The soybean aphid (Aphis glycines) is one of the most important pests of soybeans in the Northcentral region of the US. It has been hypothesized that aphids avoid effective defenses by inhibiting induction of jasmonate-regulated plant defense responses. Given the role fatty acids play in jasmonate-induced plant defenses, we analyzed the fatty acid profile of soybean leaves and seeds from aphid-infested plants. Results showed that aphids reduce the amount of polyunsaturated fatty acids in leaves with a concomitant increase in palmitic acid. In seeds, a reduction in polyunsaturated fatty acids was associated with an increase in stearic acid and oleic acid. These changes were similar in both the regular 7% seed linolenic acid soybeans as well as the low (1% and 3%) seed linolenic acid varieties. One of the polyunsaturated fatty acids, linolenic acid, is the precursor of jasmonate; thus, these changes in fatty acid metabolism may be examples of "metabolic hijacking" where one organism takes over the metabolism of another, leading to prevention of production of compounds that would otherwise be detrimental to the attacker. The pattern of fatty acid changes points to a possible interference in fatty acid biosynthesis and desaturation, especially at FAB1, leading to an increase in palmitate, and at FAD2 and FAD6, leading to a reduction in polyunsaturated fatty acids. However, the regulation does not seem to be transcriptional.

We also investigated the effects of soybean aphids on the expression of wound/JA induced defenses in soybean. From the results, transcription of two JA-regulated genes, PIN2 and GH3, was significantly repressed in aphid-infested and wounded soybeans when compared to wounded but uninfested plants. A similar result was obtained when JA was externally applied to aphid-infested soybeans. To gain insights on the mechanism of suppression of defenses, we performed an analysis of the fatty acid composition of plants under the same treatments, and found that in the treatments where repression of the wounding and JA responses occurred, i.e. aphids and aphid + wounded, there was an increase in the content of 16:0 fatty acid with a corresponding decrease in polyunsaturated fatty acids (18:2 and 18:3). A time course experiment revealed that differences in 18:3 content between infested and uninfested plants become evident 1 day after infestation but become statistically significant 7 days later. While the role of 16:0 in this interaction is not known, we hypothesize that the reduction in 18:3 may block the JA defense response pathway by minimizing the amount of precursors available to initiate the biosynthesis of JA. Reduced JA biosynthesis could explain the reduced response to wounding observed in aphid-infested plants. However, other mechanisms of suppression may still exist, since aphids were also able to block JA-responses when JA is exogenously applied. Therefore, we showed the aphids avoid induction of JA mediated defenses by multiple mechanisms, one of which involves hijacking the plants' fatty acid metabolism, reducing the production of polyunsaturated fatty acids that feed the oxylipin pathway. The reduction in transcription of JA mediated wound inducible genes in presence of aphids also implies that aphid-infested plants may become more susceptible to other insect herbivores such as caterpillars since they fail to mount a full JA mediated wound response. This is particularly important in the field conditions where multiple pests may infest the plants at the same time.