Phorate‐induced Host Defence Responses Condition Acquired Resistance to Tomato Spotted Wilt in Cultivated Peanut (Arachis hypogaea L.)

Phorate is an acetylcholinesterase‐inhibiting organophosphate pesticide used for the control of insects, mites and nematodes. In cultivated peanut (Arachis hypogaea L.), phorate is often used as an in‐furrow, systemic insecticide to reduce thrips populations which vector tomato spotted wilt tospovirus (TSWV). However, phorate‐induced suppression of disease incidence and severity is not solely due to thrips control because other pesticides control thrips but not TSWV. The present research was focused on understanding the biochemical and molecular components of the phorate‐induced host responses that may condition acquired resistance to TSWV in peanut. Phorate treatments adversely affected maximal quantum yield of the light reactions (Fᵥ/Fₘ). A dose‐dependent increase in ascorbic acid content and in activities of the oxidative stress‐related enzymes, catalase and superoxide dismutase was evident following phorate treatment, whereas the level of glutathione reductase was not affected. An RT‐PCR differential display screen identified 35 expressed sequence tags (ESTs) responsive to phorate treatment in peanut leaves. Functional annotations revealed transcriptional regulation of ESTs implicated in primary and secondary metabolism including photosynthesis‐related genes, mitigation of oxidative stress, signalling pathways and pathogenesis‐ and defence‐related proteins. Two ESTs encoding membrane trafficking functions were downregulated, which may reflect reduced internalization and/or subsequent replication of viral particles in phorate‐treated leaves. Time‐course quantitative RT‐PCR analyses further verified fidelity and sensitivity of the mRNA differential display screen and corroborated that systemic spread of TSWV in field‐grown plants is reduced following phorate application. The mélange of differentially regulated gene functions is consistent with a model in which a phorate‐induced breach of redox control culminates in hypersensitive cell death and subsequent induction of systemic acquired resistance.