© 2006 The Authors Entomologia Experimentalis et Applicata 120: 175–188, 2006 Journal compilation © 2006 The Netherlands Entomological Society 175 Blackwell Publishing Ltd Impact of chemical elicitor applications on greenhouse tomato plants and population growth of the green peach aphid, Myzus persicae Anthony J. Boughton 1 , Kelli Hoover 2 & Gary W. Felton 2 * 1 USDA-ARS Invasive Plant Research, 3225 College Avenue, Fort Lauderdale, Florida 33314, USA and 2 Department of Entomology, Pennsylvania State University, University Park, Pennsylvania 16802, USA Accepted: 3 April 2006 Key words: induced defenses, benzothiadiazole, methyl jasmonate, harpin, ethephon, protease inhibitors, polyphenol oxidases, peroxidases Homoptera, Aphididae Abstract Recent advances in the understanding of plant signaling pathways have opened the way for using elicitor-induced plant resistance as a tactic for protecting plants against arthropod pests. Four common elicitors of induced responses in tomato, Lycopersicon esculentum Mill. (Solanaceae), were evaluated with regard to phytotoxicity, induction of plant defensive proteins, and effects on population growth and fecundity of a common pest, the green peach aphid, Myzus persicae (Sulzer) (Homoptera: Aphididae). Ethephon and methyl jasmonate (MJ) treatments caused varying degrees of phytotoxicity. Ethephon caused pronounced changes in plant growth form and severe, dose-dependent negative impacts on plant growth and flowering. Effects with MJ were milder, but still caused temporary inhibition of development, leading to smaller plants and delayed flowering. The commercial elicitors benzothiadiazole (BTH) and harpin did not cause detectable phytotoxicity. The highest doses of ethephon and MJ significantly increased leaf peroxidase (POD) levels but only MJ treatments significantly increased polyphenol oxidase (PPO) levels. BTH and harpin had no detectable effects on POD and PPO. Populations of green peach aphids grew significantly more slowly on plants treated with BTH or MJ than on control plants or plants treated with harpin or ethephon. Slowed aphid population growth on BTH-treated plants was due to significant reductions in aphid fecundity, although this was independent of changes in time to onset of reproduction or time to death. Aphid fecundity was also reduced on MJ- treated plants relative to controls, but this difference was not statistically significant, suggesting that other mechanisms are involved in slowing aphid population growth on MJ-treated plants. Growth of aphid populations on plants treated with a MJ–BTH mixture was reduced almost as much as with treatments of MJ alone, suggesting that antagonism between JA-dependant and SA-dependent plant signaling pathways is only mild with regard to induced defenses against aphids. Introduction Induced resistance to herbivory or plant pathogens has been documented in over 100 plant systems (Karban & Baldwin, 1997; Heil & Bostock, 2002) including many cultivated crops (Gorlach et al., 1996; Korth & Dixon, 1997; Stout et al., 1998a; Kahl et al., 2000; Omer et al., 2001; Engelberth et al., 2004). Better understanding of the signaling pathways in plants that control induced responses has led to the discovery of natural and synthetic compounds, called elicitors, that induce responses in plants similar to those triggered by natural herbivory or pathogen infection (Karban & Kuc, 1999). At least six signal pathways have been implicated in plant responses to pathogens and herbivores (Walling, 2000). Four of the pathways, (1) the reactive oxygen species (ROS)/ nitric oxide (NO) pathway, (2) the salicylic acid (SA) pathway, (3) the jasmonic acid (JA)/ethylene sequential pathway, and (4) the JA/ethylene concomitant pathway are frequently associated with responses to pathogens. The other two pathways, (1) the JA-dependent wound pathway, and (2) the JA-independent wound pathway, are primarily associated with herbivore feeding. Many workers have * Correspondence: Gary W. Felton, Department of Entomology, Pennsylvania State University, University Park, PA 16802, USA. E-mail: gwf10@psu.edu