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Ecdysteroid induction of embryonic morphogenesis in a parasitic wasp.

Development of the parasitic wasp Copidosoma floridanum (Hymenoptera: Encyrtidae) is unusual in two ways. As many as 3000 embryos are formed from a single egg and embryonic morphogenesis is closely synchronized with the onset of the metamorphosis of its host. Given this extreme synchrony between parasite and host development, we undertook a series of experiments to determine whether host endocrine factors regulate C. floridanum embryonic morphogenesis. Here we report that C. floridanum embryos must develop for 9 days before acquiring the competence to undergo morphogenesis. Furthermore, several pieces of evidence suggest that ecdysteroids of host origin regulate induction of C. floridanum morphogenesis. First, competent embryos initiated morphogenesis when transplanted into host larvae and pupae, host stages possessing elevated ecdysteroid titers, but not when transplanted into adult moths. Second, morphogenesis was arrested by ablation of the host's source of ecdysone, but could be rescued by injection of 20-hydroxyecdysone in a dose-dependent manner. Finally, a segment of DNA encoding a zinc finger nearly identical in sequence to a portion of the ecdysone receptor of Drosophila melanogaster was isolated and characterized from C. floridanum. This putative ecdysone receptor probe indicated that expression of this gene was correlated with the initiation of C. floridanum embryonic morphogenesis. The temporal pattern of putative receptor RNA accumulation increased in association with the onset of morphogenesis, while the spatial pattern of expression was associated with the invagination of cells forming the gastrula. Together, these data suggest that ecdysone of host origin is directly involved in the induction of C. floridanum embryonic morphogenesis.

Amino Acid Sequence

AFR1 acts in conjunction with the alpha-factor receptor to promote morphogenesis and adaptation.

Mating pheromone receptors activate a G-protein signaling pathway that induces changes in transcription, cell division, and morphogenesis needed for the conjunction of Saccharomyces cerevisiae. The C terminus of the alpha-factor pheromone receptor functions in two complex processes, adaptation and morphogenesis. Adaptation to alpha-factor may occur through receptor desensitization, and alpha-factor-induced morphogenesis forms the conjugation bridge between mating cells. A plasmid overexpression strategy was used to isolate a new gene, AFR1, which acts together with the receptor C terminus to promote adaptation. The expression of AFR1 was highly induced by alpha-factor. Unexpectedly, cells lacking AFR1 showed a defect in alpha-factor-stimulated morphogenesis that was similar to the morphogenesis defect observed in cells producing C-terminally truncated alpha-factor receptors. In contrast, AFR1 overexpression resulted in longer projections of morphogenesis, which suggests that this gene may directly stimulate morphogenesis. These results indicate that AFR1 encodes a developmentally regulated function that coordinates both the regulation of receptor signaling and the induction of morphogenesis during conjugation.

Acclimatization