Publisher Summary
This chapter briefly discusses hormonal control of diapause. Diapause is an arrest in development accompanied by a major shutdown in metabolic activity. The evolution of diapause is arguably one of the most critical events bolstering the success of insects. The capacity to periodically shut down development has enabled insects and their arthropod relatives to invade environments that are seasonally hostile. Indeed, very few environments permit continuous insect development. Even in the tropics, where temperatures throughout the year may be compatible with ectotherm development, seasonal patterns of rainfall drive cycles of plant growth that favor insects with the ability to periodically become dormant. Unlike a simple quiescence that is an immediate response to an unfavorable environmental condition, diapause is a genetically programmed response that occurs at a specific stage for each species. Sometimes, the insect will enter diapause at this particular stage in each generation regardless of the environmental conditions it receives—a developmental program referred to as obligatory diapause. Much more frequently, the decision to enter diapause is determined by environmental factors, usually day length, received by that individual or its mother at an earlier developmental stage. This is referred to as facultative diapause.

10 – Hormonal Control of Diapause

7 – The Role of Ecdysteroids in Reproduction

Juvenile hormone prevents ecdysteroid-induced expression of broad complex RNAs in the epidermis of the tobacco hornworm, Manduca sexta.

The Juvenile Hormones

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.

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Kiyoshi Hiruma

Papers

Activation of the prothoracic gland by juvenile hormone and prothoracicotropic hormone in Mamestra brassicae

Possible roles of juvenile hormone in the prepupal stage of Mamestra brassicae

Larval-pupal transformation of the prothoracic glands of Mamestra brassicae

Factors affecting change in sensitivity of prophoracic glands to juvenile hormone in Mamestra brassicae