Abstract
We tested whether a tobacco, Nicotiana tabacum (L.), plant defense against tobacco aphids, Myzus nictianae (Blackman), might also inhibit the entomopathogenic fungus Pandora neoaphidis (Remaudiere & Hennebert). Growth of fungal colonies exposed to macerated and unmacerated tobacco leaves, hexanal, (E)-2-hexenal, and (E)-2-hexenol was strongly suppressed compared with controls. Large numbers of ungerminated conidia were recovered from the media surrounding the treated colonies, whereas few ungerminated conidia were found in media surrounding the controls. Conidia were then collected onto glass coverslips and exposed to the same treatments during the first 4 h after conidial relase. Relative to controls, hexanal substantially suppressed conidial germination, the leaf material suppressed germination substantially more than hexanal and (E)-2-hexenal was the strongest inhibitor indicating that the principal effect of the plant volatiles was inhibition of conidial germination. Based on scanning electron microscope examination, when conidia were deposited directly onto live aphids instead of cover slips, these volatiles had no effect on aphid infection rates, indicating that the inhibition of conidial germination does not occur when conidia are actually on an aphid surface. Finally, germination of conidia exposed to volatiles of plants previously infested with aphids was substantially suppressed relative to uninfested controls. These studies suggest that tobacco plant volatiles produced in response to wounding such as aphid feeding inhibit conidial germination by the entomopathogen unless the conidia are in direct contact with the aphid integument. We suggest that the conidia respond to presence of wound-induced volatiles by delaying germination so as to increase their probability of finding an aphid host ; the conidia use the plant's wound response as a cue to indicate host proximity. A conceptual model of this process is presented.
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