MOLECULAR MECHANISMS OF PROGRAMMED CELL DEATH BY ECDYSTEROID IN BOMBYX ANTERIOR SILK GLAND

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Programmed cell death (PCD) of anterior silk glands of the silkworm, Bombyx mori, is induced by 20E elicits its effects via binding with a heterodimeric nuclear receptor (EcR/USP) and acting as a transcriptional factor. In the PCD, however, we found various events associated with the cell death, which cannot be interpreted from the point of view of 20E action via nuclear receptor, and therefore we assumed the presence of a non-genomic action of 20E via ecdysone membrane receptor (mEcR). We confirmed the presence of the binding sites of ecdysteroids on membrane proteins. The responsible protein is embedded in plasma membrane and possesses a high binding activity with ecdysteroids. In addition, we found that 20E increases an intracellular cAMP level as rapidly as 30 seconds after 20E challenge. We also demonstrated that activation of protein kinase C and caspase 3 is involved in the 20E-induced PCD. The PCD precedes via plasma membrane blebbing, cellular shrinkage, DNA oligonucleosomal fragmentation, nuclear condensation, nuclear fragmentation and apoptotic body formation. Blebbing, cell shrinkage and apoptotic body formation are under the control of genomic action of 20E while other events are under the non-genomic action of 20E, probably through mEcR. The present results suggest that a single steroid hormone exerts its physiological effects through both genomic and nongenomic pathways.