We had shown earlier that embryos of Nauphoeta cinerea contain very high quantities of methyl farnesoate and juvenile hormone III at stages between dorsal closure and hatching, and that the increase in the titre of juvenile hormone III, but not of methyl farnesoate, could be prevented by applying ethoxy-precocene shortly after dorsal closure (Briining et al., 1985, Int. J. Invert. Reprod. Develop., 8 269-278). Here we report that [10-3 HJ methyl farnesoate injected into embryos is epoxidised only to an extremely small extent into juvenile hormone III and hardly metabolised at all. In embryos treated after dorsal closure with a dose of ethoxy-precocene, which did not alter the titre of methyl farnesoate but prevented the increase of the juvenile hormone III titre, we observed a certain delay in development, malformation of the eye and lack of larval characteristics of the cuticle, such as pigmentation and formation of hairs and bristles; using dissection and histological examination we observed that the fat body disintegrated and that the midgut did not differentiate normally, thus impeding yolk resorption. When a dose of juvenile hormone III, which was shown to restore a nearly natural titre for several days, was applied on to ethoxy-precocene treated embryos, the formation of the midgut was normalised and the disintegration of the fat body was less pronounced. We thus have direct evidence that, in embryos, juvenile hormone III plays a role in the differentiation of the midgut epithelium and probably in the development of the fat body, and our data also suggest that this hormone controls the appearance of larval characteristics of the cuticle.
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