised PTI results in a more abundant colonization of tomato roots by the endophyte. EMR appears not to rely on PTI as the endophyte-induced immune response was still observed in PTI-compromised tomato
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