Abstract
BackgroundPhloem-feeding insects can manipulate plant-induced resistance and are able to suppress effective jasmonic acid/ethylene (JA/ET) defenses by the induction of inefficient salicylic acid (SA) based responses. As a result, activation of the phenylpropanoid biosynthesis pathway in transgenic plants is anticipated to cause complex interactions between phloem-feeding insects and their host plants due to predicted contradiction between two defense forces: the toxicity of various phenylpropanoids and the accumulation of SA via a branch of the activated pathway.Methodology/Principal FindingsHere, we investigated the effect of activating the phenylpropanoids pathway in Nicotiana tabacum, by over-expression of the PAP1 transcription factor, on the whitefly Bemisia tabaci, a phloem-feeding insect model. Our performance assays indicated that the over-expression made the transgenic plants a more suitable host for B. tabaci than wild-type (WT) plants, although these plants accumulated significantly higher levels of flavonoids. Transcription analyses of indicator genes in the SA (PR1a) and JA/ET (ERF1, COI1 and AOC) pathways followed by quantification of the SA and JA hormone levels, indicated that B. tabaci infestation periods longer than 8 hours, caused higher levels of activity of SA signaling in transgenic plants and higher levels of JA/ET signaling in WT plants.Conclusions/SignificanceTaken together, these results emphasize the important role JA/ET-induced defenses play in protecting plants from successful infestation by B. tabaci and likely other phloem-feeding insects. It also indicates the necessity of phloem feeders to suppress these defenses for efficient utilization of plant hosts. Our data also indicate that the defensive chemistry produced by the phenylpropanoids pathway has only a minor effect on the insect fitness.
Highlights
Plants are in constant battle with herbivorous insects, and have evolved sophisticated defense systems to cope with insect attack, which include both induced and constitutive mechanisms [1,2]
The salicylic acid (SA) pathway is primarily activated in response to biotrophic pathogens, while the jasmonic acid/ethylene (JA/ET) pathways are induced in response to necrotrophic pathogens and in response to wounding and tissue-damaging by insect feeding [7,8], recent evidence suggests that jasmonic acid (JA) can play a role in resistance against specific types of biotrophic fungi [9]
This finding can be related to the intensive mortality of B. tabaci adults observed at this time point, after which new adults were added to the plants (Figure 3A)
Summary
Plants are in constant battle with herbivorous insects, and have evolved sophisticated defense systems to cope with insect attack, which include both induced and constitutive mechanisms [1,2]. ERF1 is induced by simultaneous action of the JA and ET signaling pathways, and plays a key role in the activation of plant defenses against necrotrophic pathogen infection by regulating defense-related genes, such as PDF1.2 [16,18]. JA/ET has been shown to negatively affect SAdependent gene expression [21] This cross-talk helps the plant to minimize fitness costs and creates a flexible signaling network that allows the plant to fine-tune its defense response to the invaders encountered [14,22]. Activation of the phenylpropanoid biosynthesis pathway in transgenic plants is anticipated to cause complex interactions between phloemfeeding insects and their host plants due to predicted contradiction between two defense forces: the toxicity of various phenylpropanoids and the accumulation of SA via a branch of the activated pathway
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