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PubMed1999

Evidence for helicity in insect diuretic peptide hormones: computational analysis, spectroscopic studies, and biological assays.

The conformation of four insect diuretic hormones has been analyzed computationally using secondary structure prediction routines and comparison with structures in the Brookhaven Protein Databank. Based on this analysis, a common seven-residue peptide fragment (DVLRQRL) had a high probability of forming an alpha-helix. Circular dichroism (CD) studies found that addition of trifluoroethanol (TFE) to an aqueous solution of the seven-residue fragment induces a change from random coil to helix. Subsequent NMR studies in water-TFE (1:1) produced nOe values and 3JalphaNH coupling constants confirming a helical conformation: 3JalphaNH coupling constants for the first five residues (D1 to Q5) were all < or = 6.0 Hz and two medium-range nOe values (dalphaN (i,i+3)) were observed between V2 and Q5, and R4 and L7. The longer fragments PLDVLRQRL in water-TFE and Lom-DH 1-26 in water alone, both containing the DVLRQRL sequence of the locust (Locusta migratoria) diuretic hormone, maintained the helicity as determined by CD analysis. However, the remaining 20 residues of the locust diuretic hormone did not maintain the same amount of helicity in water and all of the truncated fragments were not biologically active.

Amino Acid Sequence↗
PubMedDate not supplied

[Ecdysteroid agonists of the 1,2-diacyl-1-alkylhydrazine series].

The structures, properties, methods of chemical synthesis, and insect hormonal activities of insecticides of a new 1-alkyl-1,2-diacylhydrazine series are reviewed. They are agonists of ecdysteroids, insect molting hormones, in their action mechanism. The English version of the paper: Russian Journal of Bioorganic Chemistry, 2004, vol. 30, no. 6; see also http://www.maik.ru.

Animals↗
PubMedDate not supplied

Hormonal cross talk in insect development.

Two hormones, 20-hydroxyecdysone (20E) and juvenile hormone (JH), coordinately orchestrate insect growth and development. 20E initiates all major developmental transitions from egg, to larva, to pupa, to adult, but it is an interaction with the JH signal that transduces 20E pulses into stage-specific responses. Years of research have given us an understanding of 20E signaling pathway. By contrast, the molecular mechanism of JH action remains an enigma. Recent studies provide insight into the molecular background to JH-20E regulatory interplay. Two transcription factors--BR-C and E75A--contribute to the cross-talk between the two hormones. It appears that BR-C is a key target of JH status quo action, and E75A is a part of the mechanism whereby JH prevents BR-C activation.

Animals↗
PubMedDate not supplied

An established cell line from the beetle, Xylotrechus pyrrhoderus (Coleoptera: Cerambycidae).

A continuous cell line has been established from larval fat body tissues of the cerambycid beetle Xylotrechus pyrrhoderus Bates. These cells were cultured in MGM-450 medium. The cell line, designated as XP-1, showed a heterogeneous population consisting of spherical and spindle-shaped cells with some capacity to adhere and a doubling time of 5 d. The chromosome number of the cell line ranged from 18 to 42 with a mode of 20. Isozyme analysis showed that the cells had patterns distinctive from those of other insect cell lines. The cells were sensitive to insect hormones, and when continuously treated with 20-hydroxyecdysone and juvenile hormone, they assumed a floating elongated-spindle shape and became strongly adherent, respectively.

Animals↗
PubMedDate not supplied

Degradation of a radiolabeled juvenile hormone analog using two insect species.

A synthetic insect juvenile hormone analog (a juvenoid), ethyl N-[2-[4-[[2,2-(ethylenedioxy)cyclohexyl]methyl]phenox]ethyl]carbam ate, which has displayed high biological activity against different insect species and high stability under field conditions, was selected as a biologically active model compound for a study of a juvenile hormone analog degradation. The biologically active compound itself and its three diversely radiolabeled derivatives were applied to the flesh fly (Sarcophaga bullata) or the tsetse fly (Glossina palpalis), respectively. Monitoring of a fate of the applied juvenile hormone analog was carried out using a detection method of the radioactivity microdistribution within the whole insect body in combination with a radio high performance liquid chromatography (radio-HPLC), both of whole-body extracts made in different, but in advance scheduled, time intervals, and of extracts of insect excreta accumulated over an eight-day experiment.

Animals↗
PubMed2002

Molecular characterization of a Bombyx mori protein disulfide isomerase (bPDI).

