Defense remodelling by ectomycorrhizal fungi in non-hosts

Root colonizing beneficial microorganisms promote growth of host plants and protect them against biotic threats. These microbes are considered as sustainable replacements for the hazardous chemical treatments in agriculture. Ectomycorrhizal fungi, a class of beneficial fungi colonizing trees of a certain genera, protects the host’s systemic tissue from herbivory by priming defense genes and metabolites. Whether host-symbiotic interaction is a requisite for induced systemic resistance (ISR) has not been determined so far. This thesis aimed to investigate host specificity in ISR by studying the altercations in a non-mycorrhizal host, Arabidopsis thaliana (Col-0), against cabbage looper (Trichoplusia ni) after root treatment with an ectomycorrhizal fungus (L. bicolor). To find out if mycorrhization is essential for ISR, Col-0 roots were treated with L. bicolor and the foliar tissue was challenged with T. ni larvae. Though there was no visible penetration of L. bicolor in Col-0 roots, ISR was triggered by negatively affecting T. ni weight gain. The expression of defense genes (VSP, PDF1.2 or PR1) or phytohormone accumulation (JA, JA-Ile, ABA, SA) in Col-0 leaves was not significantly influenced by L. bicolor. However, L. bicolor-triggered ISR was attributed by increasing the accumulation of the secondary metabolite, camalexin, in systemic leaves. Further characterization of the ISR signalling pathway using Arabidopsis mutants, showed that L. bicolor-induced ISR is dependent on the CYP79B2/B3 and CYP81F2 of the tryptophan pathway, jasmonic acid signalling via COI1 and salicylic acid signalling via SID2 and NPR3/4 and the iron homeostasis regulator, MYB72. Unlike other beneficial microbes that suppress basal plant defenses, L. bicolor induced oxidative burst and activated the mitogen-activated protein kinase signalling cascade in Col-0. Also, Col-0 root treatment with heat-killed L. bicolor induced ISR against the larvae. These observations indicated that cell wall component(s) of L. bicolor can trigger ISR. The fungal cell wall component, chitin, when treated on Col-0 roots, reduced T. ni growth by 38% and L. bicolor-triggered ISR was dependent on the chitin receptor, CERK1. Moreover, at the expense of triggering ISR against herbivory, chitin induced susceptibility in Col-0 against the hemibiotrophic pathogen, Pseudomonas syringae. Data from this thesis highlights that host adaptability or symbiotic association is not necessary for altering systemic defense responses. Screening other microbial patterns with hosts and non-hosts can provide us answers whether ISR is a broadly conserved mechanism in systemic plant immunity