Abstract

Juvenile hormone (JH) is a key agent in the regulation of insect development, and thus it must effect proper gene management during ontogeny. How this occurs is as yet a mystery, but JH can alter chromosome function as assayed by puffing in polytene chromosomes of Diptera (Lezzi and Gilbert, 1969) and models based on gene regulation have been presented for its action (Williams and Kafatos, 1971). Therefore it seems appropriate to approach the study of JH action from a genetic standpoint. Mutant genes causing defects in JH action in Drosophila might be expected to develop lethal morphogenetic irregularities during embryonic, larval, or pupal stages (Dearden, 1964; Bryant and Sang, 1968; Ashburner, 1970; Madhavan, 1973; Postlethwait, 1974). Studying the biochemistry of these moribund animals might reveal only frustrating artifacts. A more convenient system might involve a tissue which responds to JH but which is unnecessary for the individual’s survival. For example, in many insects JH is required for some step in oogenesis (see Doan, 1973; Engelmann, 1970). A genetic approach to the hormonal control of oogenesis in Drosophila seems appropriate due to several factors. Drosophila females can lay up to 60% of their weight per day in eggs (King et al., 1955; David et al., 1968), which indicates the prodigious biosynthetic activity directed toward oogenesis. Furthermore, the ultrastructure of normal oogenesis has been very carefully described by King (1970). Finally, a great many female sterile mutants are known (King and Mohler, 1975). Our investigation exploits these properties to approach the following three points regarding JH control of oogenesis: (1) What is the endocrinology of oogenesis in Drosophila melanogaster? (2) How are female sterile mutants altered in JH action? (3) How does JH act to control the appearance of specific proteins in developing oocytes?

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