Understand the Potential Role of Aureobasidium pullulans, a Resident Microorganism From Grapevine, to Prevent the Infection Caused by Diplodia seriata.

Cátia Pinto,Florence Fontaine,Barbara Courteaux,Mariana Nunes,Ana Catarina Gomes,Christophe Clément,Valéria Custódio,Aurélie Songy,Fanja Rabenoelina

doi:10.3389/fmicb.2018.03047

Abstract

Grapevine trunk diseases (GTDs) are one of the major concern amongst grapevine diseases, responsible for the decline of vineyards and for several economical losses. Since grapevine is naturally colonized by resident microorganisms such as Aureobasidium pullulans, the present challenge is to understand their biocontrol potential and how such microorganisms can be successfully integrated in the control of GTDs. In this context, the first priority consists to exploit the plant-beneficial-phytopathogen interactions in plant model systems, to identify the most prevalent equilibrium limiting expression of GTDs. In the current study, we deep characterized the interaction of a resident and abundant microorganism from grapevine – Aureobasidium pullulans strain Fito_F278 – against D. seriata F98.1, a Botryosphaeria dieback agent, and with plant (cv Chardonnay). Results revealed that A. pullulans strain Fito_F278 was able to reduce significantly the mycelium growth of D. seriata F98.1 at 33.41 ± 0.55%, under in vitro conditions, though this reduction is possibly dependent on a direct interaction between strain Fito_F278 and pathogen. Furthermore, strain Fito_F278 was able to promote an induction of some plant defense responses in cutting plants, 1 week after the D. seriata F98.1 infection. Results evidenced that strain Fito_F278 colonized efficiently grapevine at both epiphyte and endophyte level, could persist on plant roots for long-periods (up to 2 months after its inoculation) and grow at different pH and high salinity conditions. Moreover, a significant decrease of the microbial load from soil and rhizosphere was observed in plants treated with the strain Fito_F278, suggesting its competitivity potential in a microbial ecosystem. Altogether, the present study gives the first insights about the interaction of A. pullulans strain Fito_F278, a resident microorganism, with grapevine, its potential role against a Botryosphaeria dieback agent, and highlights its importance to toward more resilient grapevine.

Highlights

Grapevine is largely attacked by different phytopathogens such as those responsible for powdery mildew, downy mildew, and gray mold (Armijo et al, 2016)
Effect of Aureobasidium pullulans Strain Fito_F278 on Grapevine Defense Responses In order to determine how grapevine responds to strain Fito_F278 in the presence or absence of D. seriata F98.1, a a deep characterization of Aureobasidium pullulans strain Fito_F278, a resident microorganism from grapevine microbiome (Grube et al, 2011; Pinto et al, 2014, 2015), was performed as no evidence of its antagonistic potential was reported against D. seriata, a Botryosphaeria dieback agent
These genes encoded for plant defense proteins (PR6, Gluc), detoxification and stress tolerance (Hahl, heat shock protein (HSP), GST5), phenylpropanoid pathway (STS), cell wall, and water stress (Pip 2.2) were selected from previous studies focusing on grapevine responses to Grapevine trunk diseases (GTDs) (Magnin-Robert et al, 2011; Reis et al, 2016; Spagnolo et al, 2017)

Summary

Introduction

Grapevine is largely attacked by different phytopathogens such as those responsible for powdery mildew, downy mildew, and gray mold (Armijo et al, 2016). Those causing grapevine trunk diseases (GTDs) such as Esca disease, Eutypa and Botryosphaeria diebacks, are of utmost concern to wine industry as these are the most destructive grapevine diseases worldwide (Mugnai et al, 1999; Larignon et al, 2009; Bertsch et al, 2012; Fontaine et al, 2016a). Botryosphaeria dieback is caused by Botryosphaeriaceae species such as Diplodia seriata, Botryosphaeria dothidea, Diplodia mutila, or Neofusicoccum parvum and are the causal agents of trunk cankers and grapevine decline (Larignon et al, 2009; Úrbez-Torres, 2011; Fontaine et al, 2016a,b)

Methods

Discussion

Conclusion