Abstract

During metamorphosis of the hawkmoth, Manduca sexta, accessory planta retractor (APR) motoneurons undergo a segment-specific pattern of programmed cell death (PCD): e.g., APRs from abdominal segment six [APR(6)s] die at pupation in direct response to the prepupal rise in 20-hydroxyecdysone (20E), whereas APR(4)s survive through the pupal stage and die at eclosion (adult emergence). The hypothesis that the death of APR(4)s is triggered by the decline in 20E at eclosion was supported by findings that injection of 20E into developing pupae to delay the fall in 20E delayed APR(4) death. Furthermore, abdomen isolation to advance the fall in 20E caused precocious APR(4) death. In other experiments, APR(4)s were placed in primary cell culture 4 days before eclosion in medium containing 1 μg/ml 20E. A switch to hormone-free medium induced PCD in a significant proportion of APR(4)s, compared to APR(4)s that remained in 20E. Process fragmentation was a reliable early indicator of PCD. These results show that a decline in 20E triggers cell-autonomous PCD of APR(4)s, in contrast to the rise in 20E that triggers cell-autonomous PCD of APR(6)s. Thus, the PCD of homologous motoneurons in different body segments at different developmental times is triggered by different steroid hormone signals.

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