Mixed infections of fungal trunk pathogens and induced systemic phenolic compound production in grapevines

Authors: Wallis, Christopher; Gorman, Zachary; Galarneau, Erin; Baumgartner, Kendra

Submitted to: Frontiers in Fungal Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/1/2022
Publication Date: 9/15/2022
Citation: Wallis, C.M., Gorman, Z.J., Galarneau, E.R., Baumgartner, K. 2022. Mixed infections of fungal trunk pathogens and induced systemic phenolic compound production in grapevines. Frontiers in Fungal Biology. 3. Article 1001143. https://doi.org/10.3389/ffunb.2022.1001143.
DOI: https://doi.org/10.3389/ffunb.2022.1001143

Interpretive Summary: Grapevines, like many perennial plants, will inevitably become infected by multiple pathogens, such as infections by fungal canker causing fungi Diplodia seriata, Neofusicoccum parvum, and Phaeomoniella chlamydospora. Studies were undertaken to see how these pathogens affect one another as well as host defense-related chemistry. Prior infections only affected Diplodia seriata lesion development, but not the other pathogens. Most phenolic compound levels were significantly greater in plants previously infected with Diplodia seriata as well, but there were no significant correlations between phenolic levels and lesion sizes overall. These results expand our knowledge about how fungal canker pathogens interact with grapevine hosts.

Technical Abstract: Within vineyards, grapevines will inevitably become infected with fungal canker pathogens including Diplodia seriata, Neofusicoccum parvum, and Phaeomoniella chlamydospora. Despite initial studies examining grapevine host interactions with these pathogens, more knowledge is needed about systemic changes that infections may occur as these could result in indirect interactions among multiple pathogens. Thus, this study examined changes in phenolic compounds away from lesion sites for grapevines infected with Diplodia seriata, Neofusicoccum parvum, or Phaeomoniella chlamydospora, and then subsequently evaluate if such changes could affect secondary infections. Prior fungal infections only affected the development of subsequent Diplodia seriata infections. Effects of fungal infections on phenolic compounds was variable, yet prior infection by Diplodia seriata appeared to significantly increase most phenolic compounds distally. It was reasonable to hypothesize that pre-existing phenolic levels can slow initial lesion development of fungal canker pathogens, especially for Diplodia seriata, but over time the pathogens can overcome or neutralize phenolic compounds and grow unimpeded. These results demonstrate that effects of one fungal canker pathogen infection is generally unable to distally affect another long-term, albeit shifts in host phenolics and other plant defenses do indeed occur.