Abstract
Summary The intimate association of host and fungus in arbuscular mycorrhizal (AM) symbiosis can potentially trigger induction of host defence mechanisms against the fungus, implying that successful symbiosis requires suppression of defence.We addressed this phenomenon by using AM‐defective vapyrin (vpy) mutants in Petunia hybrida, including a new allele (vpy‐3) with a transposon insertion close to the ATG start codon. We explore whether abortion of fungal infection in vpy mutants is associated with the induction of defence markers, such as cell wall alterations, accumulation of reactive oxygen species (ROS), defence hormones and induction of pathogenesis‐related (PR) genes.We show that vpy mutants exhibit a strong resistance against intracellular colonization, which is associated with the generation of cell wall appositions (papillae) with lignin impregnation at fungal entry sites, while no accumulation of defence hormones, ROS or callose was observed. Systematic analysis of PR gene expression revealed that several PR genes are induced in mycorrhizal roots of the wild‐type, and even more in vpy plants. Some PR genes are induced exclusively in vpy mutants.Our results suggest that VPY is involved in avoiding or suppressing the induction of a cellular defence syndrome that involves localized lignin deposition and PR gene induction.
Highlights
Arbuscular mycorrhiza (AM) is a mutualistic association of the majority of land plants with fungi of the subphylum Glomeromycotina (Smith & Read, 2008; Spatafora et al, 2016), which confers various benefits to the plant host (Chen, M et al, 2018)
Microscopic and molecular analysis using a range of defence markers indicates that the abortion of the arbuscular mycorrhizal (AM) fungus in vpy mutants involves a cellular defence response that is independent of callose deposition and of the classical stress hormones salicylic acid, jasmonic acid and ethylene, but is associated with induction of several PR genes, and with cell wall lignification during intracellular invasion. 121
None of the mutants accumulated significant amounts of lignin at infection points, either (Fig. S10c-g), including the vpy-2 mutant, while prominent lignin deposition was observed along the vasculature in the stele (Fig. S10h), as in all other genotypes. These results indicate that lignin accumulation at AMF infection points is not part of the phenotype of symbiosis mutants in Medicago. 539 Resistance of vpy-3 does not correlate with accumulation of SA, JA, or ethylene We tested whether papilla formation in mycorrhizal vpy mutants is accompanied by accumulation of the defence hormones salicylic acid (SA), jasmonic acid (JA), or ethylene
Summary
Arbuscular mycorrhiza (AM) is a mutualistic association of the majority of land plants with fungi of the subphylum Glomeromycotina (Smith & Read, 2008; Spatafora et al, 2016), which confers various benefits to the plant host (Chen, M et al, 2018). Characteristic markers of defence include the stress hormones salicylic acid (Loake & Grant, 2007), jasmonic acid (Browse, 2009) and ethylene (van Loon et al, 2006a), cell wall reinforcements such as callose and lignin (Millet et al, 2010; Miedes et al, 2014; Chowdhury et al, 2016; Liu et al, 2018), induction of reactive oxygen species (Jones & Dangl, 2006), and the induction of pathogenesis-related (PR) proteins that are thought to have antimicrobial functions and contribute to disease resistance (van Loon et al, 2006b) In this context it is important to note that most of our knowledge on plant defence mechanisms were gained in the shoot (mainly from leaves), while defence mechanisms in the roots are considerably different (Chuberre et al, 2018), and have been explored to a lesser extent. Microscopic and molecular analysis using a range of defence markers indicates that the abortion of the AM fungus in vpy mutants involves a cellular defence response that is independent of callose deposition and of the classical stress hormones salicylic acid, jasmonic acid and ethylene, but is associated with induction of several PR genes, and with cell wall lignification during intracellular invasion. 121
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