scholarly journals Hormonally mediated reprogramming of muscles and motoneurones during the larval-pupal transformation of the tobacco hornworm, Manduca sexta

1986 ◽  
Vol 125 (1) ◽  
pp. 1-13 ◽  
Author(s):  
J. C. Weeks ◽  
J. W. Truman

The larval-pupal transformation of Manduca sexta results from an exposure to ecdysteroids in the absence of juvenile hormone (the commitment pulse), followed by a larger exposure to ecdysteroids (the prepupal peak) with a reappearance of juvenile hormone (JH). The prepupal ecdysteroid peak triggers the degeneration of abdominal muscles, and the dendritic regression and death of identified motoneurones. The present experiments examined the role of the commitment pulse in the larval-pupal reprogramming of these cells. The commitment pulse did not overtly affect the muscles and motoneurones, but it switched their hormonal responsiveness; before the commitment pulse, exposure to ecdysteroids in the presence of JH had no effect on the larval cells, whereas after the commitment pulse the same treatment caused regression and death. Thus, JH lost its ability to prevent pupal development. Furthermore, treatment with ecdysteroids in the absence of JH before the commitment pulse promoted pupal development much less effectively than did the same treatment given after the commitment pulse, indicating that the commitment pulse facilitates the subsequent responsiveness to ecdysteroids. Thus, the commitment pulse covertly causes both qualitative and quantitative changes in the hormonal sensitivity of the larval muscles and motoneurones.

1986 ◽  
Vol 120 (1) ◽  
pp. 41-58 ◽  
Author(s):  
D. B. Rountree ◽  
W. E. Bollenbacher

Pupal development is elicited early in the last larval instar of the tobacco hornworm, Manduca sexta (Johannson), by a precise temporal and quantitative increase in the haemolymph titre of 20-hydroxyecdysone. This increase in the titre is referred to as the pupal commitment peak, and it occurs once the titre of juvenile hormone (JH) has dropped. If the haemolymph titre of JH remains elevated at this time due to topical application of the hormone or of its analogue ZR512, commitment is delayed or inhibited in a dose-dependent manner. This delay or inhibition is due to the curtailment of the commitment peak in the ecdysteroid titre, which results from a failure of the prothoracic glands (PG) to increase the synthesis/secretion of the premoulting hormone, ecdysone. Since the PG from ZR512- and JH 1-treated larvae are capable of being activated in vitro by the prothoracicotropic hormone (PTTH), the effect of JH on the PG does not involve suppression of gland sensitivity to PTTH. The locus of the JH effect was determined to be the brain-retrocerebral complexes (Br-CC-CA), on the basis of experiments which tested the effect of implanted Br-CC-CA from pre-commitment larvae treated with JH on the occurrence of pupal commitment in head-ligated larval hosts. The implanted, JH-treated Br-CC-CA exhibited a delayed release of PTTH, and the effect was at concentrations of JH that were physiological. These results argue that JH functions to control the time during the last larval instar when pupal commitment occurs by dictating when PTTH will undergo gated release.


1989 ◽  
Vol 35 (3) ◽  
pp. 259-274 ◽  
Author(s):  
István Ujváry ◽  
György Matolcsy ◽  
Lynn M. Riddiford ◽  
Kiyoshi Hiruma ◽  
Kathleen L. Horwath

BMC Biology ◽  
2015 ◽  
Vol 13 (1) ◽  
Author(s):  
Nicole E. Hatem ◽  
Zhou Wang ◽  
Keelin B. Nave ◽  
Takashi Koyama ◽  
Yuichiro Suzuki

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