LAUSR

Many studies have shown that virus infection alters phytohormone signaling and insect vector contact with hosts. Increased vector contact and movement among plants should increase virus survival and host range. In this study we examine the role of virus-induced changes in phytohormone signaling in plant-aphid interactions, using Pea enation mosaic virus (PEMV), pea aphids ( Acyrthosiphon pisum ), and pea ( Pisum sativum ) as a model. We observed that feeding by aphids carrying PEMV increases salicylic acid and jasmonic acid accumulation in pea plants compared to feeding by virus-free aphids. To determine if induction of the oxylipin jasmonic acid is critical for aphid settling, attraction, and retention on PEMV-infected plants, we conducted insect bioassays using virus-induced gene silencing (VIGS), an oxylipin signaling inducer, methyl jasmonate (MeJA), and a chemical inhibitor of oxylipin signaling, phenidone. Surprisingly, there was no impact of phenidone treatment on jasmonic acid or salicylic acid levels in virus-infected plants, though aphid attraction and retention were altered. These results suggest that the observed impacts of phenidone on aphid attraction to and retention on PEMV-infected plants are independent of the jasmonic acid and salicylic acid pathway but may be mediated by another component of the oxylipin signaling pathway. These results shed light on the complexity of viral manipulation of phytohormone signaling and vector-plant interactions.