The endocrine mechanisms controlling the development and reproduction of flight-capable (long-winged) and flightless (short-winged or wingless) morphs of wing-polymorphic insects have been intensively investigated. The “classical model,” put forward in the early 1960s, postulates that morph-specific differences in development and reproduction are caused by variation in the titers of juvenile hormone (JH) and/or ecdysone. Despite decades of study, the importance of these hormones in regulating wing polymorphism in aphids and planthoppers remains uncertain. This uncertainly is largely a consequence of technical and size constraints which have severely limited the types of endocrine approaches that can be used in these insects. Recent studies in wing-polymorphic crickets (Gryllus) have provided the first direct evidence that the in vivo blood titers of juvenile hormone and ecdysone, and especially the activity of the JH regulator, juvenile hormone esterase, differ between nascent morphs. Morph differences are largely consistent with the classical model, although some types of data are problematic, and other explanations are possible. Adult morphs differ dramatically in the JH titer but titer differences are more complex than those proposed by the classical model. Detailed endocrine information is thus far available only for a few species of crickets, and the hormonal control of wing polymorphism for insects as a whole remains poorly understood. Future studies should continue to investigate the role of JH and ecdysteroids in morph development and reproduction, and should expand to include studies of morph-specific differences in hormone receptors and neurohormones.

For almost a century, biologists have used trait scaling relationships (bi-variate scatter-plots of trait size versus body size) to characterize phenotypic variation within populations, and to compare animal shape across populations or species. Scaling relationships are a popular metric because they have long been thought to reflect underlying patterns of trait growth and development. However, the physiological mechanisms generating animal scaling are not well understood, and it is not yet clear how scaling relationships evolve. Here we review recent advances in developmental biology, genetics, and physiology as they pertain to the control of growth of adult body parts in insects. We summarize four mechanisms known to influence either the rate or the duration of cell proliferation within developing structures, and suggest how mutations in these mechanisms could affect the relative sizes of adult body parts. By reviewing what is known about these four processes, and illustrating how they may contribute to patterns of trait scaling, we reveal genetic mechanisms likely to be involved in the evolution of insect form.

The ability to change reproductive tactics during adult development in response to environmental variation is predicted to enhance fitness. Many organisms show phenotypic plasticity early in non-embryonic development, but later exhibit phases of developmental inflexibility (=canalization). Therefore, we studied reproduction-related hormones and proteins and their relationships to plasticity in the Eastern lubber grasshopper. Diet-switching experiments demonstrated plasticity early in the egg production cycle, but a switch to canalization late in the cycle. We measured developmental titers of 4 hemolymph compounds from single individuals from adult molt until first oviposition. These 4 compounds were the egg-yolk precursor protein vitellogenin, juvenile hormone (the central regulator of insect reproduction), major hemolymph proteins, and ecdysteroids (the arthropod molting hormone that ultimately is stored in the egg). Using diet manipulations, we investigated how these developmental titers relate to the switch from plastic to canalized egg production. All 4 hemolymph compounds reached their peak levels during the canalized phase, about 12 day before oviposition. Diet switches after these peak levels did not affect the timing to oviposition. Therefore, these peak titers were physiological events that occurred after the individual committed to laying. We compared these patterns in reproduction to the development toward adult molt, another major life-history event in insects. We observed an extended canalized phase before the adult molt. This canalized phase always included a peak of ecdysteroids. The similar patterns in the physiology of these life-history events suggested that common limitations may exist in major developmental processes of insects that are directed by hormones.

Amphibian larvae respond to heterogeneous environments by varying their rates of growth and development. Several amphibian species are known to accelerate metamorphosis in response to pond drying or resource restriction. Some of the most extensive studies to date on developmental responses to pond drying have been conducted on species of spadefoot toads (family Pelobatidae). We have found that tadpoles of two species of spadefoot toad accelerate metamorphosis when exposed to water volume reduction in the laboratory (to simulate a drying pond). Furthermore, Western spadefoot toad (Spea hammondii) tadpoles accelerated metamorphosis in response to food restriction, which was intended to simulate a decline in resource availability in the larval habitat. Metamorphic acceleration was accompanied by increased whole body 3,5,3′-triiodothyronine and hindbrain corticotropin-releasing hormone content by 24 hr after transfer of tadpoles from high to low water. Food restriction for 4 day accelerated metamorphosis and elevated whole body thyroid hormone content. Although tadpoles accelerated metamorphosis and activated their thyroid axis in response to the two environmental manipulations, the kinetics of the responses were greater for water volume reduction than for resource restriction. The modulation of hormone secretion and action by environmental factors provides a mechanistic basis for plasticity in the timing of amphibian metamorphosis, and the neuroendocrine stress axis may play a central role in developmental plasticity.

In many species of animals, males may achieve reproductive success via one of several alternative reproductive tactics. Over the past decade or so, there has been a concerted effort to investigate endocrine mechanisms that underlie such discrete behavioral (and often morphological) variation. In vertebrates, the first generation of studies focused on potential organizational or activational effects of steroid hormones (Moore, 1991; Moore et al., 1998). Some of these studies have made it clear that, in addition to circulating hormone levels, one must also consider other aspects of the endocrine system, including hormone receptors, binding globulins and potential interactions among endocrine axes. In this paper, I review recent work on endocrine mechanisms and suggest possibilities for future investigation. I highlight how individual variation in sensitivity to environmental conditions, particularly with respect to various stressors, may account for the existence of alternative male reproductive phenotypes. Along these lines, I briefly explain the logic behind our work with male phenotypes of longear sunfish (Lepomis megalotis) that is aimed at determining the tissue-specific distribution and activity of two enzymes that are common to androgen and glucocorticoid metabolism. A major goal of our work is to examine the potential role of steroidogenic enzymes in the transduction of environmental information to influence the expression of alternative male reproductive phenotypes.