Target muscles and sensory afferents do not influence steroid-regulated, segment-specific death of identified motoneurons inManduca sexta

The eclosion of the adult Manduca sexta moth is followed by a wave of cell death that eliminates up to 50% of the neurons of the central nervous system within the first few days of imaginal life. While the identity of some of the dying motoneurons has been established, that of most doomed neurons is unknown. Here, we show that the dying cells include peptidergic neurons involved in the control of ecdysis behavior. These cells belong to a small population of 50 neurons that express crustacean cardioactive peptide (CCAP), a potent regulator of the ecdysis motor program, and show increases in cyclic 3′,5′‐guanosine monophosphate at each ecdysis. First, we describe new markers for these neurons and show that they are expressed in these CCAP‐immunoreactive neurons in a complex temporal pattern during development. We then show that these neurons die within 36 h after adult eclosion, the last performance of ecdysis behavior in the life of the animal, via the active, genetically determined process of programmed cell death. The death of these neurons supports the hypothesis that outmoded or unused neurons are actively eliminated. © 1998 John Wiley & Sons, Inc. J Neurobiol 37: 265–280, 1998

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Segment-specific muscle degeneration is triggered directly by a steroid hormone during insect metamorphosis

Hazelett

Weeks

2004

J. Neurobiol.

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During metamorphosis of the hawkmoth, Manduca sexta, some larval muscles degenerate while others are respecified for new functions. In larvae, accessory planta retractor muscles (APRMs) are present in abdominal segments 1 to 6 (A1 to A6). APRMs serve as proleg retractors in A3 to A6 and body wall muscles in A1 and A2. At pupation, all APRMs degenerate except those in A2 and A3, which are respecified to circulate hemolymph in pupae. The motoneurons that innervate APRMs, the APRs, likewise undergo segment-specific programmed cell death (PCD), as a direct, cell-autonomous response to the prepupal peak of ecdysteroids. The segment-specific patterns of APR and APRM death differ. The present study tested the hypothesis that APRM death is a direct, cell-autonomous response to the prepupal peak of ecdysteroids. Prevention of the prepupal peak prevented APRM degeneration, and replacement of the peak by infusion of 20-hydroxyecdysone restored the correct segment-specific pattern of APRM degeneration. Surgical denervation of APRMs did not perturb their segment-specific degeneration at pupation, indicating that signals from APRs are not required for the muscles' segment-specific responses to ecdysteroids. The possibility that instructive signals originate from APRMs' epidermal attachment points was tested by treating the epidermis with a juvenile hormone analog to prevent pupal development. This manipulation likewise did not alter APRM fate. We conclude that both the muscles and motoneurons in this motor system respond directly and cell-autonomously to prepupal ecdysteroids to produce a segment-specific pattern of PCD that is matched to the functional requirements of the pupal body.

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Target muscles and sensory afferents do not influence steroid-regulated, segment-specific death of identified motoneurons inManduca sexta

Cited by 13 publications

References 51 publications

Programmed cell death of an identified motoneuronin vitro: Temporal requirements for steroid exposure and protein synthesis

Programmed cell death of an identified motoneuronin vitro: Temporal requirements for steroid exposure and protein synthesis

Programmed cell death of identified peptidergic neurons involved in ecdysis behavior in the moth,Manduca sexta

Segment-specific muscle degeneration is triggered directly by a steroid hormone during insect metamorphosis

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