Insect hormones control a broad range of processes in the insect life cycle, both developmental and physiological. These include the metabolism of carbohydrates and lipids, the maintenance of water balance, including excretion of water after a blood meal, stimulation and inhibition of the circulatory system and the firing of muscles, growth, including molting and metamorphosis, diapause (a period of suspended growth or development), apoptosis, reproduction, caste determination (which occurs in social insects, such as bees and ants, whose fate as queen or worker is determined not by genes but by differential feeding and pheromone exposure at the larval stage), and aspects of behavior during molting and migration, reproductive and other social behaviors, and response to pheromones.
Insects produce two general classes of hormones, as do vertebrates, lipid or steroid (lipophilic) hormones and polar (hydrophilic) peptides, and their mode of action depends on how the hormone interacts with the cell membrane (peptide hormones are coded directly by genes; the other forms are the product of enzymatic reactions for which the enzymes, but not the final hormone product, are genetically coded). Being hydrophobic, the lipid hormones pass readily through the cell wall to bind with receptors in the cytoplasm or nucleus of the cell. The hormone-receptor complex in turn binds with specific DNA sequences to initiate, enhance, or inhibit gene expression. The peptide hormones, however, do not easily pass through the cell membrane but instead bind with receptors on the cell surface, which transduce the signal to second messengers inside the cell, often via a G protein cascade. Target cells are not continuously receptive to hormone stimulation. There are "hormonesensitive periods," and although hormones circulate throughout the hemolymph, exposing all tissues to the same levels of hormone at the same time, the tissues are not all equally receptive. What controls the timing of the sensitivity of a tissue is not known, but clearly both the signaling and receiving cells need to be prepared, implying a prior element of differentiation in these two, often distant, locations in the body.
Insects synthesize hormones in two distinct organ systems: endocrine tissues and neurosecretory cells. The glandular endocrine tissues are specialized for the synthesis and release of hormones. The most important endocrine glands in insects are the prothoracic glands, which secrete ecdysteroids during development, and the corpora allata, where the juvenile hormones are produced and secreted.The ovaries and testes of many adult insects also produce ecdysteroids.
The gross morphology of the prothoracic glands varies widely throughout insect phylogenies, both in size and in location in the body, but the cellular structure is quite uniform (Nijhout 1994). As in vertebrates, probably because of shared ancestry, the distinction between the nervous and endocrine systems is not clear-cut; homologous nerves of the CNS in all species generally innervate the prothoracic glands, and some of these are neurosecretory and are involved in regulating secre-
Site of Synthesis
Ecdysone (an ecdysteroid) Thoracic glands
Stimulate secretion hormone of ecdysone
Promote growth, control molting, embryonic development
Ecdysone (an ecdysteroid) Thoracic glands
Induce apolysis, cell division, degradation of old cuticle, production of new
Development, metabolism, behavior
Control of hardening of new cuticle tions from the prothoracic glands (Nijhout 1994). These glands secrete, but do not store, ecdysone, a steroid that promotes growth and controls molting. In most insects, the prothoracic glands undergo apoptosis during the metamorphosis of the larva to adult stage and ecdysone is then no longer synthesized and released.
Molting is essential if an insect is to change size or shape because the insect's hard outer shell, or cuticle, cannot accommodate growth by expanding (in contrast to the endoskeleton of vertebrates, which grows along with the individual). The process is complex, involving the formation of a new cuticle within the old one while the old one is digested and the proteins reused. Therefore, the new cuticle must be protected against degradation by the digestive enzymes and at the same time remain pliable enough to expand when the old cuticle is shed (Nijhout 1994). Chemical assault to interfere with normal molting is one insecticide strategy.
Molting cycles are triggered by the secretion of the prothoracicotropic hormone (PTTH), which is produced by neurosecretory cells in the brain. The only known function of PTTH is to stimulate the secretion of the molting hormone ecdysone by the two prothoracic glands in the thorax. These two hormones trigger every molt, whether larva to larva or pupa to adult. Levels of a different set of hormones, the juvenile hormones (JHs), control metamorphosis.