We have isolated a complementary deoxyribonucleic acid clone that encodes the protein disulfide isomerase of Bombyx mori (bPDI). This protein has a putative open reading frame of 494 amino acids and a predicted size of 55.6 kDa. In addition, 2 thioredoxin active sites, each with a CGHC sequence, and an endoplasmic reticulum (ER) retention signal site with a KDEL motif were found at the C-terminal. Both sites are typically found in members of the PDI family of proteins. The expression of bPDI messenger ribonucleic acid (mRNA) was markedly increased during ER stress induced by stimulation with calcium ionophore A23187, tunicamycin, and dithiothreitol, all of which are known to cause an accumulation of unfolded proteins in the ER. We also examined the tissue distribution of bPDI mRNA and found pronounced expression in the fat body of insects. Hormonal regulation studies showed that juvenile hormone, insulin, and a combination of juvenile hormone and transferrin (although not transferrin alone) affected bPDI mRNA expression. A challenge with exogenous bacteria also affected expression, and the effect peaked 16 hours after infection. These results suggest that bPDI is a member of the ER-stress protein group, that it may play an important role in exogenous bacterial infection of the fat body, and that its expression is hormone regulated.

Amino Acid Sequence↗
PubMed2003

Conservation of ecdysis-triggering hormone signalling in insects.

Pre-ecdysis- and ecdysis-triggering hormones (PETH and ETH) from endocrine Inka cells initiate ecdysis in moths and Drosophila through direct actions on the central nervous system (CNS). Using immunohistochemistry, we found Inka cells in representatives of all major insect orders. In most insects, Inka cells are numerous, small and scattered throughout the tracheal system. Only some higher holometabolous insects exhibit 8-9 pairs of large Inka cells attached to tracheae in each prothoracic and abdominal segment. The number and morphology of Inka cells can be very variable even in the same individuals or related insects, but all produce peptide hormones that are completely released at each ecdysis. Injection of tracheal extracts prepared from representatives of several insect orders induces pre-ecdysis and ecdysis behaviours in pharate larvae of Bombyx, indicating functional similarity of these peptides. We isolated several PETH-immunoreactive peptides from tracheal extracts of the cockroach Nauphoeta cinerea and the bug Pyrrhocoris apterus and identified the gene encoding two putative ETHs in the mosquito Anopheles gambiae. Inka cells also are stained with antisera to myomodulin, FMRFamide and other peptides sharing RXamide carboxyl termini. However, our enzyme immunoassays show that these antisera cross-react with PETH and ETH. Our results suggest that Inka cells of different insects produce only peptide hormones closely related to PETH and ETH, which are essential endocrine factors required for activation of the ecdysis behavioural sequence.

Animals↗
PubMed1996

Synapse loss and axon retraction in response to local muscle degeneration.

During metamorphosis in the moth, Manduca sexta, the abdominal body-wall muscle DEO1 is remodeled to form the adult muscle DE5. As the larval muscle degenerates, its motoneuron loses its end plates and retracts axon branches from the degenerating muscle. Muscle degeneration is under the control of the insect hormones, the ecdysteroids. Topical application of an ecdysteroid mimic resulted in animals that produced a localized patch of pupal cuticle. Muscle fibers underlying the patch showed a gradient of degeneration. The motoneuron showed end-plate loss and axon retraction from degenerating regions of a given fiber but maintained its fine terminal branches and end plates on intact regions. The results suggest that local steroid treatments that result in local muscle degeneration bring about a loss of synaptic contacts from regions of muscle degeneration.

Animals↗
PubMed1990

Diversity and unity in the nuclear hormone receptors: a terpenoid receptor superfamily.

The remarkable structural unity among the different members of the nuclear hormone receptor superfamily stands in striking contrast to the diversity of the chemical structures of their ligands. Of the three currently known classes of ligands, steroids, retinoids, and thyroid hormones, the first two share a common biosynthetic pathway. Both are terpenes, which are derived by assembly of isoprene units. This biosynthetic link suggests that the receptors for three other classes of terpenoid hormones, the insect juvenile hormones and the plant hormones gibberellic acid and abscissic acid, may also be members of the superfamily. A number of putative nuclear hormone receptors that do not have known ligands have been isolated. At least some of the ligands for these orphan members of the receptor superfamily may be found on the list of biologically active terpenes. Finally, the terpenoid connection raises interesting issues for the evolution of the receptor superfamily.

Animals↗
PubMed1996

An insect juvenile hormone-specific epoxide hydrolase is related to vertebrate microsomal epoxide hydrolases.

