Abstract
Programmed cell death (PCD) of the silkworm silk glands is triggered by the insect steroid hormone, 20-hydroxyecdysone (20E), and proceeds sequentially through cell shrinkage, nuclear condensation, DNA fragmentation, nuclear fragmentation and apoptotic body formation. A protein synthesis inhibitor, cycloheximide (CHX, 2 mM) induced a cell death that exhibited only nuclear and DNA fragmentation. A concentration of 0.2 mM CHX was ineffective at inducing the cell death when added alone, but in the presence of 20E, a cell death similar to that induced by 2 mM CHX was resulted with accompanying nuclear condensation. Since 2 and 0.2 mM CHX inhibited protein synthesis equally, the DNA and nuclear fragmentation appear to be mediated by a nongenomic action of 20E. In addition, we show a possible involvement of Ca 2+–PKC–caspase-3 like protease pathway in the nongenomic action. The data suggest that 20E-induced PCD is accomplished through the integration of genomic and nongenomic actions.
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