The corpora allata are a pair of small glands found along the main vessel in the neck of most insects and are attached to the brain by a nerve that passes through the corpora cardiaca (additional small glands just anterior to the corpora allata). The corpora allata produce JHs. Innervation of the corpora allata is by nerves that conduct impulses, as well as by neurosecretory neurons. In some insects the corpora allata are also neurohemal organs for some neural secretions from the brain. The brain and these associated neurohemal glands form the brain-retrocerebral neuroendocrine complex, a control, synthesis, and excretion system that is the most important neuroendocrine organ in the insect endocrine system.
JHs serve both as regulatory and developmental hormones and have a role in every aspect of insect life, from development to metabolism to some behaviors. Three major forms of JH are known; some insects secrete only one, others two or all three. After secretion from the corpora allata, JHs bind to the juvenile hormone binding proteins, which increase the solubility of the hormones in the hemolymph and protect them from degradation. JHs are lipid hormones, but their mode of entry into the cell, and subsequently into the nucleus, is not yet definitively known (Davey
2000). It may be that juvenile hormone binding proteins chaperone JHs into the cell and regulate their binding to JH-specific receptors once there.
As in plants, insect hormones have an antagonistic or complementary relationship with each other and highly tissue-localized, specifically timed gene expression. The presence of JHs prevents a juvenile insect from becoming an adult (thus the nomenclature) by suppressing secretion by the brain of hormones involved in molting and metamorphosis. The process is complicated and depends on JH-sensitive periods during the molting cycle. Basically, when the insect is JH sensitive and JH is present, the insect does not molt. If JH is absent, the developmental stage changes. This generally depends on the secretion of ecdysone having already initiated the next molt. Different sections of the epidermis have different JH-sensitive periods. The onset of JH-sensitive periods is independent of presence or absence of JH, and it is during this period that a cell can be committed to a specific developmental fate. Usually, it requires the action of ecdysteroids, however. JHs are pleiotropic and play different roles at different stages in the life cycle (see below).
Ecdysteroids are a family of steroids that includes ecdysone and its analogs and metabolites. These compounds are found in insects and crustaceans and in some plants as phytoecdysone. Nearly 100 of these compounds have been described in insects and other arthropods, and more than 200 have been isolated from plants (Sadikov et al. 2000). These hormones promote growth and control molting and play a role in embryonic development. Ecdysteroids are lipid hormones and act by enhancing or inhibiting gene transcription. The hormone-receptor complex usually binds a G protein inside the cell to initiate the signaling cascade.
Ecdysone is produced by the thoracic glands and is a relatively inactive prohormone that becomes active when converted by the fat body and epidermal cells into 20-hydroxyecdysone, the most important molting hormone in insects (Nijhout 1994). Ecdysteroid action is the same at all stages of insect life; these hormones act on epidermal cells to induce apolysis (the first step in the synthesis of a new exoskeleton), cell division, degradation of the old cuticle, and production of the new. As with other hormones, ecdysteroid concentrations are affected by the concentration of other hormones. In this case, ecdysteroid secretion depends on the pattern of PTTH secretion in the brain.
When the new-stage insect emerges from the old cuticle of the previous stage, initiating a new instar (the phase between molts) in a process called ecdysis, the new cuticle must harden or tan. This is controlled by a neurosecretory hormone called bursicon, except in the higher Diptera in which it is controlled by a set of neurose-cretory hormones called pupariation factors. The principal source of bursicon is the abdominal ganglia, and the hormone is released into the hemolymph from the abdominal previsceral organs, although it is synthesized throughout the nervous system, including the brain.
The ecdysone signal is transduced by the ecdysone receptor, a heterodimer formed by the joining of two nuclear receptor proteins, EcR (Ecdysone receptor) and Usp (Drosophila Ultraspiracle receptor), a homolog of the vertebrate nuclear receptor RXR (Retinoid X receptor) family of ligand-dependent transcription factors (TFs) (Arbeitman and Hogness 2000; Ghbeish et al. 2001; Mouillet et al.
