THE PHYSIOLOGY OF INSECT DIAPAUSE. IX. THE CYTOCHROME OXIDASE SYSTEM IN RELATION TO THE DIAPAUSE AND DEVELOPMENT OF THE CECROPIA SILKWORM

Abstract
The effects of mixtures of CO and O2 on growth and metamorphosis of the Cecropia silkworm were examined at successive stages of embryonic and post-embryonic development. Embryos, mature larvae, and adults are killed by 5 days of exposure to CO/O2 ratios of 20:1 or 25:1. Diapausing pupae, by contrast, survive at least 21 days of exposure to CO/O2 ratios as high as 33:1. While failing to interfere with the viability of diapausing pupae, CO blocks or greatly retards termination of the pupal diapause; it also inhibits healing of exptl. wounds in the pupal integument. The ability to survive in the presence of high pressures of CO persists throughout the early stages of adult development. Exposure of the developing, post-diapausing insect to suitable pressures of CO establishes and enforces an artificial diapause which is reversed upon return to air. Inhibition of adult development by CO is light-reversible; the degree of inhibition is a function of the CO/O2 ratio. These findings indicate that the effects of CO are due to the poisoning of cytochrome oxidase. Resistance to CO, as in the diapausing pupa, signals the presence and utilization of an oxidase other than cytochrome oxidase. On the basis of these several lines of evidence, it is concluded that growth and metamorphosis, at all stages in the life history, are dependent on metabolism catalyzed by cytochrome oxidase. The function of cytochrome oxidase is likewise prerequisite for the maintenance of life of the embryo, larva, and adult. Only the diapausing pupa survives without regard to the presence or function of cytochrome oxidase, the maintenance metabolism of the pupae being served by an unidentified oxidase which is insensitive to CO. With the termination of pupal diapause the growth and differentiation of the adult moth again requires the function of the cytochrome oxidase system. This fact is considered in relation to the endocrine control of the pupal diapause.