期刊
ENTOMOLOGIA EXPERIMENTALIS ET APPLICATA
卷 131, 期 2, 页码 178-188出版社
WILEY
DOI: 10.1111/j.1570-7458.2009.00836.x
关键词
volatile organic compounds; Euschistus heros; semiochemicals; tritrophic interactions; Glycine max; Hymenoptera; cis-jasmone; Scelionidae; Fabaceae; Homoptera; Pentatomidae
类别
资金
- Brazilian Council for Scientific and Technological Development (CNPq)
- Distrito Federal Research Foundation (FAPDF)
- Empresa Brazileira de Pesquisa Agropecuaria (EMBRAPA)
- Biotechnology and Biological Sciences Research Council
After herbivore attack or chemical activation, plants release a blend of volatile organic compounds (VOCs) that is qualitatively or quantitatively different to the blend emitted by an undamaged plant. The altered blend of VOCs is then usually attractive to the herbivore's natural enemies. Soybean, Glycine max (L.) (Fabaceae), when damaged by stink bug herbivory, has been shown to emit a blend of VOCs that attracts the stink bug egg parasitoid Telenomus podisi (Ashmead) (Hymenoptera: Scelionidae) to the plant. In this study, our aim was to investigate changes in the VOC profile of soybean (var. BR16) elicited by the naturally occurring plant activator cis-jasmone, and to determine whether these changes elicited the attraction of T. podisi. cis-Jasmone elicited chemical defence in soybean similar to that previously reported for stink bug damage. The main components induced by cis-jasmone were camphene, myrcene, (E)-ocimene, methyl salicylate, and (E,E)-4,8,12-trimethyltrideca-1,3,7,11-tetraene. In Y-tube behavioural bioassays, T. podisi preferred cis-jasmone treated plants over untreated plants. Thus, cis-jasmone appears to induce defence pathways in soybean similar to those induced by stink bug damage, and this phenomenon appears to be a promising tool for the manipulation of beneficial natural enemies in future sustainable stink bug control strategies. The delay in response demonstrates that cis-jasmone treatment is not directly causing the response, but, more importantly, that it is causing activation of induced defence, long after initial treatment.
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