2001).The RXR receptors have two signature domains, the DNA binding and ligand binding domains. The ecdysone receptor requires not only heterodimerization for DNA binding, as do the RXR family of receptors, but also for ligand binding, a characteristic it does not share with the RXR receptors. Through alternative splicing and two promoters, the EcR gene encodes three protein isoforms, EcRA, EcRBl, and EcRB2, each with different quantitative control over transcription (Mouillet, Henrich et al. 2001). Each of the three isoforms is able to dimerize with the Usp receptor, and this may explain how it is that ecdysone can initiate the large variety of responses, at various stages in the life cycle, that it does (Mouillet, Henrich et al. 2001).
The ecdysone signal activates a hierarchical response when bound to the receptor, turning on a small set of early genes that in turn activate a larger set of genes downstream. In vertebrates, activation of the homodimeric steroid receptors depends on the presence of a molecular chaperone-containing heterocomplex (MCH), which interacts with the receptors, probably to facilitate protein folding and DNA binding by their ligands. The presence of an MCH seems to be required to activate the ecdysone pathway as well (Arbeitman and Hogness 2000).
Molting is a good example to illustrate the importance under some circumstances of centrally coordinated signaling. We mentioned in Chapter 9 that some structures like limbs or teeth cannot develop until a place has been prepared for that to happen. In this case, prepatterning of cells to respond to later signals is likely to be a mechanism that enables this delayed, context-specific response to occur. An entire insect must be ready before molting can occur. At the appropriate time, a central signal is released that affects the whole body.
The second insect organ system that secretes hormones consists of the neurosecre-tory cells of the CNS, neurons that produce small polypeptides, or neurohormones. These cells tend to be localized in the brain, although they are found in all the ganglia of the CNS; they have axons that end in neurohemal organs or areas, where the secretions are released directly into the hemolymph.
Adult insects do not undergo molting or development, so in adults the same ecdysteroids, JHs, and various neuroendocrine hormones that controlled these processes earlier in life control adult processes like diapause, migratory behavior, and reproduction—the production of yolk proteins, maturation of the ovaries, and synthesis of eggs (Hartfelder 2000; Nijhout 1994). As a generalization about hormone action in insects, a given hormone can have different effects in different target tissues and different effects on the same tissue at a different time in the life cycle. Once again we see the use and reuse of a mechanism, showing the importance of context specificity in the inducing mechanisms (which themselves may have multiple uses). As we have mentioned in Chapter 9 in context with the apparently inconsistent inductive/inhibitory effects of Dorsal protein, the specific effect of a signaling substance ultimately depends on the nature of the regulatory regions associated with a gene, and the combination of factors that must bind jointly there to activate or inhibit a gene.
Crustaceans have a number of endocrine mechanisms in common with insects, including production of methyl farnesoate (MF), a hormone that is the precursor of insect JH. MF seems to play a role in reproduction in crustaceans. Interestingly, although many of these substances are found in insects and crustaceans, they do not necessarily play the same role in both.
The eyestalk neurosecretory complex of decapod crustaceans is the location of the sinus gland, the source of a number of neuropeptide hormones, including those involved in pigment migration (red pigment-concentrating hormone and pigment-dispersing hormone), regulation of carbohydrate metabolism (crustacean hyper-glycemic hormone, CHH), molting (molt-inhibiting hormone, MIH), and gonadal growth (gonad-inhibiting hormone, GIH) (Webster 1998). These neuropeptides have been found to play an inhibitory role, acting on endocrine tissues that produce the hormones that initiate reproduction and molting. DNA sequencing has shown that the genes for these hormones are structurally related. Again, they are also pleiotropic; CHH, for example, has a role in molting and in reproduction as well as in carbohydrate metabolism. Other neuroendocrine centers are located throughout the CNS, including, as well as the eyestalk, the brain and the subesophageal ganglion.
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