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Published online by Cambridge University Press: 10 July 2009
Only a few symbionts and mycetocytes in the bird cherry–oat aphid Rhopalosiphum padi (Linnaeus) reared for three days were affected on plants treated with 50 ppm benomyl. The symbionts of aphids reared for the same time on plants treated with 100 ppm benomyl, however, were abnormal and at an early stage of degeneration. Mycetocytes contained more residual bodies than normal. The symbionts and mycetocytes of embryonic aphids on such plants were also abnormal. When aphids were reared for 3 days on plants treated with 200 ppm benomyl, the symbionts and mycetocytes were drastically affected. Most of the symbionts were very abnormal and had degenerated. The mycetocytes were full of electron-lucent and electron-dense structures intermixed with abnormal cell organelles. Symbionts and mycetocytes of embryonic aphids were abnormal. In contrast, when the systemic insecticide pirimicarb was used to kill aphids, it did not affect the symbionts and mycetocytes. When aphids were reared for 6 days on plants treated with 50 ppm benomyl, their symbionts and mycetocytes and those of their offspring were also degenerate and abnormal, as were those of Fl generation aphids from mothers reared from birth on plants treated with 50 ppm benomyl. From a consideration of the known mode of action of benomyl on tubulin and the presence of tubulin only in the mycetocyte cells, it is concluded that the degeneration of symbionts in benomyl-treated aphids is a secondary consequence of the degeneration of the aphid mycetocytes.