Summary 1. The process of oosorption in insects is discussed with regard to the chronology of events which occur during resorption of oocytes and the role of their auxiliary cells. 2. A theory of neuroendocrine control of oosorption is put forward, suggesting that cessation of juvenile hormone secretion is the most important factor leading to this degradative process in spite of the fact that oosorption and vitellogenesis can occur simultaneously. 3. The diversity of behavioural, ecological and physiological factors which promote oosorption is discussed with an emphasis on differences and similarities among representatives of major insect groups, and the manner in which oosorption provides an ovipositional strategy.

The ovaries of the mosquito Aedes aegypti cultured in vitro secrete material that behaves like ecdysone in a radioimmunoassay. The material was identified as aecdysone by high-resolution liquid and gas-liquid chromatography. Secretion reached a maximum 16 hr after a blood meal as shown by bioassay and direct determination. Ovariectomy reduced the concentration of ecdysone in the adult after a blood meal. Qualitative analysis of whole-body extracts indicated fi-ecdysone to be the principal species present. Thus the ovaries appear to secrete a prohormone, a-ecdysone, which is converted to,-ecdysone. ,-ecdysone plays a significant role in stimulating egg development in the adult mosquito and may have reproductive roles in other insects.In mosquitoes the blood meal triggers egg development. This process, which has been found to be quite complex (1), involves the elaboration of yolk for later use by the developing embryo. The major proteins which become yolk are synthesized by the fat body, secreted into the hemolymph, and selectively taken up by the developing oocyte (2, 3). These proteins have been termed vitellogenins (4). Recent investigations into the control of this process showed that, in contrast with most insects, the mosquito ovary was the source of a hormonal factor which activated and maintained vitellogenin synthesis by the fat body (5). Thus synthesis by the fat body was abolished by ovariectomy and restored by reimplantation. Further, when ovaries from blood-fed females were incubated in vitro with the inactive fat body from unfed females, synthesis of vitellogenin was activated. This ovarian hormone was designated the vitellogenin stimulating hormone, VSH (1).The discovery that injected f3-ecdysone stimulates egg development (6) and dopa decarboxylase activity (7) in the absence of a blood meal led us to investigate the possibility that VSH might be f3-ecdysone. Our results indicated that f3-ecdysone mimicked VSH in vivo and in vitro (8) and that material with ecdysone-like activity could be detected in mosquitoes after a blood meal (9). These lines of evidence strongly suggested that VSH was fl-ecdysone or a closely related steroid. We here describe experiments designed to identify the secretory product of the ovary. METHODSMosquitoes (Aedes aegypti) were reared at 27 + 0.50 using standard techniques (8, 9). The assay for vitellogenin synthesis has been described in detail (1, 8). The radioimmunoassay (RIA) was performed as previously described (10, 11).Ovaries were removed from females 15 hr after a rabbit blood meal and incubated at 250 with gentle shaking in groups of 100 in 100,ul of a defined medium (8). After 24 hr the medium was removed and the ovaries were rinsed with saline. An equal volume of methanol was added to the combined medium and rinse. Particulates were removed by filtration. The extract was evaporated to dryness under reduced pressure, redissolved in chloroform:methanol (2:1) and partitioned against water according to Folch et al. (12). The epiphase was dried under vacuum ...

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In the blood-fed mosquito, peak vitellogenin synthesis occurs 24-32 h after the meal, dropping t o resting levels by 40 h. Challenging fat body with ecdysterone in vitro at various times after a blood meal demonstrated a refractory period at about 50 h, when there was also a drastic decrease in mitochondria, rough endoplasmic reticulum, ribosomes, and glycogen in fat body cells. When fat bodies from sugar-fed females were incubated with continuous ecdysterone in vitro, vitellogenin synthesis reached a peak a t 30 h, but then declined even in the presence of ecdysteron;. This was not due t o the in vitro conditions since fat bodies were responsive, even if first exposed to ecdysterone, after 80 h in vitro. If ecdysterone was removed, vitellogenin synthesis ceased. If it was replaced, the fat body responded again only if the initial removal was done during the first 30 h. It is proposed that the falling ecdysterone titre is the major cause of cessation of vitellogenin synthesis, but that synthesis is programmed t o decline even if exposure t o ecdysterone is abnormally prolonged.