scholarly journals The release of the prothoracicotropic hormone in the tobacco hornworm, Manduca sexta, is controlled intrinsically by juvenile hormone

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.

1974 ◽  
Vol 61 (2) ◽  
pp. 493-501 ◽  
Author(s):  
H. FREDERIK NIJHOUT ◽  
CARROLL M. WILLIAMS

During the final larval instar of the tobacco hornworm the presence of juvenile hormone (JH) inhibits the secretion of the brain's prothoracicotropic hormone (PTTH). The corpora allata cease to secrete JH when the larvae attain a weight of approximately 5 g. The JH is cleared from the haemolymph in about 24 h. This process in itself renders the brain competent to release PTTH. The actual release of PTTH occurs at the very first photo-periodic gate after the JH has disappeared from the haemolymph. A functional failure of this normal mechanism is apparently responsible for the developmental standstill of Lepidoptera which diapause as mature larvae.


1987 ◽  
Vol 128 (1) ◽  
pp. 159-173
Author(s):  
R. D. Watson ◽  
T. K. Williams ◽  
W. E. Bollenbacher

A recently isolated haemolymph protein appears to be an important regulator of ecdysone biosynthesis by prothoracic glands in Manduca sexta. Using a dose-response titration protocol, the haemolymph titre of this stimulatory factor was determined during the last larval instar. The titre was high (greater than 2.0 U ml-1) on days 0 and 1, then dropped significantly to 0.55 U ml-1 on day 2, and remained depressed until day 4. The titre of the stimulatory factor then increased to a peak of 1.62 U ml-1 on day 7, and remained elevated (approx. 1.1 U ml-1) until the end of the instar. A set of physical and biochemical criteria was used to confirm that the stimulatory activity present in haemolymph on different days of the instar represented the presence of the factor. The data are consistent with the hypothesis that fluctuations in the titre of the haemolymph stimulatory factor play a critical role in regulating ecdysone biosynthesis during larval-pupal development.


1987 ◽  
Vol 128 (1) ◽  
pp. 175-192
Author(s):  
W. E. Bollenbacher ◽  
N. A. Granger ◽  
E. J. Katahira ◽  
M. A. O'Brien

A larval moult in the tobacco hornworm, Manduca sexta, involves an endocrine cascade that begins with the release of a cerebral peptide hormone, the prothoracicotropic hormone (PTTH). The release of PTTH is gated, occurs during the scotophase and appears to be developmentally cued. In fourth instar Manduca larvae, PTTH release into the haemolymph occurs as a single burst over a few hours during the head critical period, i.e. the time during which the head (brain) is needed for the initiation of the moult to the fifth (last) instar. Released PTTH activates the prothoracic glands (PGs), and within a few hours the cumulative effect of this event results in a dramatic increase in the haemolymph ecdysteroid titre, which then elicits the moult. An assessment of the capacity of the corpora allata (CA) to synthesize juvenile hormone (JH) in vitro indicates that the above sequence of endocrine events begins only when JH synthesis has reached a nadir for the instar. Since CA activity is an indirect measure of the haemolymph titre of the hormone, it is conceivable that the developmentally cued release of PTTH is permissively controlled by a decreasing haemolymph titre of JH. With the increase in the ecdysteroid titre which marks the end of this endocrine cascade, the CA again become active, presumably to cause the increase in the JH haemolymph titre which directs the larval moult. This investigation has thus established the temporal and quantitative dynamics of the PTTH-PG axis that drive larval moulting and provides insight into the interendocrine regulatory relationships that may exist between the ecdysteroids and JHs. These possible relationships and the role of the brain in their regulation are discussed.


1971 ◽  
Vol 26 (2) ◽  
pp. 154-157 ◽  
Author(s):  
Ch. Hintze-Podufal

The two synthetic farnesol derivatives, farnesyl methyl ether and the dihydrochloride of ethylfarnesoate were found to be morphogenetically effective in a distinguishable manner in the last larval instar of Cerura vinula L. by topical application assays. The juvenile hormone-like activity of the two substances correlates with the amount of applied substances and a critical time interval to the prepupal processes. In spite of the deficiency of some prepupal processes, it is possible, that the pupal moult occurs after a long period of delay.The time lapse of the pupal development is suggested to be dependent upon some balance of the hormones of the prothoracic glands, ecdysone, and the juvenile hormone of the corpora allata.


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.


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