Progressive hypertrophy of fat body, muscles, gonads and pleuropodial glands was observed with lengthening diapause incubation in embryos of Aulocara elliotti. Embryonic hemolymph stained more darkly and lipoid materials accumulated in the fat body and other tissues. Gradual increase in volumes was observed in the corpora cardiaca, corpora allata and ventral head glands (ecdysial glands). Termination of diapause was achieved in embryos treated with juvenile hormone analogue (JHA) (4 ethyl phenyl 6.7 epoxy geranyl ether--87%, Stauffer Chemical) applied directly to the egg undiluted or when eggs were immersed in a 10% solution in methanol. Treated embryos terminating diapause underwent rapid teratological morphogenesis, achieving pigmentation and sclerotization as in definitive embryos without engulfing their yolk. In treated embryos which remained in diapause, unusual paired masses of pigmented cells, resembling the melanotic pseudotumors of Drosophila, were observed ventral and lateral to the stomodeum and are thought to be subesophageal body cells (pericardial cell homologues). In some embryos these cells were enlarged, lysed or their nuclei rhexic and pycnotic. This response suggests these cells are target organs for JHA, or perhaps for ecdysone or its precursor released by JHA treatment. Endocrine glands in treated embryos had significantly larger volumes (.01) than those of controls or untreated embryos. The ventral head glands of treated embryos appeared to be cytoplasmically depleted. It is suggested that JHA triggered the release of stored ecdysone (or its precursor produced in the ventral head gland) at a rate too rapid for normal morphogenetic processes, such as dorsal closure, to accompany epidermal maturation. The response to JHA cannot be interpreted as juvenilization, but rather must be considered to be precocious maturation. These results indicate that: 1. diapause development involves a transfer of nutrient materials from the yolk into the fat body and other embryonic tissues where they are available to meet the demands of post-diapause morphogenesis; 2. that embryonic diapause in A. elliotti is a consequence of endocrine deficiency which probably results ultimately from the lack of neurosecretory stimulus from the brain-corpora cardiaca complex; and 3. that the subesophageal body cells, and perhaps the pericardial cells, play an essential role in the embryonic physiology, perhaps in the production of carrier protein and/or an essential growth regulator.