We describe the first cDNA sequence encoding a juvenile hormone-specific epoxide hydrolase from an insect. A full-length cDNA clone revealed a 462-amino-acid open reading frame encoding an amino acid sequence with 44% identity and 64% similarity to human microsomal epoxide hydrolase. All residues in the catalytic triad (residues Asp227-His428-Asp350 in the M. sexta protein) were present, as was the conserved Trp154 corresponding to the oxyanion hole. The surprising similarity of insect juvenile hormone epoxide hydrolase to vertebrate microsomal epoxide hydrolases, coupled with the ancient lineage of the epoxide hydrolases and haloalkane dehalogenases, suggests that this catabolic enzyme evolved from an original ubiquitous detoxication function to a more recent role in hormonal regulation.

Amino Acid Sequence↗
PubMed1987

Chemistry of pheromone and hormone metabolism in insects.

Chemical evidence is needed in both insect endocrinology and sensory physiology to understand hormone and pheromone action at the molecular level. Radiolabeled pheromones and hormones have been synthesized and used to identify binding and catabolic proteins from insect tissues. Chemically modified analogs, including photoaffinity labels and enzyme inhibitors, are among the tools used to covalently modify the specific acceptor or catalytic sites. Such targeted agents can also provide leads for the design of growth and mating disruptants by allowing manipulation of the physiologically important interactions of the chemical signals with macromolecules.

Animals↗
PubMed1994

Larva lights: a decade of photoaffinity labeling with juvenile hormone analogues.

The introduction of photoaffinity labeling into the mode of action of insect hormones and pheromones started 12 yr ago with the photoaffinity labeling of juvenile hormone binding proteins (JHBPs) from cockroaches in the laboratory of the late John K. Koeppe. Applying this technique to Manduca sexta led ultimately to a three-laboratory collaborative project that has begun to dissect the molecular basis for JH transport, metabolism, and nuclear binding and gene activation in Lepidoptera. This review provides (1) a history of the first experiments; (2) an idea of the breadth of the technique in the arthropod classes Insecta, Crustacea, and Arachnida; and (3) evidence for the depth of the technique in unearthing key details about three different types of the molecular action of JH in M. sexta.

Affinity Labels↗
PubMed1993

Hormonal control of transmitter plasticity in insect peptidergic neurons. I. Steroid regulation of the decline in cardioacceleratory peptide 2 (CAP2) expression.

Transmitter plasticity, the ability to alter transmitter expression, has been documented in several different preparations both in vivo and in vitro. One of these is the tobacco hawkmoth, Manduca sexta, whose central nervous system contains four individually identified lateral neurosecretory cells (LNCs) that undergo a postembryonic transmitter switch in vivo. In larvae, the LNCs express high levels of a myoregulatory peptide, cardioacceleratory peptide 2 (CAP2). In contrast, the predominant LNC transmitter in adult moths in bursicon, a classic insect peptide hormone responsible for cuticular tanning. Here we show that the CAP2-to-bursicon conversion by the LNCs is a multi-step process beginning with a decline in CAP2 levels midway through the final larval stage. We provide several lines of evidence that this CAP2 drop is regulated by the insect steroid hormone 20-hydroxyecdysone (20-HE). The LNCs exhibit a fall in CAP2 levels at the beginning of metamorphosis, immediately after the commitment pulse of 20-HE when steroid levels are elevated. LNCs not exposed to this 20-HE rise do not exhibit a decline in CAP2 level. The transmitter switch can also be prevented by using an analog of juvenile hormone to create a larval hormonal environment during the commitment pulse of 20-HE. The CAP2 decline in the LNCs could be directly induced by exogenous steroid application, but only under conditions where the LNCs remained connected to the brain. Thus, the first step in the transmitter switch by the LNCs, the decline in CAP2 levels, is triggered by the commitment pulse of 20-HE, which may act indirectly through a set of steroid-sensitive cells in the brain.

Animals↗
PubMedDate not supplied

[The role of microsporidia in the disturbance of the hormonal balance in the infected insects].

Since investigations of Fisher and Sanborn (1964), the most popular point of view on pathological alterations in the development of insects is the statement that microsporidians can produce and secrete the insect juvenile hormone in infected tissues. We suppose that the juvenilizing effect of microsoporidian infection may be a consequence of stress induced by the protozoan invasion. To our opinion, microsporidians can not be a source of juvenile hormone in parasitized insects because of several reasons. 1. The juvenilizing effect of infection may be explained by other reason, that is the stress effect of invasion. 2. Until now nobody can find juvenile hormone in microsporidians. 3. An increase of juvenile hormone titre either alters non-metabolic activity of fat body or alters it in a way that is not favorable for microsporidias. 4. Some effects of the microsporidian infection more resemble an action of ecdysone, but not juvenile hormone. Hypothesis of parasitic stress can explain this, while hypothesis of production JH by microsporidians can not. 5. An effect of invasion by parasites of other systematic groups onto the hormone balance is of the same type. But nobody thinks that other parasites can produce juvenile hormone. Nevertheless it is clear that a high titre of the juvenile hormone is favorable for the microsporidian infection in larvae, especially the last instars. The most descriptions of microsporidian infections are related with this age of insects. Juvenilizing effect of Nosema implantant in the work of Fisher and Sanborn (1964) may be easily explained by decreasing of JH-esterase activity. But in this case the decrease of JH-esterase activity after the implantation of infected tissue in a healthy insect should be explained. We suppose that this fact witness the existence of stress-factor produced by damaged cells of fat body that can enter the healthy cells of fat body and inhibit the activity of JH-esterases.

Animals↗
PubMed1990

Resistance to juvenile hormone and an insect growth regulator in Drosophila is associated with an altered cytosolic juvenile hormone-binding protein.

The Met mutant of Drosophila melanogaster is highly resistant to juvenile hormone III (JH III) or its chemical analog, methoprene, an insect growth regulator. Five major mechanisms of insecticide resistance were examined in Met and susceptible Met+ flies. These two strains showed only minor differences when penetration, excretion, tissue sequestration, or metabolism of [3H]JH III was measured. In contrast, when we examined JH III binding by a cytosolic binding protein from a JH target tissue, Met strains had a 10-fold lower binding affinity than did Met+ strains. Studies using deficiency-bearing chromosomes provide strong evidence that the Met locus controls the binding protein characteristics and may encode the protein. These studies indicate that resistance in Met flies results from reduced binding affinity of a cytosolic binding protein for JH III.

Adipose Tissue↗
PubMedDate not supplied

[Impact of microsporidia on hormonal balance in insect hosts].

Microsporidia (M) is a phylum of protists parasitizing obligatory in animal cells. Long way of adaptation of M to intracellular parasitism resulted in establishment of quite close relationships between the parasite and its host. Different species of M induce in their hosts symptoms similar to those caused by misbalance of juvenile hormone (JH) and ecdysone. M infection leads to pathology of different hormone-dependent functions such as cell differentiation and specialization, molting, metamorphosis, diapause and reproduction of insects. The signs of hormonal dysfunction evidence for elevated titer of JH in M-infected insects. Two possible explanation of this could be offered: JH secretion by M or specific influence of the parasites on the insect endocrine systems. Impact on insect endogenous JH titer by M could be mediated by affection of secretory activity of corpora allata or by suppression of enzymatic degradation of JH. According to different hypotheses, insect hormonal status during microsporidiosis could be modified by a) insect host stress-reaction, b) exhaustion of insect host reserves, characteristic for acute phase of the disease, c) destruction of infected insect cells and tissues during mass sporogenesis of M. Data found in literature and provided by our experiments evidence for presence of JH analogues or juvenilizing substance in the extracts of M spores. From detailed examination of pathological process it is also seen that juvenilizing effect of M infection is usually restricted to the invaded regions of tissues (i.e. expressed locally) but not a systemic one. Ability of M to modify morpho-functional features of infected tissues at the level of hormonal regulation is undoubtfully a prominent adaptation for stabilizing "microsporidia-insect" parasite-host systems.

Adaptation, Physiological↗
PubMed2007

The role of allatostatins in juvenile hormone synthesis in insects and crustaceans.

Allatostatins are pleiotropic neuropeptides for which one function in insects is the inhibition of juvenile hormone synthesis. Juvenile hormone, an important regulator of development and reproduction in insects, is produced by the corpora allata. Mandibular organs, the crustacean homologs of insect corpora allata, produce precursors of juvenile hormone with putatively similar functions. Three types of allatostatins in insects have been isolated: FGLamides, W(X)(6)Wamides, and PISCFs. All act rapidly and reversibly; however, although these types occur in all groups of insects studied, they act as inhibitors of juvenile hormone production in only some groups. Only the FGLamide-type peptides have been isolated in crustaceans, in which they may function to stimulate production of hormone by the mandibular glands, as occurs in early cockroach embryos. Much remains to be learned in order to understand the role of allatostatins in the modulation of hormone production.

Animals↗